A condition characterized by an abnormal increase of BILIRUBIN in the blood, which may result in JAUNDICE. Bilirubin, a breakdown product of HEME, is normally excreted in the BILE or further catabolized before excretion in the urine.
Accumulation of BILIRUBIN, a breakdown product of HEME PROTEINS, in the BLOOD during the first weeks of life. This may lead to NEONATAL JAUNDICE. The excess bilirubin may exist in the unconjugated (indirect) or the conjugated (direct) form. The condition may be self-limiting (PHYSIOLOGICAL NEONATAL JAUNDICE) or pathological with toxic levels of bilirubin.
A bile pigment that is a degradation product of HEME.
Yellow discoloration of the SKIN; MUCOUS MEMBRANE; and SCLERA in the NEWBORN. It is a sign of NEONATAL HYPERBILIRUBINEMIA. Most cases are transient self-limiting (PHYSIOLOGICAL NEONATAL JAUNDICE) occurring in the first week of life, but some can be a sign of pathological disorders, particularly LIVER DISEASES.
A term used pathologically to describe BILIRUBIN staining of the BASAL GANGLIA; BRAIN STEM; and CEREBELLUM and clinically to describe a syndrome associated with HYPERBILIRUBINEMIA. Clinical features include athetosis, MUSCLE SPASTICITY or hypotonia, impaired vertical gaze, and DEAFNESS. Nonconjugated bilirubin enters the brain and acts as a neurotoxin, often in association with conditions that impair the BLOOD-BRAIN BARRIER (e.g., SEPSIS). This condition occurs primarily in neonates (INFANT, NEWBORN), but may rarely occur in adults. (Menkes, Textbook of Child Neurology, 5th ed, p613)
A benign familial disorder, transmitted as an autosomal dominant trait. It is characterized by low-grade chronic hyperbilirubinemia with considerable daily fluctuations of the bilirubin level.
Treatment of disease by exposure to light, especially by variously concentrated light rays or specific wavelengths.
Inborn errors of bilirubin metabolism resulting in excessive amounts of bilirubin in the circulating blood, either because of increased bilirubin production or because of delayed clearance of bilirubin from the blood.
Repetitive withdrawal of small amounts of blood and replacement with donor blood until a large proportion of the blood volume has been exchanged. Used in treatment of fetal erythroblastosis, hepatic coma, sickle cell anemia, disseminated intravascular coagulation, septicemia, burns, thrombotic thrombopenic purpura, and fulminant malaria.
Mutant strain of Rattus norvegicus which is used as a disease model of kernicterus.
A clinical manifestation of HYPERBILIRUBINEMIA, characterized by the yellowish staining of the SKIN; MUCOUS MEMBRANE; and SCLERA. Clinical jaundice usually is a sign of LIVER dysfunction.
A family of enzymes accepting a wide range of substrates, including phenols, alcohols, amines, and fatty acids. They function as drug-metabolizing enzymes that catalyze the conjugation of UDPglucuronic acid to a variety of endogenous and exogenous compounds. EC 2.4.1.17.
A familial form of congenital hyperbilirubinemia transmitted as an autosomal recessive trait. It is characterized by icterus and brain damage caused by a glucuronyl transferase deficiency in the liver and faulty bilirubin conjugation.
A benign, autosomally recessive inherited hyperbilirubinemia characterized by the presence of a dark pigment in the centrilobular region of the liver cells. There is a functional defect in biliary excretion of bilirubin, cholephilic dyes, and porphyrins. Affected persons may be asymptomatic or have vague constitutional or gastrointestinal symptoms. The liver may be slightly enlarged, and oral and intravenous cholangiography fails to visualize the biliary tract.
An infant during the first month after birth.
CHILDBIRTH at the end of a normal duration of PREGNANCY, between 37 to 40 weeks of gestation or about 280 days from the first day of the mother's last menstrual period.
The identification of selected parameters in newborn infants by various tests, examinations, or other procedures. Screening may be performed by clinical or laboratory measures. A screening test is designed to sort out healthy neonates (INFANT, NEWBORN) from those not well, but the screening test is not intended as a diagnostic device, rather instead as epidemiologic.
A disease-producing enzyme deficiency subject to many variants, some of which cause a deficiency of GLUCOSE-6-PHOSPHATE DEHYDROGENASE activity in erythrocytes, leading to hemolytic anemia.
An organic anion transporter found in human liver. It is capable of transporting a variety organic anions and mediates sodium-independent uptake of bile in the liver.
An antigenic mismatch between donor and recipient blood. Antibodies present in the recipient's serum may be directed against antigens in the donor product. Such a mismatch may result in a transfusion reaction in which, for example, donor blood is hemolyzed. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984).
A condition characterized by the abnormal presence of ERYTHROBLASTS in the circulation of the FETUS or NEWBORNS. It is a disorder due to BLOOD GROUP INCOMPATIBILITY, such as the maternal alloimmunization by fetal antigen RH FACTORS leading to HEMOLYSIS of ERYTHROCYTES, hemolytic anemia (ANEMIA, HEMOLYTIC), general edema (HYDROPS FETALIS), and SEVERE JAUNDICE IN NEWBORN.
Porphyrins which are combined with a metal ion. The metal is bound equally to all four nitrogen atoms of the pyrrole rings. They possess characteristic absorption spectra which can be utilized for identification or quantitative estimation of porphyrins and porphyrin-bound compounds.
Graphical representation of a statistical model containing scales for calculating the prognostic weight of a value for each individual variable. Nomograms are instruments that can be used to predict outcomes using specific clinical parameters. They use ALGORITHMS that incorporate several variables to calculate the predicted probability that a patient will achieve a particular clinical endpoint.
The degree of antigenic similarity between tissues of the mother and those of the FETUS. Maternal-fetal histocompatibility can determine the acceptance and health of the fetus.
A mixed function oxidase enzyme which during hemoglobin catabolism catalyzes the degradation of heme to ferrous iron, carbon monoxide and biliverdin in the presence of molecular oxygen and reduced NADPH. The enzyme is induced by metals, particularly cobalt. EC 1.14.99.3.
Hearing loss due to disease of the AUDITORY PATHWAYS (in the CENTRAL NERVOUS SYSTEM) which originate in the COCHLEAR NUCLEI of the PONS and then ascend bilaterally to the MIDBRAIN, the THALAMUS, and then the AUDITORY CORTEX in the TEMPORAL LOBE. Bilateral lesions of the auditory pathways are usually required to cause central hearing loss. Cortical deafness refers to loss of hearing due to bilateral auditory cortex lesions. Unilateral BRAIN STEM lesions involving the cochlear nuclei may result in unilateral hearing loss.
Porphyrins with four methyl, two vinyl, and two propionic acid side chains attached to the pyrrole rings. Protoporphyrin IX occurs in hemoglobin, myoglobin, and most of the cytochromes.
A potent and specific HIV protease inhibitor that appears to have good oral bioavailability.
The major human blood type system which depends on the presence or absence of two antigens A and B. Type O occurs when neither A nor B is present and AB when both are present. A and B are genetic factors that determine the presence of enzymes for the synthesis of certain glycoproteins mainly in the red cell membrane.
The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.
A human infant born before 37 weeks of GESTATION.
A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
A test to detect non-agglutinating ANTIBODIES against ERYTHROCYTES by use of anti-antibodies (the Coombs' reagent.) The direct test is applied to freshly drawn blood to detect antibody bound to circulating red cells. The indirect test is applied to serum to detect the presence of antibodies that can bind to red blood cells.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
The use of ultraviolet electromagnetic radiation in the treatment of disease, usually of the skin. This is the part of the sun's spectrum that causes sunburn and tanning. Ultraviolet A, used in PUVA, is closer to visible light and less damaging than Ultraviolet B, which is ionizing.
Impairment of bile flow due to obstruction in small bile ducts (INTRAHEPATIC CHOLESTASIS) or obstruction in large bile ducts (EXTRAHEPATIC CHOLESTASIS).
Proteins involved in the transport of organic anions. They play an important role in the elimination of a variety of endogenous substances, xenobiotics and their metabolites from the body.
Imino acids are organic compounds containing a nitrogen atom in their structure, classified as derivatives of amino acids, where the carbon atom adjacent to the carboxyl group is bonded to a nitrogen atom instead of a hydrogen atom, forming a characteristic imino functional group.
A condition of inadequate circulating red blood cells (ANEMIA) or insufficient HEMOGLOBIN due to premature destruction of red blood cells (ERYTHROCYTES).
'Infant, Premature, Diseases' refers to health conditions or abnormalities that specifically affect babies born before 37 weeks of gestation, often resulting from their immature organ systems and increased vulnerability due to preterm birth.
Removal of plasma and replacement with various fluids, e.g., fresh frozen plasma, plasma protein fractions (PPF), albumin preparations, dextran solutions, saline. Used in treatment of autoimmune diseases, immune complex diseases, diseases of excess plasma factors, and other conditions.
A radiopharmaceutical used extensively in cholescintigraphy for the evaluation of hepatobiliary diseases. (From Int Jrnl Rad Appl Inst 1992;43(9):1061-4)
A legal requirement that designated types of information acquired by professionals or institutions in the course of their work be reported to appropriate authorities.
Peptides composed of between two and twelve amino acids.
Minute intercellular channels that occur between liver cells and carry bile towards interlobar bile ducts. Also called bile capillaries.
Glucose-6-Phosphate Dehydrogenase (G6PD) is an enzyme that plays a critical role in the pentose phosphate pathway, catalyzing the oxidation of glucose-6-phosphate to 6-phosphoglucono-δ-lactone while reducing nicotinamide adenine dinucleotide phosphate (NADP+) to nicotinamide adenine dinucleotide phosphate hydrogen (NADPH), thereby protecting cells from oxidative damage and maintaining redox balance.
Subsequent admissions of a patient to a hospital or other health care institution for treatment.
The age of the conceptus, beginning from the time of FERTILIZATION. In clinical obstetrics, the gestational age is often estimated as the time from the last day of the last MENSTRUATION which is about 2 weeks before OVULATION and fertilization.
Diversion of blood flow through a circuit located outside the body but continuous with the bodily circulation.

A patient with hypertrophic cardiomyopathy accompanied by right ventricular dilation of unknown cause. (1/291)

Hypertrophic cardiomyopathy (HCM) is a disease characterized by an unknown cause of hypertrophy in the left or right ventricle. The dilated phase of HCM shows disease conditions resembling dilated cardiomyopathy, such as ventricular dilation, thin ventricular wall, and reduction of the ejection fraction. A patient presented with left ventricular concentric hypertrophy accompanied by right ventricular dilatation of unknown cause. Right ventricular endomyocardial biopsy specimens showed characteristic myocardial disarray. Therefore, there is the possibility that the patient had right and left ventricular HCM in the process toward the dilated phase, in which dilatation first occurred in the right ventricle.  (+info)

Co-inherited Gilbert's syndrome: a factor determining hyperbilirubinemia in homozygous beta-thalassemia. (2/291)

BACKGROUND AND OBJECTIVE: Patients with thalassemia major and intermedia show a marked variability of serum indirect bilirubin levels. In this paper we tested the hypothesis related to the variability of the glucuronidation bilirubin rate which depends on the configuration of the A(TA)nTAA motif of the UGT1*1 glucuronosyltransferase gene promoter. DESIGN AND METHODS: We studied the configuration of the A(TA)nTAA motif in 26 patients with thalassemia major and 34 with thalassemia intermedia. RESULTS: In patients with thalassemia major and in those with thalassemia intermedia significantly higher bilirubin levels were found in patients with the (TA)7/(TA)7 genotype, than in those with the (TA)7/(TA)6 or (TA)6/(TA)6 genotype. INTERPRETATION AND CONCLUSIONS: These results indicate that the (TA)7/(TA)7 genotype, the configuration found in patients with Gilbert's syndrome, is capable of modifying the clinical phenotype of homozygous beta-thalassemia. This is an example of the role played by co-inherited modifying gene(s) on the extent of clinical heterogeneity of monogenic disorders.  (+info)

Serum malondialdehyde concentration in babies with hyperbilirubinaemia. (3/291)

AIM: To determine lipid peroxide concentrations in the first 10 days of life. METHODS: Malondialdehyde concentrations were investigated in neonates with or without hyperbilirubinaemia during the first 10 days of life. RESULTS: Serum malondialdehyde concentrations were higher in infants with hyperbilirubinaemia than in controls. A positive correlation was found between malondialdehyde and bilirubin concentrations in the study group. When the study group was categorised according to the presence of haemolysis, a significant correlation was found between malondialdehyde and bilirubin concentrations in those infants with hyperbilirubinaemia due to haemolysis. There was no such correlation in those without haemolysis. CONCLUSION: Exchange transfusion rapidly produces variable changes in pro-oxidant and antioxidant plasma concentrations in neonates, which may be responsible for free radical metabolism. The fall in malondialdehyde concentration is probably directly related to its exogenous removal by exchange transfusion.  (+info)

Effect of liver disease and transplantation on urea synthesis in humans: relationship to acid-base status. (4/291)

It has been suggested that hepatic urea synthesis, which consumes HCO-3, plays an important role in acid-base homeostasis. This study measured urea synthesis rate (Ra urea) directly to assess its role in determining the acid-base status in patients with end-stage cirrhosis and after orthotopic liver transplantation (OLT). Cirrhotic patients were studied before surgery (n = 7) and on the second postoperative day (n = 11), using a 5-h primed-constant infusion of [15N2]urea. Six healthy volunteers served as controls. Ra urea was 5.05 +/- 0.40 (SE) and 3.11 +/- 0.51 micromol. kg-1. min-1, respectively, in controls and patients with cirrhosis (P < 0. 05). Arterial base excess was 0.6 +/- 0.3 meq/l in controls and -1.1 +/- 1.3 meq/l in cirrhotic patients (not different). After OLT, Ra urea was 15.05 +/- 1.73 micromol. kg-1. min-1, which accompanied an arterial base excess of 7.0 +/- 0.3 meq/l (P < 0.001). We conclude that impaired Ra urea in cirrhotic patients does not produce metabolic alkalosis. Concurrent postoperative metabolic alkalosis and increased Ra urea indicate that the alkalosis is not caused by impaired Ra urea. It is consistent with, but does not prove, the concept that the graft liver responds to metabolic alkalosis by augmenting Ra urea, thus increasing HCO-3 consumption and moderating the severity of metabolic alkalosis produced elsewhere.  (+info)

MRP3, a new ATP-binding cassette protein localized to the canalicular domain of the hepatocyte. (5/291)

Bile secretion in liver is driven in large part by ATP-binding cassette (ABC)-type proteins that reside in the canalicular membrane and effect ATP-dependent transport of bile acids, phospholipids, and non-bile acid organic anions. Canalicular ABC-type proteins can be classified into two subfamilies based on membrane topology and sequence identity: MDR1, MDR3, and SPGP resemble the multidrug resistance (MDR) P-glycoprotein, whereas MRP2 is similar in structure and sequence to the multidrug resistance protein MRP1 and transports similar substrates. We now report the isolation of the rMRP3 gene from rat liver, which codes for a protein 1522 amino acids in length that exhibits extensive sequence similarity with MRP1 and MRP2. Northern blot analyses indicate that rMRP3 is expressed in lung and intestine of Sprague-Dawley rats as well as in liver of Eisai hyperbilirubinemic rats and TR- mutant rats, which are deficient in MRP2 expression. rMRP3 expression is also transiently induced in liver shortly after birth and during obstructive cholestasis. Antibodies raised against MRP3 recognize a polypeptide of 190-200 kDa, which is reduced in size to 155-165 kDa after treatment with endoglycosidases. Immunoblot analysis and immunoconfocal microscopy indicate that rMRP3 is present in the canalicular membrane, suggesting that it may play a role in bile formation.  (+info)

Neonatal bilirubin production, reflected by carboxyhaemoglobin concentrations, in Down's syndrome. (6/291)

AIM: To determine whether increased bilirubin production, reflected by blood carboxyhaemoglobin (COHb) values, is responsible for hyperbilirubinaemia in cases of Down's syndrome with no obvious cause for excessive jaundice. METHODS: Blood was sampled on the third day of life for COHb, total haemoglobin (tHb), and serum total bilirubin, from 19 consecutively born neonates with Down's syndrome (a subset of 34 term babies), who had developed hyperbilirubinaemia (serum bilirubin >/= 256 micromol), and from 32 term controls. COHb, measured by gas chromatography, was corrected for inspired CO (COHbc) and expressed as a percentage of tHb. RESULTS: Significantly more of the Down's syndrome subset developed hyperbilirubinaemia than the controls (10/19 (52%) vs 7/32 (22%), relative risk 2.4, 95% confidence intervals (CI) 1.10 to 5.26). Third day serum bilirubin values (mean (SD)) were higher in the Down's syndrome neonates than in controls (214 +- 63 micromol/l vs 172 +- 54 micromol/l, respectively, p=0.015). Mean (SD) COHbc values were significantly higher in the Down's syndrome neonates than in controls (0.92 +- 0. 24% vs 0.63 +- 0.17%; p<0.0001). However, Down's syndrome neonates who became hyperbilirubinaemic had similar COHbc values to those who did not (0.87 +- 0.26% and 0.95 +- 0.23%, respectively). These values contrast with those of the controls, in whom a significant increase in COHbc was associated with hyperbilirubinaemia (0.74 +- 0. 15% vs 0.60 +- 0.16%, respectively; p<0.05). tHb values were similar in both groups. CONCLUSIONS: Down's syndrome neonates had a greater risk of hyperbilirubinaemia, and higher COHbc values, than controls. However, excessive bilirubin production could not be exclusively responsible for the hyperbilirubinaemia. By inference, decreased bilirubin elimination probably plays a greater part in its pathogenesis than in controls. Down's syndrome neonates may have abnormal erythropoiesis, leading to increased haem turnover.  (+info)

Retrospective review of cystic fibrosis presenting as infantile liver disease. (7/291)

The mode of presentation, clinical course, and outcome of 12 infants with cystic fibrosis and liver disease referred over an 18 year period were investigated retrospectively. Median age at presentation was 6.5 weeks (range, 5-12). Two thirds were boys. Conjugated hyperbilirubinaemia was the presenting symptom in 11 patients, and hypoalbuminaemia in one. Jaundice was cleared over a median period of 7.36 months. Eight patients had bile duct proliferation on liver biopsy and one required cholangiography to exclude biliary atresia. Classic histological features of cystic fibrosis were only present in two children biopsied at 8 and 18 months. Three patients had meconium ileus, including one infant with concomitant alpha(1) antitrypsin deficiency, who required early liver transplantation. All other patients had no signs of significant chronic liver disease during a median follow up of 42 months (range, 10-205). Children with cystic fibrosis and infantile liver disease have a good short and medium term prognosis.  (+info)

Zinc protoporphyrin: A metabolite with a mission. (8/291)

Zinc protoporphyrin (ZnPP) is a normal metabolite that is formed in trace amounts during heme biosynthesis. The final reaction in the biosynthetic pathway of heme is the chelation of iron with protoporphyrin. During periods of iron insufficiency or impaired iron utilization, zinc becomes an alternative metal substrate for ferrochelatase, leading to increased ZnPP formation. Evidence suggests that this metal substitution is one of the first biochemical responses to iron depletion, causing increased ZnPP to appear in circulating erythrocytes. Because this zinc-for-iron substitution occurs predominantly within the bone marrow, the ZnPP/heme ratio in erythrocytes reflects iron status in the bone marrow. In addition, ZnPP may regulate heme catabolism through competitive inhibition of heme oxygenase, the rate-limiting enzyme in the heme degradation pathway that produces bilirubin and carbon monoxide. Physiological roles, especially relating to carbon monoxide and possibly nitric oxide production, have been suggested for ZnPP. Clinically, ZnPP quantification is valuable as a sensitive and specific tool for evaluating iron nutrition and metabolism. Diagnostic determinations are applicable in a variety of clinical settings, including pediatrics, obstetrics, and blood banking. ZnPP analytical methodologies for clinical studies are discussed. In addition to diagnostic tests and metabolic studies, ZnPP has a potential therapeutic application in controlling bilirubin formation in neonates as a preventive measure for hyperbilirubinemia. Biochemical research techniques, both in vivo and in vitro, are described for further studies into the role of ZnPP in metabolism and physiology.  (+info)

Hyperbilirubinemia is a medical condition characterized by an excessively high level of bilirubin in the bloodstream. Bilirubin is a yellowish pigment produced by the liver when it breaks down old red blood cells. Normally, bilirubin is conjugated (made water-soluble) in the liver and then excreted through the bile into the digestive system. However, if there is a problem with the liver's ability to process or excrete bilirubin, it can build up in the blood, leading to hyperbilirubinemia.

Hyperbilirubinemia can be classified as either unconjugated or conjugated, depending on whether the bilirubin is in its direct (conjugated) or indirect (unconjugated) form. Unconjugated hyperbilirubinemia can occur due to increased production of bilirubin (such as in hemolytic anemia), decreased uptake of bilirubin by the liver, or impaired conjugation of bilirubin in the liver. Conjugated hyperbilirubinemia, on the other hand, is usually caused by a problem with the excretion of conjugated bilirubin into the bile, such as in cholestatic liver diseases like hepatitis or cirrhosis.

Symptoms of hyperbilirubinemia can include jaundice (yellowing of the skin and eyes), dark urine, light-colored stools, itching, and fatigue. Treatment depends on the underlying cause of the condition and may involve medications, dietary changes, or surgery.

Neonatal hyperbilirubinemia is a condition characterized by an excessively high level of bilirubin in the blood of newborn infants. Bilirubin is a yellowish pigment produced by the normal breakdown of red blood cells. Normally, bilirubin is processed by the liver and excreted through the bile into the digestive system. However, in neonatal hyperbilirubinemia, the liver may be unable to process bilirubin quickly enough, leading to its accumulation in the bloodstream. This can cause the skin and eyes of the newborn to appear yellow, a condition known as jaundice.

Neonatal hyperbilirubinemia is relatively common and usually resolves on its own within a few days or weeks. However, if bilirubin levels become too high, they can cause brain damage (kernicterus) in severe cases. Treatment may include phototherapy to help break down bilirubin, exchange transfusions, or other interventions to support liver function and reduce bilirubin levels.

Bilirubin is a yellowish pigment that is produced by the liver when it breaks down old red blood cells. It is a normal byproduct of hemoglobin metabolism and is usually conjugated (made water-soluble) in the liver before being excreted through the bile into the digestive system. Elevated levels of bilirubin can cause jaundice, a yellowing of the skin and eyes. Increased bilirubin levels may indicate liver disease or other medical conditions such as gallstones or hemolysis. It is also measured to assess liver function and to help diagnose various liver disorders.

Neonatal jaundice is a medical condition characterized by the yellowing of a newborn baby's skin and eyes due to an excess of bilirubin in the blood. Bilirubin is a yellowish substance produced by the normal breakdown of red blood cells, which are then processed by the liver and excreted through the bile. In neonatal jaundice, the liver is not yet fully developed and cannot process bilirubin quickly enough, leading to its accumulation in the body.

Neonatal jaundice typically appears within the first 2-4 days of life and can range from mild to severe. Mild cases may resolve on their own without treatment, while more severe cases may require medical intervention such as phototherapy or a blood transfusion. Risk factors for neonatal jaundice include prematurity, bruising during birth, blood type incompatibility between mother and baby, and certain genetic disorders.

It is important to monitor newborns closely for signs of jaundice and seek medical attention if concerned, as untreated neonatal jaundice can lead to serious complications such as brain damage or hearing loss.

Kernicterus is a severe form of brain damage caused by high levels of bilirubin, a yellow pigment that forms when red blood cells break down. It's most commonly seen in newborns, particularly those with a condition called ABO or Rh incompatibility, where the baby's blood type is different from the mother's. This can lead to an increased breakdown of the baby's red blood cells and a buildup of bilirubin.

In kernicterus, the bilirubin reaches such high levels that it becomes toxic and can damage the brain, particularly areas like the basal ganglia and brainstem. This can result in symptoms such as severe jaundice (a yellowing of the skin and eyes), lethargy, high-pitched crying, poor feeding, and eventually seizures, hearing loss, and developmental delays.

Kernicterus is preventable with timely treatment, which may include phototherapy (using light to break down bilirubin) or exchange transfusion (replacing the baby's blood with fresh donor blood). If you suspect your newborn has jaundice or if their skin appears yellow, it's important to seek medical attention immediately.

Gilbert's disease, also known as Gilbert's syndrome, is a common and mild condition characterized by **intermittent** elevations in bilirubin levels in the bloodstream without any evidence of liver damage or disease. Bilirubin is a yellowish pigment that forms when hemoglobin breaks down. Normally, it gets processed in the liver and excreted through bile.

In Gilbert's disease, there is an impaired ability to conjugate bilirubin due to a deficiency or dysfunction of the enzyme UDP-glucuronosyltransferase 1A1 (UGT1A1), which is responsible for the glucuronidation process. This results in mild unconjugated hyperbilirubinemia, where bilirubin levels may rise and cause mild jaundice, particularly during times of fasting, illness, stress, or dehydration.

Gilbert's disease is typically an incidental finding, as it usually does not cause any significant symptoms or complications. It is often discovered during routine blood tests when bilirubin levels are found to be slightly elevated. The condition is usually harmless and does not require specific treatment, but avoiding triggers like fasting or dehydration may help minimize the occurrence of jaundice.

Phototherapy is a medical treatment that involves the use of light to manage or improve certain conditions. It can be delivered in various forms, such as natural light exposure or artificial light sources, including lasers, light-emitting diodes (LEDs), or fluorescent lamps. The wavelength and intensity of light are carefully controlled to achieve specific therapeutic effects.

Phototherapy is most commonly used for newborns with jaundice to help break down bilirubin in the skin, reducing its levels in the bloodstream. This type of phototherapy is called bilirubin lights or bili lights.

In dermatology, phototherapy can be applied to treat various skin conditions like psoriasis, eczema, vitiligo, and acne. Narrowband ultraviolet B (UVB) therapy, PUVA (psoralen plus UVA), and blue or red light therapies are some examples of dermatological phototherapies.

Phototherapy can also be used to alleviate symptoms of seasonal affective disorder (SAD) and other mood disorders by exposing patients to bright artificial light, which helps regulate their circadian rhythms and improve their mood. This form of phototherapy is called light therapy or bright light therapy.

It's essential to consult a healthcare professional before starting any phototherapy treatment, as inappropriate use can lead to adverse effects.

Hyperbilirubinemia is a condition characterized by an excess of bilirubin in the blood. Bilirubin is a yellowish substance produced by the liver when it breaks down old red blood cells. Normally, bilirubin is processed by the liver and excreted through the bile ducts and into the digestive system. However, if there is a problem with the liver or the bile ducts, bilirubin can build up in the blood, causing hyperbilirubinemia.

Hereditary hyperbilirubinemia refers to forms of the condition that are caused by genetic mutations. There are several types of hereditary hyperbilirubinemia, including:

1. Dubin-Johnson syndrome: This is a rare autosomal recessive disorder characterized by chronic conjugated hyperbilirubinemia and a dark brownish-black pigmentation of the liver. It is caused by mutations in the MRP2 gene, which provides instructions for making a protein that helps to remove bilirubin from the liver cells into the bile ducts.

2. Rotor syndrome: This is another rare autosomal recessive disorder characterized by chronic conjugated hyperbilirubinemia. It is caused by mutations in the SLCO1B1 and SLCO1B3 genes, which provide instructions for making proteins that help to transport bilirubin into the liver cells.

3. Crigler-Najjar syndrome: This is a rare autosomal recessive disorder characterized by severe unconjugated hyperbilirubinemia. It is caused by mutations in the UGT1A1 gene, which provides instructions for making an enzyme that helps to conjugate bilirubin in the liver.

4. Gilbert syndrome: This is a common autosomal recessive disorder characterized by mild unconjugated hyperbilirubinemia. It is caused by mutations in the UGT1A1 gene, but to a lesser degree than Crigler-Najjar syndrome.

In general, hereditary hyperbilirubinemias are managed with close monitoring of bilirubin levels and may require treatment with phototherapy or exchange transfusion in severe cases. In some cases, liver transplantation may be necessary.

An exchange transfusion of whole blood is a medical procedure in which a patient's blood is gradually replaced with donor whole blood. This procedure is typically performed in newborns or infants who have severe jaundice caused by excessive levels of bilirubin, a yellowish pigment that forms when hemoglobin from red blood cells breaks down.

During an exchange transfusion, the baby's blood is removed through a vein or artery and replaced with donor whole blood through another vein or artery. The process is repeated several times until a significant portion of the baby's blood has been exchanged with donor blood. This helps to reduce the levels of bilirubin in the baby's blood, which can help prevent or treat brain damage caused by excessive bilirubin.

Exchange transfusions are typically performed in a neonatal intensive care unit (NICU) and require close monitoring by a team of healthcare professionals. The procedure carries some risks, including infection, bleeding, and changes in blood pressure or heart rate. However, it can be a lifesaving treatment for newborns with severe jaundice who are at risk of developing serious complications.

I'm sorry for any confusion, but "Rats, Gunn" is not a recognized medical term or phrase. It appears to be a nonsensical expression without specific meaning in the context of medicine or healthcare. If you have any questions about medical terminology or concepts, I would be happy to try and help answer those for you!

Jaundice is a medical condition characterized by the yellowing of the skin, sclera (whites of the eyes), and mucous membranes due to an excess of bilirubin in the bloodstream. Bilirubin is a yellow-orange pigment produced when hemoglobin from red blood cells is broken down. Normally, bilirubin is processed by the liver and excreted through bile into the digestive system. However, if there's an issue with bilirubin metabolism or elimination, it can accumulate in the body, leading to jaundice.

Jaundice can be a symptom of various underlying conditions, such as liver diseases (hepatitis, cirrhosis), gallbladder issues (gallstones, tumors), or blood disorders (hemolysis). It is essential to consult a healthcare professional if jaundice is observed, as it may indicate a severe health problem requiring prompt medical attention.

Glucuronosyltransferase (UDP-glucuronosyltransferase) is an enzyme belonging to the family of glycosyltransferases. It plays a crucial role in the process of biotransformation and detoxification of various endogenous and exogenous substances, including drugs, hormones, and environmental toxins, in the liver and other organs.

The enzyme functions by transferring a glucuronic acid moiety from a donor molecule, uridine diphosphate glucuronic acid (UDP-GlcUA), to an acceptor molecule, which can be a variety of hydrophobic compounds. This reaction results in the formation of a more water-soluble glucuronide conjugate, facilitating the excretion of the substrate through urine or bile.

There are multiple isoforms of glucuronosyltransferase, classified into two main families: UGT1 and UGT2. These isoforms exhibit different substrate specificities and tissue distributions, allowing for a wide range of compounds to be metabolized through the glucuronidation pathway.

In summary, Glucuronosyltransferase is an essential enzyme in the detoxification process, facilitating the elimination of various substances from the body by conjugating them with a glucuronic acid moiety.

Crigler-Najjar Syndrome is a rare inherited genetic disorder that affects the metabolism of bilirubin, a yellow pigment produced when hemoglobin breaks down. This condition is characterized by high levels of unconjugated bilirubin in the blood, which can lead to jaundice, kernicterus, and neurological damage if left untreated.

There are two types of Crigler-Najjar Syndrome: Type I and Type II.

Type I is the more severe form, and it is caused by a mutation in the UGT1A1 gene, which encodes for an enzyme responsible for conjugating bilirubin. People with this type of Crigler-Najjar Syndrome have little to no functional enzyme activity, leading to very high levels of unconjugated bilirubin in the blood. This form is usually diagnosed in infancy and requires regular phototherapy or a liver transplant to prevent neurological damage.

Type II is a milder form of the disorder, caused by a mutation that results in reduced enzyme activity but not complete loss of function. People with this type of Crigler-Najjar Syndrome usually have milder symptoms and may not require regular phototherapy or a liver transplant, although they may still be at risk for neurological damage if their bilirubin levels become too high.

Both types of Crigler-Najjar Syndrome are inherited in an autosomal recessive manner, meaning that an individual must inherit two copies of the mutated gene (one from each parent) to develop the condition.

Chronic Idiopathic Jaundice is not a widely accepted medical diagnosis and the term "idiopathic" is used to denote that the cause of the jaundice is unknown. However, it is generally used to describe a condition where a person has persistent jaundice without any identifiable underlying cause.

Jaundice itself refers to the yellowing of the skin, sclera (whites of the eyes), and mucous membranes due to an accumulation of bilirubin in the body. Bilirubin is a yellowish substance that is produced when hemoglobin, the protein in red blood cells that carries oxygen, breaks down. Normally, bilirubin is processed by the liver and excreted through the bile ducts into the digestive system.

In Chronic Idiopathic Jaundice, the bilirubin level remains elevated over an extended period of time without any apparent explanation. The condition may be asymptomatic or associated with symptoms such as fatigue, itching, and abdominal discomfort. It is important to note that while "idiopathic" implies an unknown cause, further investigation and monitoring are often necessary to rule out any underlying liver disease or other conditions that may contribute to the jaundice.

A newborn infant is a baby who is within the first 28 days of life. This period is also referred to as the neonatal period. Newborns require specialized care and attention due to their immature bodily systems and increased vulnerability to various health issues. They are closely monitored for signs of well-being, growth, and development during this critical time.

A "term birth" is a medical term that refers to a delivery or pregnancy that has reached 37 weeks or more. It is the normal length of a full-term pregnancy and is considered a healthy and low-risk period for childbirth. Babies born at term have the best chance of being healthy and not experiencing any significant medical issues, compared to those born preterm (before 37 weeks) or postterm (after 42 weeks). The different types of term births are:

* Early Term: Between 37 weeks and 38 weeks, 6 days.
* Full Term: Between 39 weeks and 40 weeks, 6 days.
* Late Term: Between 41 weeks and 41 weeks, 6 days.
* Postterm: 42 weeks or later.

It is important to note that while a term birth is generally considered low-risk, there can still be variations in the health of babies born at different points within this range. For example, research has shown that babies born at 39 weeks have better outcomes than those born at 37 or 38 weeks. Therefore, it is always best to consult with a healthcare provider for individualized guidance and recommendations regarding pregnancy and childbirth.

Neonatal screening is a medical procedure in which specific tests are performed on newborn babies within the first few days of life to detect certain congenital or inherited disorders that are not otherwise clinically apparent at birth. These conditions, if left untreated, can lead to serious health problems, developmental delays, or even death.

The primary goal of neonatal screening is to identify affected infants early so that appropriate treatment and management can be initiated as soon as possible, thereby improving their overall prognosis and quality of life. Commonly screened conditions include phenylketonuria (PKU), congenital hypothyroidism, galactosemia, maple syrup urine disease, sickle cell disease, cystic fibrosis, and hearing loss, among others.

Neonatal screening typically involves collecting a small blood sample from the infant's heel (heel stick) or through a dried blood spot card, which is then analyzed using various biochemical, enzymatic, or genetic tests. In some cases, additional tests such as hearing screenings and pulse oximetry for critical congenital heart disease may also be performed.

It's important to note that neonatal screening is not a diagnostic tool but rather an initial step in identifying infants who may be at risk of certain conditions. Positive screening results should always be confirmed with additional diagnostic tests before any treatment decisions are made.

Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is a genetic disorder that affects the normal functioning of an enzyme called G6PD. This enzyme is found in red blood cells and plays a crucial role in protecting them from damage.

In people with G6PD deficiency, the enzyme's activity is reduced or absent, making their red blood cells more susceptible to damage and destruction, particularly when they are exposed to certain triggers such as certain medications, infections, or foods. This can lead to a condition called hemolysis, where the red blood cells break down prematurely, leading to anemia, jaundice, and in severe cases, kidney failure.

G6PD deficiency is typically inherited from one's parents in an X-linked recessive pattern, meaning that males are more likely to be affected than females. While there is no cure for G6PD deficiency, avoiding triggers and managing symptoms can help prevent complications.

Organic anion transport polypeptide C (OATPc or OATPC) is not a widely recognized or established term in the medical field. It seems that this terminology might be referring to one or more members of the organic anion transporting polypeptides (OATPs) family, specifically those localized to the canalicular membrane of hepatocytes.

OATPs are a group of membrane transporters primarily responsible for the uptake of various amphipathic organic molecules, including bile salts, steroid conjugates, thyroid hormones, and various drugs. They play a crucial role in the hepatic clearance and disposition of many endogenous and exogenous substances.

The term "OATPc" might be referring to OATP1B1 (SLCO1B1) and/or OATP1B3 (SLCO1B3), which are the two major isoforms found in the human liver's canalicular membrane. However, it is essential to note that there isn't a universally accepted or standardized definition for "OATPc."

To obtain accurate and reliable information, consult scientific literature, textbooks, or databases specializing in medical definitions and terminology.

Blood group incompatibility refers to a situation where the blood type of a donor and a recipient are not compatible, leading to an immune response and destruction of the donated red blood cells. This is because the recipient's immune system recognizes the donor's red blood cells as foreign due to the presence of incompatible antigens on their surface.

The most common type of blood group incompatibility occurs between individuals with different ABO blood types, such as when a person with type O blood receives type A, B, or AB blood. This can lead to agglutination and hemolysis of the donated red blood cells, causing potentially life-threatening complications such as hemolytic transfusion reaction.

Another type of blood group incompatibility occurs between Rh-negative mothers and their Rh-positive fetuses. If a mother's immune system is exposed to her fetus's Rh-positive red blood cells during pregnancy or childbirth, she may develop antibodies against them. This can lead to hemolytic disease of the newborn if the mother becomes pregnant with another Rh-positive fetus in the future.

To prevent these complications, it is essential to ensure that donated blood is compatible with the recipient's blood type before transfusion and that appropriate measures are taken during pregnancy and childbirth to prevent sensitization of Rh-negative mothers to Rh-positive red blood cells.

Erythroblastosis, fetal is a medical condition that occurs in the fetus or newborn when there is an incompatibility between the fetal and maternal blood types, specifically related to the Rh factor or ABO blood group system. This incompatibility leads to the destruction of the fetal red blood cells by the mother's immune system, resulting in the release of bilirubin, which can cause jaundice, anemia, and other complications.

In cases where the mother is Rh negative and the fetus is Rh positive, the mother may develop antibodies against the Rh factor during pregnancy or after delivery, leading to hemolysis (breakdown) of the fetal red blood cells in subsequent pregnancies if preventive measures are not taken. This is known as hemolytic disease of the newborn (HDN).

Similarly, incompatibility between the ABO blood groups can also lead to HDN, although it is generally less severe than Rh incompatibility. In this case, the mother's immune system produces antibodies against the fetal red blood cells, leading to their destruction and subsequent complications.

Fetal erythroblastosis is a serious condition that can lead to significant morbidity and mortality if left untreated. Treatment options include intrauterine transfusions, phototherapy, and exchange transfusions in severe cases. Preventive measures such as Rh immune globulin (RhIG) injections can help prevent the development of antibodies in Rh-negative mothers, reducing the risk of HDN in subsequent pregnancies.

Metalloporphyrins are a type of porphyrin molecule that contain a metal ion at their center. Porphyrins are complex organic compounds containing four modified pyrrole rings connected to form a planar, aromatic ring known as a porphine. When a metal ion is incorporated into the center of the porphyrin ring, it forms a metalloporphyrin.

These molecules have great biological significance, as they are involved in various essential processes within living organisms. For instance, heme, a type of iron-containing porphyrin, plays a crucial role in oxygen transport and storage in the body by forming part of hemoglobin and myoglobin molecules. Chlorophyll, another metalloporphyrin with magnesium at its center, is essential for photosynthesis in plants, algae, and some bacteria.

Metalloporphyrins have also found applications in several industrial and medical fields, including catalysis, sensors, and pharmaceuticals. Their unique structure and properties make them valuable tools for researchers and scientists to study and utilize in various ways.

A nomogram is a graphical representation of a mathematical formula or equation that allows the user to quickly solve a problem by simply drawing a line between different values on the chart. In the field of medicine, nomograms are often used as a tool for predicting patient outcomes, assessing risk, or making diagnostic decisions based on specific clinical data.

For example, a nomogram may be used to estimate the probability of survival in patients with a particular type of cancer, based on factors such as age, tumor size, and stage of disease. The user would locate the appropriate values for each factor on the nomogram, draw a line connecting them, and read off the estimated probability at the intersection point.

Nomograms can be a useful and intuitive way to communicate complex medical information and help clinicians make informed decisions in a timely manner. However, it is important to note that nomograms are only as accurate as the data they are based on, and should always be used in conjunction with clinical judgment and other relevant factors.

Histocompatibility, maternal-fetal, refers to the compatibility between the human leukocyte antigens (HLAs) and other antigenic proteins expressed on the fetal tissues and those present in the mother's immune system. The HLAs are a group of proteins encoded by the major histocompatibility complex (MHC) and play a crucial role in the recognition and presentation of foreign peptides to the immune cells.

During pregnancy, the fetal tissues express paternal HLA antigens that can be recognized as non-self by the mother's immune system. However, the maternal-fetal interface, which includes the placenta and decidua, has several mechanisms to prevent the activation of the maternal immune response against the fetus. These mechanisms include the expression of unique HLA molecules (HLA-G, -C, and -E) by the trophoblast cells, which have immunomodulatory functions, as well as the production of anti-inflammatory cytokines and the suppression of pro-inflammatory responses.

Despite these immune tolerance mechanisms, in some cases, the maternal immune system may still recognize the fetal tissues as foreign and mount an immune response, leading to pregnancy complications such as preeclampsia, recurrent miscarriage, or intrauterine growth restriction. The degree of histocompatibility between the mother and fetus can influence the risk of these complications, with a higher degree of mismatch increasing the risk.

In transplantation medicine, the concept of histocompatibility is critical in matching donors and recipients to minimize the risk of rejection. However, in pregnancy, the unique immune environment at the maternal-fetal interface allows for the coexistence of two genetically distinct individuals without the need for full histocompatibility.

Central hearing loss is a type of hearing disorder that occurs due to damage or dysfunction in the central auditory pathways of the brain, rather than in the ear itself. This condition can result from various causes, such as stroke, tumors, trauma, infection, or degenerative diseases affecting the brain.

In central hearing loss, the person may have difficulty understanding and processing speech, even when they can hear sounds at normal levels. They might experience problems with sound localization, discriminating between similar sounds, and comprehending complex auditory signals. This type of hearing loss is different from sensorineural or conductive hearing loss, which are related to issues in the outer, middle, or inner ear.

Protoporphyrins are organic compounds that are the immediate precursors to heme in the porphyrin synthesis pathway. They are composed of a porphyrin ring, which is a large, complex ring made up of four pyrrole rings joined together, with an acetate and a propionate side chain at each pyrrole. Protoporphyrins are commonly found in nature and are important components of many biological systems, including hemoglobin, the protein in red blood cells that carries oxygen throughout the body.

There are several different types of protoporphyrins, including protoporphyrin IX, which is the most common form found in humans and other animals. Protoporphyrins can be measured in the blood or other tissues as a way to diagnose or monitor certain medical conditions, such as lead poisoning or porphyrias, which are rare genetic disorders that affect the production of heme. Elevated levels of protoporphyrins in the blood or tissues can indicate the presence of these conditions and may require further evaluation and treatment.

Indinavir is an antiretroviral medication used in the treatment and management of HIV (Human Immunodeficiency Virus) infection. It belongs to a class of drugs known as protease inhibitors, which work by blocking the action of protease enzymes that are necessary for the HIV virus to replicate. By inhibiting this process, indinavir helps prevent the spread of HIV in the body and reduces the risk of developing AIDS (Acquired Immunodeficiency Syndrome).

Indinavir is often prescribed as part of a combination therapy regimen with other antiretroviral drugs. It is available in capsule form and is typically taken several times a day, usually on an empty stomach. As with all medications, indinavir can have side effects, which may include nausea, diarrhea, headache, and changes in liver function. Regular monitoring of blood tests is necessary to ensure that the drug is working effectively and not causing any harmful side effects.

It's important to note that while antiretroviral therapy can help manage HIV infection and improve quality of life, it does not cure the disease. Therefore, it is essential for individuals with HIV to continue taking their medications as prescribed and to follow up regularly with their healthcare provider.

The ABO blood-group system is a classification system used in blood transfusion medicine to determine the compatibility of donated blood with a recipient's blood. It is based on the presence or absence of two antigens, A and B, on the surface of red blood cells (RBCs), as well as the corresponding antibodies present in the plasma.

There are four main blood types in the ABO system:

1. Type A: These individuals have A antigens on their RBCs and anti-B antibodies in their plasma.
2. Type B: They have B antigens on their RBCs and anti-A antibodies in their plasma.
3. Type AB: They have both A and B antigens on their RBCs but no natural antibodies against either A or B antigens.
4. Type O: They do not have any A or B antigens on their RBCs, but they have both anti-A and anti-B antibodies in their plasma.

Transfusing blood from a donor with incompatible ABO antigens can lead to an immune response, causing the destruction of donated RBCs and potentially life-threatening complications such as acute hemolytic transfusion reaction. Therefore, it is crucial to match the ABO blood type between donors and recipients before performing a blood transfusion.

Hemolysis is the destruction or breakdown of red blood cells, resulting in the release of hemoglobin into the surrounding fluid (plasma). This process can occur due to various reasons such as chemical agents, infections, autoimmune disorders, mechanical trauma, or genetic abnormalities. Hemolysis may lead to anemia and jaundice, among other complications. It is essential to monitor hemolysis levels in patients undergoing medical treatments that might cause this condition.

A premature infant is a baby born before 37 weeks of gestation. They may face various health challenges because their organs are not fully developed. The earlier a baby is born, the higher the risk of complications. Prematurity can lead to short-term and long-term health issues, such as respiratory distress syndrome, jaundice, anemia, infections, hearing problems, vision problems, developmental delays, and cerebral palsy. Intensive medical care and support are often necessary for premature infants to ensure their survival and optimal growth and development.

Porphyrins are complex organic compounds that contain four pyrrole rings joined together by methine bridges (=CH-). They play a crucial role in the biochemistry of many organisms, as they form the core structure of various heme proteins and other metalloproteins. Some examples of these proteins include hemoglobin, myoglobin, cytochromes, and catalases, which are involved in essential processes such as oxygen transport, electron transfer, and oxidative metabolism.

In the human body, porphyrins are synthesized through a series of enzymatic reactions known as the heme biosynthesis pathway. Disruptions in this pathway can lead to an accumulation of porphyrins or their precursors, resulting in various medical conditions called porphyrias. These disorders can manifest as neurological symptoms, skin lesions, and gastrointestinal issues, depending on the specific type of porphyria and the site of enzyme deficiency.

It is important to note that while porphyrins are essential for life, their accumulation in excessive amounts or at inappropriate locations can result in pathological conditions. Therefore, understanding the regulation and function of porphyrin metabolism is crucial for diagnosing and managing porphyrias and other related disorders.

I'm sorry for any confusion, but "Pyridines" is not a medical term. It is a chemical term that refers to a class of organic compounds with the chemical structure of a six-membered ring containing one nitrogen atom and five carbon atoms (heterocyclic aromatic compound).

In a biological or medical context, pyridine derivatives can be found in various natural and synthetic substances. For example, some medications contain pyridine rings as part of their chemical structure. However, "Pyridines" itself is not a medical term or condition.

The Coombs test is a laboratory procedure used to detect the presence of antibodies on the surface of red blood cells (RBCs). It is named after the scientist, Robin Coombs, who developed the test. There are two types of Coombs tests: direct and indirect.

1. Direct Coombs Test (DCT): This test is used to detect the presence of antibodies directly attached to the surface of RBCs. It is often used to diagnose hemolytic anemia, a condition in which RBCs are destroyed prematurely, leading to anemia. A positive DCT indicates that the patient's RBCs have been coated with antibodies, which can occur due to various reasons such as autoimmune disorders, blood transfusion reactions, or drug-induced immune hemolysis.
2. Indirect Coombs Test (ICT): This test is used to detect the presence of antibodies in the patient's serum that can agglutinate (clump) foreign RBCs. It is commonly used before blood transfusions or during pregnancy to determine if the patient has antibodies against the RBCs of a potential donor or fetus, respectively. A positive ICT indicates that the patient's serum contains antibodies capable of binding to and agglutinating foreign RBCs.

In summary, the Coombs test is a crucial diagnostic tool in identifying various hemolytic disorders and ensuring safe blood transfusions by detecting the presence of harmful antibodies against RBCs.

The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:

1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.

Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.

Ultraviolet (UV) therapy, also known as phototherapy, is a medical treatment that uses ultraviolet light to treat various skin conditions. The UV light can be delivered through natural sunlight or artificial sources, such as specialized lamps or lasers.

In medical settings, controlled doses of UV light are used to target specific areas of the skin. The most common type of UV therapy is narrowband UVB (NB-UVB) phototherapy, which uses a specific wavelength of UVB light to treat conditions such as psoriasis, eczema, vitiligo, and dermatitis.

The goal of UV therapy is to reduce inflammation, slow skin cell growth, and improve the overall appearance of the skin. It is important to note that while UV therapy can be effective in treating certain skin conditions, it also carries risks such as skin aging and an increased risk of skin cancer. Therefore, it should only be administered under the supervision of a qualified healthcare professional.

Cholestasis is a medical condition characterized by the interruption or reduction of bile flow from the liver to the small intestine. Bile is a digestive fluid produced by the liver that helps in the breakdown and absorption of fats. When the flow of bile is blocked or reduced, it can lead to an accumulation of bile components, such as bilirubin, in the blood, which can cause jaundice, itching, and other symptoms.

Cholestasis can be caused by various factors, including liver diseases (such as hepatitis, cirrhosis, or cancer), gallstones, alcohol abuse, certain medications, pregnancy, and genetic disorders. Depending on the underlying cause, cholestasis may be acute or chronic, and it can range from mild to severe in its symptoms and consequences. Treatment for cholestasis typically involves addressing the underlying cause and managing the symptoms with supportive care.

Organic anion transporters (OATs) are membrane transport proteins that are responsible for the cellular uptake and excretion of various organic anions, such as drugs, toxins, and endogenous metabolites. They are found in various tissues, including the kidney, liver, and brain, where they play important roles in the elimination and detoxification of xenobiotics and endogenous compounds.

In the kidney, OATs are located in the basolateral membrane of renal tubular epithelial cells and mediate the uptake of organic anions from the blood into the cells. From there, the anions can be further transported into the urine by other transporters located in the apical membrane. In the liver, OATs are expressed in the sinusoidal membrane of hepatocytes and facilitate the uptake of organic anions from the blood into the liver cells for metabolism and excretion.

There are several isoforms of OATs that have been identified, each with distinct substrate specificities and tissue distributions. Mutations in OAT genes can lead to various diseases, including renal tubular acidosis, hypercalciuria, and drug toxicity. Therefore, understanding the function and regulation of OATs is important for developing strategies to improve drug delivery and reduce adverse drug reactions.

Imino acids are organic compounds that contain a nitrogen atom as part of an amide-like structure. They are structurally similar to amino acids, which contain a carboxyl group and an amino group, but instead of the amino group, imino acids have a structural unit known as an imine or Schiff base, which is a carbon-nitrogen double bond with a hydrogen atom attached to the nitrogen atom.

One example of an imino acid is proline, which is a cyclic imino acid that plays important roles in protein structure and function. Proline is unique among the 20 standard amino acids because its side chain is linked to the nitrogen atom of the backbone, forming a ring-like structure. This structural feature gives proline unique properties, such as restricted rotation around the bond between the nitrogen and alpha carbon atoms, which can affect protein folding and stability.

Other imino acids may be formed through chemical reactions or enzymatic processes, and they can play important roles in various biological pathways, including the biosynthesis of amino acids, nucleotides, and other biomolecules. However, imino acids are not typically considered to be part of the standard set of 20 amino acids that make up proteins.

Hemolytic anemia is a type of anemia that occurs when red blood cells are destroyed (hemolysis) faster than they can be produced. Red blood cells are essential for carrying oxygen throughout the body. When they are destroyed, hemoglobin and other cellular components are released into the bloodstream, which can lead to complications such as kidney damage and gallstones.

Hemolytic anemia can be inherited or acquired. Inherited forms of the condition may result from genetic defects that affect the structure or function of red blood cells. Acquired forms of hemolytic anemia can be caused by various factors, including infections, medications, autoimmune disorders, and certain medical conditions such as cancer or blood disorders.

Symptoms of hemolytic anemia may include fatigue, weakness, shortness of breath, pale skin, jaundice (yellowing of the skin and eyes), dark urine, and a rapid heartbeat. Treatment for hemolytic anemia depends on the underlying cause and may include medications, blood transfusions, or surgery.

A "premature infant" is a newborn delivered before 37 weeks of gestation. They are at greater risk for various health complications and medical conditions compared to full-term infants, due to their immature organ systems and lower birth weight. Some common diseases and health issues that premature infants may face include:

1. Respiratory Distress Syndrome (RDS): A lung disorder caused by the lack of surfactant, a substance that helps keep the lungs inflated. Premature infants, especially those born before 34 weeks, are at higher risk for RDS.
2. Intraventricular Hemorrhage (IVH): Bleeding in the brain's ventricles, which can lead to developmental delays or neurological issues. The risk of IVH is inversely proportional to gestational age, meaning that the earlier the infant is born, the higher the risk.
3. Necrotizing Enterocolitis (NEC): A gastrointestinal disease where the intestinal tissue becomes inflamed and can die. Premature infants are at greater risk for NEC due to their immature digestive systems.
4. Jaundice: A yellowing of the skin and eyes caused by an accumulation of bilirubin, a waste product from broken-down red blood cells. Premature infants may have higher rates of jaundice due to their liver's immaturity.
5. Infections: Premature infants are more susceptible to infections because of their underdeveloped immune systems. Common sources of infection include the mother's genital tract, bloodstream, or hospital environment.
6. Anemia: A condition characterized by a low red blood cell count or insufficient hemoglobin. Premature infants may develop anemia due to frequent blood sampling, rapid growth, or inadequate erythropoietin production.
7. Retinopathy of Prematurity (ROP): An eye disorder affecting premature infants, where abnormal blood vessel growth occurs in the retina. Severe ROP can lead to vision loss or blindness if not treated promptly.
8. Developmental Delays: Premature infants are at risk for developmental delays due to their immature nervous systems and environmental factors such as sensory deprivation or separation from parents.
9. Patent Ductus Arteriosus (PDA): A congenital heart defect where the ductus arteriosus, a blood vessel that connects two major arteries in the fetal heart, fails to close after birth. Premature infants are at higher risk for PDA due to their immature cardiovascular systems.
10. Hypothermia: Premature infants have difficulty maintaining body temperature and are at risk for hypothermia, which can lead to increased metabolic demands, poor feeding, and infection.

Plasma exchange, also known as plasmapheresis, is a medical procedure where the liquid portion of the blood (plasma) is separated from the blood cells. The plasma, which may contain harmful substances such as antibodies, clotting factors, or toxins, is then removed and replaced with fresh plasma or a plasma substitute. This process helps to remove the harmful substances from the blood and allows the body to replenish its own plasma with normal components. Plasma exchange is used in the treatment of various medical conditions including autoimmune diseases, poisonings, and certain types of kidney diseases.

Technetium Tc 99m Disofenin is not a medical condition, but rather a radiopharmaceutical used in diagnostic imaging. It is a radioactive tracer used in nuclear medicine scans, specifically for liver and biliary system imaging. The compound consists of the radioisotope Technetium-99m (Tc-99m) bonded to the pharmaceutical Disofenin.

The Tc-99m is a gamma emitter with a half-life of 6 hours, making it ideal for diagnostic imaging. When administered to the patient, the compound is taken up by the liver and excreted into the bile ducts and gallbladder, allowing medical professionals to visualize these structures using a gamma camera. This can help detect various conditions such as tumors, gallstones, or obstructions in the biliary system.

It's important to note that Technetium Tc 99m Disofenin is used diagnostically and not for therapeutic purposes. The radiation exposure from this compound is generally low and considered safe for diagnostic use. However, as with any medical procedure involving radiation, the benefits and risks should be carefully weighed and discussed with a healthcare professional.

Mandatory reporting is a legal requirement that healthcare professionals, as well as other designated individuals or organizations, must report suspected or confirmed cases of abuse, neglect, or exploitation of vulnerable populations to the appropriate authorities. These vulnerable populations often include children, elderly persons, and individuals with disabilities. The purpose of mandatory reporting is to ensure the protection and safety of these at-risk individuals and to facilitate interventions that can address and prevent further harm.

Healthcare professionals who are mandated reporters typically include doctors, nurses, mental health professionals, social workers, and teachers, among others. Mandatory reporting requirements vary by jurisdiction but generally involve immediate notification upon suspicion or knowledge of maltreatment. Failing to report as required can result in legal consequences for the mandated reporter, including potential penalties such as fines, license suspension, or even criminal charges.

The specifics of mandatory reporting laws and regulations differ between countries, states, and provinces; therefore, it is essential for healthcare professionals to be familiar with the requirements applicable to their particular practice settings.

Oligopeptides are defined in medicine and biochemistry as short chains of amino acids, typically containing fewer than 20 amino acid residues. These small peptides are important components in various biological processes, such as serving as signaling molecules, enzyme inhibitors, or structural elements in some proteins. They can be found naturally in foods and may also be synthesized for use in medical research and therapeutic applications.

Bile canaliculi are the smallest bile-transporting structures in the liver. They are formed by the close apposition of hepatocyte (liver cell) plasma membranes, and they are responsible for the majority of bile production. The bile canaliculi merge to form bile ductules, which then merge to form larger bile ducts that transport bile to the gallbladder and small intestine. Bile is a fluid that contains water, electrolytes, bile salts, cholesterol, phospholipids, and bilirubin, which are produced by the liver and play important roles in digestion and elimination of waste products.

Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), also known as Glucosephosphate Dehydrogenase, is an enzyme that plays a crucial role in cellular metabolism, particularly in the glycolytic pathway. It catalyzes the conversion of glyceraldehyde 3-phosphate (G3P) to 1,3-bisphosphoglycerate (1,3-BPG), while also converting nicotinamide adenine dinucleotide (NAD+) to its reduced form NADH. This reaction is essential for the production of energy in the form of adenosine triphosphate (ATP) during cellular respiration. GAPDH has been widely used as a housekeeping gene in molecular biology research due to its consistent expression across various tissues and cells, although recent studies have shown that its expression can vary under certain conditions.

Patient readmission refers to the event when a patient who was previously discharged from a hospital or healthcare facility returns for further treatment, often within a specified period. It is measured as a percentage of patients who are readmitted within a certain time frame, such as 30, 60, or 90 days after discharge. Readmissions may be planned or unplanned and can occur due to various reasons, including complications from the initial illness or treatment, inadequate post-discharge follow-up care, or the patient's inability to manage their health conditions effectively at home. High readmission rates are often considered an indicator of the quality of care provided during the initial hospitalization and may also signify potential issues with care coordination and transitions between healthcare settings.

Gestational age is the length of time that has passed since the first day of the last menstrual period (LMP) in pregnant women. It is the standard unit used to estimate the age of a pregnancy and is typically expressed in weeks. This measure is used because the exact date of conception is often not known, but the start of the last menstrual period is usually easier to recall.

It's important to note that since ovulation typically occurs around two weeks after the start of the LMP, gestational age is approximately two weeks longer than fetal age, which is the actual time elapsed since conception. Medical professionals use both gestational and fetal age to track the development and growth of the fetus during pregnancy.

Extracorporeal circulation (ECC) is a term used in medicine to describe the process of temporarily taking over the functions of the heart and lungs by using a machine. This allows the surgeon to perform certain types of surgery, such as open-heart surgery, on a still and bloodless operating field.

During ECC, the patient's blood is circulated outside the body through a pump and oxygenator. The pump helps to maintain blood flow and pressure, while the oxygenator adds oxygen to the blood and removes carbon dioxide. This allows the surgeon to stop the heart and arrest its motion, making it easier to perform delicate procedures on the heart and surrounding structures.

Extracorporeal circulation is a complex and high-risk procedure that requires careful monitoring and management by a team of healthcare professionals. It carries risks such as bleeding, infection, and injury to blood vessels or organs. However, when performed correctly, it can be a life-saving measure for patients undergoing certain types of surgery.

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Hyperbilirubinemia may be observed when hemolysis produces too much bilirubin through the excessive breakdown of red blood ... For infants with hemolytic jaundice, severe and prolonged cases of hyperbilirubinemia, or high serum bilirubin that does not ... Watson RL (March 2009). "Hyperbilirubinemia". Critical Care Nursing Clinics of North America. The High-Risk Neonate: Part I. 21 ... Murki S, Kumar P (June 2011). "Blood exchange transfusion for infants with severe neonatal hyperbilirubinemia". Seminars in ...
Hyperbilirubinemia, more precisely hyperbilirubinemia due to the unconjugated fraction, may cause bilirubin to accumulate in ... While this may occur in children with hyperbilirubinemia, tooth discoloration due to hyperbilirubinemia is not observed in ... In developing children, hyperbilirubinemia may cause a yellow or green discoloration of teeth due to bilirubin deposition ... Amin SB, Karp JM, Benzley LP (May 2010). "Unconjugated hyperbilirubinemia and early childhood caries in a diverse group of ...
American Academy of Pediatrics Subcommittee on Hyperbilirubinemia (July 2004). "Management of hyperbilirubinemia in the newborn ... "Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation". Pediatrics. doi:10.1542/peds.2022-058859 ... This pattern of hyperbilirubinemia has been classified into two functionally distinct periods. Phase one Term infants - ... Total bilirubin more than 331.5 μmol/L (19.5 mg/dL) (hyperbilirubinemia). Direct bilirubin more than 34 μmol/L (2.0 mg/dL). The ...
Liver failure and hepatitis are the most etiological in liver-genesis hyperbilirubinemia. In case of hyperbilirubinemia due to ... Moreover, the unconjugated hyperbilirubinemia arises in case the components of liver transfer the indirect bilirubin into ... "Diseases Associated with Hyperbilirubinemia". library.med.utah.edu. 1995-01-05. Archived from the original on 2019-05-06. ... Up to 8% to 11% neonates will develop hyperbilirubinemia in the first week of their lives. In jaundice owing to hemolysis ( ...
The syndrome cannot cause severe indirect hyperbilirubinemia in neonates by itself, but it may have a summative effect on ... J L Gollan; C Bateman; B H Billing (1976). "Effect of dietary composition on the unconjugated hyperbilirubinaemia of Gilbert's ... This substance then accumulates in the body, causing mild hyperbilirubinemia. Gilbert syndrome is a phenotypic effect, mostly ... Rennie, Janet M.; Beer, Jeanette; Upton, Michele (2019). "Learning from claims: hyperbilirubinaemia and kernicterus". Archives ...
CETP Hyperbilirubinemia, familial transcient neonatal; 237900; UGT1A1 Hypercarotenemia and vitamin A deficiency, autosomal ...
October 2001). "Mechanism of indinavir-induced hyperbilirubinemia". Proceedings of the National Academy of Sciences of the ...
Birth weight less than 1,500g (3.3 lbs). Hyperbilirubinemia at levels quiring exchange transfusion. Bacterial meningitis. ...
Unconjugated hyperbilirubinemia in a newborn can lead to accumulation of bilirubin in certain brain regions (particularly the ... Aside from specific chronic medical conditions that may lead to hyperbilirubinemia, neonates in general are at increased risk ... The neurotoxicity of neonatal hyperbilirubinemia manifests because the blood-brain barrier has yet to develop fully,[dubious - ... "Unconjugated Hyperbilirubinemia: Practice Essentials, Background, Pathophysiology". Medscape Reference. 4 March 2019. Retrieved ...
Unconjugated hyperbilirubinemia above 15% is present. The differential diagnoses are rifampicin or probenecid use, inherited ...
This causes a primarily conjugated hyperbilirubinemia and jaundice; the liver conjugates the bile to make it water-soluble and ... This is in contrast to primarily unconjugated hyperbilirubinemia which is the water-insoluble form that is bound to serum ... Unconjugated hyperbilirubinemia does not typically cause pruritus. It is thought that bile salts that deposit into the skin are ...
Huang MJ, Kua KE, Teng HC, Tang KS, Weng HW, Huang CS (2005). "Risk factors for severe hyperbilirubinemia in neonates". Pediatr ... Huang CS, Huang MJ, Lin MS, Yang SS, Teng HC, Tang KS (2005). "Genetic factors related to unconjugated hyperbilirubinemia ... "Inhibition of human organic anion transporting polypeptide OATP 1B1 as a mechanism of drug-induced hyperbilirubinemia". Chem. ...
American Academy of Pediatrics Subcommittee on Hyperbilirubinemia (July 2004). "Management of hyperbilirubinemia in the newborn ... Jerold Lucey demonstrated that hyperbilirubinemia of prematurity (a form of neonatal jaundice) could be successfully treated ... Lucey, Jerold; Ferreiro, Mario; Hewitt, Jean (1968-06-01). "Prevention of hyperbilirubinemia of prematurity by phototherapy". ...
"Genetic factors related to unconjugated hyperbilirubinemia amongst adults". Pharmacogenetics and Genomics. 15 (1): 43-50. doi: ...
American Academy of Pediatrics Subcommittee on Hyperbilirubinemia (July 2004). "Management of hyperbilirubinemia in the newborn ... Phenobarbital - Phenobarbital is sometimes given to the mother to help mature the fetal liver and reduce hyperbilirubinemia. ... High at birth or rapidly rising bilirubin Prolonged hyperbilirubinemia Bilirubin Induced Neurological Dysfunction Cerebral ...
American Academy of Pediatrics Subcommittee on Hyperbilirubinemia (July 2004). "Management of hyperbilirubinemia in the newborn ...
Causes of unconjugated hyperbilirubinemia are divided into three main categories, namely, excessive bilirubin synthesis, liver ... Sanjiv Chopra; Shilpa Grover (eds.). "Diagnostic approach to the adult with jaundice or asymptomatic hyperbilirubinemia". ... which is characterized by unconjugated hyperbilirubinemia. It is also associated with Crigler-Najjar syndrome, a more serious ... and extravasation of blood into tissues such as angioedema and edema can also lead to indirect hyperbilirubinemia, along with ...
Rotor type hyperbilirubinemia is a distinct yet similar disorder to Dubin-Johnson syndrome - both diseases cause an increase in ... Increased conjugated hyperbilirubinemia is the hallmark for diagnosing Rotor syndrome. There is no distinct black pigmentation ... Rotor syndrome (also known as Rotor type hyperbilirubinemia) is a rare cause of mixed direct (conjugated) and indirect ( ... Imaging studies cannot diagnose Rotor syndrome but can help rule out other diseases that cause hyperbilirubinemia. For example ...
Extensive bruising may increase the likelihood of clinically significant hyperbilirubinemia. Most of the time increased levels ... Watchko JF (June 2009). "Identification of neonates at risk for hazardous hyperbilirubinemia: emerging clinical insights". ...
Complications the baby may face include cephalohematomas, hyperbilirubinemia, and intracranial hemorrhages. Asynclitic birth ...
The conjugated hyperbilirubinemia is a result of defective endogenous and exogenous transfer of anionic conjugates from ... Strassburg CP (2010). "Hyperbilirubinemia syndromes (Gilbert-Meulengracht, Crigler-Najjar, Dubin-Johnson, and Rotor syndrome ... Up-to-date: "Inherited disorders associated with conjugated hyperbilirubinemia" Dubin, IN; Johnson, F (September 1954). " ... the condition so as not to confuse it with other hepatobiliary disorders associated with conjugated hyperbilirubinemia that ...
Bili lights may also be used to treat newborn jaundice (hyperbilirubinemia). Water can be carefully provided to prevent ... and hyperbilirubinemia (jaundice) that can lead to kernicterus. Infection, including sepsis, pneumonia, and urinary tract ...
... is contraindicated in patients with hyperbilirubinaemia.[citation needed] editor, Emilio Jirillo (2008). ...
Dickey W, McAleer JJ, Callender ME (April 1991). "The Nicotinic Acid Provocation Test and Unconjugated Hyperbilirubinaemia". ...
Livestock ingesting large amounts can experience weight loss, hyperbilirubinemia, photosensitization, and polyuria. The plant's ...
In this case phenobarbital treatment helps to lower bilirubin lever by more than 30%. Hyperbilirubinemia, familial transient ... which causes a hyperbilirubinemia with levels of total serum bilirubin from 6 to 20 mg/dL. ... which causes a severe hyperbilirubinemia with levels of total serum bilirubin from 20 to 45 mg/dL. Phenobarbital treatment does ... actually develop UGT1A1-associated hyperbilirubinemia, so it appears that this mutation alone may be a necessary but not ...
American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. (2004). "Management of hyperbilirubinemia in the newborn ... Phenobarbital - Phenobarbital is sometimes given to the mother to help mature the fetal liver and reduce hyperbilirubinemia. ... The hemolytic process can result in anemia, hyperbilirubinemia, neonatal thrombocytopenia, and neonatal neutropenia. With the ... High at birth or rapidly rising bilirubin Prolonged hyperbilirubinemia Bilirubin Induced Neuorlogical Dysfunction Cerebral ...
American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. (2004). "Management of hyperbilirubinemia in the newborn ... Phenobarbital - Phenobarbital is sometimes given to the mother to help mature the fetal liver and reduce hyperbilirubinemia. ... The hemolytic process can result in anemia, hyperbilirubinemia, neonatal thrombocytopenia, and neonatal neutropenia. With the ... High at birth or rapidly rising bilirubin Prolonged hyperbilirubinemia Bilirubin-induced neurological dysfunction Cerebral ...
Hereditary hyperbilirubinemia refers to the condition where levels of bilirubin are elevated, for reasons that can be ... Eventually it causes unconjugated hyperbilirubinemia and jaundice as substance accumulates in the body due to the reduced ... "Hepatobiliary transport of glutathione and glutathione conjugate in rats with hereditary hyperbilirubinemia". J. Clin. Invest. ...
Transient familial hyperbilirubinemia is a metabolic disorder that is passed down through families. Babies with this disorder ... Transient familial hyperbilirubinemia is a metabolic disorder that is passed down through families. Babies with this disorder ... Transient familial hyperbilirubinemia is a metabolic disorder that is passed down through families. Babies with this disorder ... Transient familial hyperbilirubinemia is an inherited disorder. It occurs when the body does not properly break down ( ...
encoded search term (Conjugated Hyperbilirubinemia) and Conjugated Hyperbilirubinemia What to Read Next on Medscape ... Hyperbilirubinemia in infants with Gram-negative sepsis does not affect mortality. Early Hum Dev. 2011 Aug. 87(8):515-9. [QxMD ... Differential Diagnosis of Conjugated Hyperbilirubinemia (Open Table in a new window). I. Acute or Chronic Hepatocellular ... Conjugated hyperbilirubinemia in infants: Is there still a role for ERCP?. Can J Gastroenterol Hepatol. 2021. 2021:9969825. [ ...
A common feature of congenital nonhemolytic hyperbilirubinemias is an abnormal serum bilirubin level without other ... Congenital nonhemolytic hyperbilirubinemias (CNH) are quite rare pathology of liver. They occur most often in children, but are ... Congenital nonhemolytic hyperbilirubinemias Ann Univ Mariae Curie Sklodowska Med. 2004;59(1):449-52. ... Congenital nonhemolytic hyperbilirubinemias (CNH) are quite rare pathology of liver. They occur most often in children, but are ...
Hyperbilirubinemia in the Newborn. What is hyperbilirubinemia in a newborn?. Hyperbilirubinemia happens when there is too much ... Key points about hyperbilirubinemia in the newborn. *Hyperbilirubinemia happens when there is too much bilirubin in your babys ... How is hyperbilirubinemia in a newborn diagnosed?. The timing of when your childs jaundice first starts matters. It may help ... How is hyperbilirubinemia in a newborn treated?. Treatment will depend on your childs symptoms, age, and general health. It ...
This child was born via emergency C-section and at age 2 weeks, had meconium ileus with perforation and DIC secondary to peritonitis. Enterococcus faecalis sepsis developed and terminal ileal resection was performed. Bilirubin levels remained elevated for 5 months.
... Zeinab Nabil Ahmed Said, Safinaz Adel El ... COVID-19-induced transaminitis and hyperbilirubinemia: Presentation and outcomes. World J Gastroenterol 2023; 29(7): 1123-1130 ...
Stanford Medicine Childrens Health Hyperbilirubinemia happens when there is too much bilirubin in your babys blood. Bilirubin ... Hyperbilirubinemia in the Newborn. What is hyperbilirubinemia in a newborn?. Hyperbilirubinemia happens when there is too much ... Key points about hyperbilirubinemia in the newborn. * Hyperbilirubinemia happens when there is too much bilirubin in your ... How is hyperbilirubinemia in a newborn diagnosed?. The timing of when your childs jaundice first starts matters. It may help ...
... concludes that the evidence is insufficient to recommend screening infants for hyperbilirubinemia to prevent chronic bilirubin ... Harms of detection and early treatment.Hyperbilirubinemia is commonly treated with phototherapy, and severe hyperbilirubinemia ... Phototherapy is commonly used to treat hyperbilirubinemia. Exchange transfusion is used to treat extreme hyperbilirubinemia. ... American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or ...
Neonatal Hyperbilirubinemia - Etiology, pathophysiology, symptoms, signs, diagnosis & prognosis from the Merck Manuals - ... Consequences of hyperbilirubinemia Hyperbilirubinemia may be harmless or harmful depending on its cause and the degree of ... Treatment of Neonatal Hyperbilirubinemia Treatment of hyperbilirubinemia is directed at the underlying disorder. In addition, ... It also can be classified by mechanism ( see Table: Causes of Neonatal Hyperbilirubinemia Causes of Neonatal Hyperbilirubinemia ...
Searching News Database: hyperbilirubinemia HSMN NewsFeed - 25 Sep 2020. Blueprint Medicines Announces European Commission ...
American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. . Management of hyperbilirubinemia in the newborn infant 35 ... Long-Awaited AAP Hyperbilirubinemia Guidelines Have Arrived Laura R. Kair, MD, MAS; Laura R. Kair, MD, MAS ... Since the 2004 guideline and 2009 clarification,6,12 the evidence base for hyperbilirubinemia has expanded,4,13-20 providing ... Laura R. Kair, Carrie A. Phillipi, Kelly E. Wood; Long-Awaited AAP Hyperbilirubinemia Guidelines Have Arrived. Hosp Pediatr ...
Hyperbilirubinemia can lead to brain complications in rare instances, which the guidelines work to prevent. ... Hyperbilirubinemia most often leads to jaundice, a condition where the skin and whites of the eyes take on a yellow appearance ... AAP announces revisions to clinical guidelines for hyperbilirubinemia treatment in infants August 5, 2022. Celeste Krewson, ... Hyperbilirubinemia can lead to brain complications in rare instances, which the guidelines work to prevent. ...
Molecular diagnosis of a familial non heamolytic hyperbilirubinemia (Gilberts Syndrome) in healthy subjects. ...
Background: A recent study proposed a risk factor scoring system for prediction of hyperbilirubinaemia that assigned increased ...
Which patients are at high risk for severe hyperbilirubinemia or acute bilirubin encephalopathy? Which patients need ... What characteristics differentiate the different types of nonpathologic and pathologic hyperbilirubinemia? ... The presence of hyperbilirubinemia risk factors is used to help interpret the results of the hour-specific nomogram. ... Hyperbilirubinemia risk factors include: * A newborn nursery predischarge TSB in the high-risk zone ...
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De Luca, Federico (2016) Umbilical cord blood base deficit predicts the development of hyperbilirubinemia in healthy term and ... Umbilical cord blood base deficit predicts the development of hyperbilirubinemia in healthy term and near term newborns ... Umbilical cord blood base deficit predicts the development of hyperbilirubinemia in healthy term and near term newborns ... Umbilical cord blood base deficit predicts the development of hyperbilirubinemia in healthy term and near term newborns ...
Impact of switching total bilirubin assays on the classification of neonates at high risk for hyperbilirubinemia Journal ... Isotonic versus hypotonic fluid supplementation in term neonates with severe hyperbilirubinemia - a double‐blind, randomized, ... controlled trial of compact fluorescent lamp versus standard phototherapy for the treatment of neonatal hyperbilirubinemia. ...
Detection, management and prevention of hyperbilirubinemia in term and late preterm newborn infants. Standard Treatment ...
Postnatal hyperbilirubinemia. Hyperbilirubinemia occurs in approximately 25% of infants of diabetic mothers, a rate ... The causes of hyperbilirubinemia in infants of diabetic mothers are multiple, but prematurity and polycythemia are the primary ... High hematocrit values in the neonate lead to vascular sludging, poor circulation, and postnatal hyperbilirubinemia. ... What is the frequency of postnatal hyperbilirubinemia in gestational diabetes mellitus (GDM)? ...
NICU-PEDIA is the complete resource for NICU families from admission to discharge and beyond. The website presents a wealth of information from neonatologists for families with preterm babies.
Keep in mind at one point this was 17! Im not sure if were safe to cross hyperbilirubinemia off her problem list just yet, ...
"Hyperbilirubinemia" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical ... This graph shows the total number of publications written about "Hyperbilirubinemia" by people in this website by year, and ... UGT1A1 promoter polymorphisms and the development of hyperbilirubinemia and gallbladder disease in children with sickle cell ... Variation in Care and Clinical Outcomes Among Infants Hospitalized With Hyperbilirubinemia. Hosp Pediatr. 2020 10; 10(10):844- ...
hyperbilirubinemia Tularemia in Cats - Thumper & Mickey Mouse are not Garfields Friends!. 16-10-17. by CriticalCareDVM ... Posted in: Diseases Tagged: fever, Francisella tularensis, hematuria, hyperbilirubinemia, hypoglycemia, hyponatremia, icterus, ... hyperbilirubinemia, icterus, jaundice, liver, post-hepatic, pre-hepatic, ultrasonography, urinalysis ...
"Hyperbilirubinemia" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical ... This graph shows the total number of publications written about "Hyperbilirubinemia" by people in UAMS Profiles by year, and ... Below are the most recent publications written about "Hyperbilirubinemia" by people in Profiles over the past ten years. ... Cadmium and arsenic override NF-?B developmental regulation of the intestinal UGT1A1 gene and control of hyperbilirubinemia. ...
encoded search term (Conjugated Hyperbilirubinemia) and Conjugated Hyperbilirubinemia What to Read Next on Medscape ... Hyperbilirubinemia in infants with Gram-negative sepsis does not affect mortality. Early Hum Dev. 2011 Aug. 87 (8):515-9. [QxMD ... Etiologies of conjugated hyperbilirubinemia in infancy: a systematic review of 1692 subjects. BMC Pediatr. 2015 Nov 20. 15:192 ... Dani C, Pratesi S, Raimondi F, Romagnoli C, for the Task Force for Hyperbilirubinemia of the Italian Society of Neonatology. ...
Evaluation of Hyperbilirubinemia: 3. References:. *Heathcote, E. J. (2007). Diagnosis and Management of Cholestatic Liver ...
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Neonatal Hyperbilirubinemia - Etiology, pathophysiology, symptoms, signs, diagnosis & prognosis from the MSD Manuals - Medical ... Consequences of hyperbilirubinemia Hyperbilirubinemia may be harmless or harmful depending on its cause and the degree of ... Treatment of Neonatal Hyperbilirubinemia Treatment of hyperbilirubinemia is directed at the underlying disorder. In addition, ... It also can be classified by mechanism ( see Table: Causes of Neonatal Hyperbilirubinemia Causes of Neonatal Hyperbilirubinemia ...
  • Eventually it causes unconjugated hyperbilirubinemia and jaundice as substance accumulates in the body due to the reduced ability of the enzyme. (wikipedia.org)
  • Hyperbilirubinaemia, presenting as jaundice, is a ubiquitous and frequently benign condition in newborn babies but is a leading cause of hospitalisation in the first week of life. (nih.gov)
  • For most babies, hyperbilirubinemia leads only to jaundice , a yellow appearance to the skin and whites of the eyes. (healthychildren.org)
  • Jaundice is a yellow discoloration of the skin and eyes caused by hyperbilirubinemia (elevated serum bilirubin concentration). (msdmanuals.com)
  • Neonatal Cholestasis Cholestasis is failure of bilirubin secretion, resulting in conjugated hyperbilirubinemia and jaundice. (msdmanuals.com)
  • [1] [2] In neonates, jaundice typically occurs due to unconjugated hyperbilirubinemia, which is characterized by the increased levels of indirect or unconjugated bilirubin (UCB) in the serum. (statpearls.com)
  • Hyperbilirubinemia itself resolves within 14 days (except for jaundice from breast milk). (wikilectures.eu)
  • Although the efficacy of exchange transfusion in the treatment of neonatal jaundice is known and quickly reduces blood bilirubin levels, but severe neonatal hyperbilirubinemia is associated with significant morbidity and mortality. (ac.ir)
  • Objective: To observe the incidence, causes of jaundice requiring Exchange and any adverse event of exchange transfusion in newborns with unconjugated hyperbilirubinemia. (journalcra.com)
  • Hyperbilirubinemia is universally present in the newborn period and is recognized as clinical jaundice in approximately 50% infants. (ijpediatrics.com)
  • Jaundice and hyperbilirubinemia in the Newborn. (ijpediatrics.com)
  • Raising phototherapy thresholds and revising risk assessment are among the key changes in the American Academy of Pediatrics' updated guidelines for managing hyperbilirubinemia in infants 35 weeks' gestation and older. (medscape.com)
  • The rate of increase in TSB or TcB, if more than one measure is available, may identify infants at higher risk of hyperbilirubinemia, according to the guidelines, and a possible delay of hospital discharge may be needed for infants if appropriate follow-up is not feasible. (medscape.com)
  • The American Academy of Pediatrics (AAP) has revised clinical guidelines on treating infants born at least 35 weeks into pregnancy for hyperbilirubinemia. (healthychildren.org)
  • Phototherapy can be used to prevent severe hyperbilirubinemia in infants with a moderately elevated TSB concentration and as initial therapy in those with severe hyperbilirubinemia. (medscape.com)
  • The most common symptom of hyperbilirubinemia in both infants and adults is a change in skin and eye color. (mfine.co)
  • Neural damage to infants from hyperbilirubinemia was thought to be a problem solved in the last century. (austinpublishinggroup.com)
  • Conjugated hyperbilirubinemia affects approximately 1 in every 2500 infants and is much less common than unconjugated hyperbilirubinemia. (mhmedical.com)
  • In the formative phase, we conducted eight focus group discussions with parents and grandparents of infants and eight key informant interviews with public and private healthcare providers and managers to explore their current knowledge , perceptions , practices, and challenges regarding identification and management of neonatal hyperbilirubinemia . (bvsalud.org)
  • Tan İ, Salihoğlu Ö, Demirelli Y, Hatipoğlu S. Clinical and laboratory characteristics and associated risk factors of infants hospitalized in newborn unit for indirect hyperbilirubinemia. (jceionline.org)
  • For assessment and monitoring, the guidelines advise the use of total serum bilirubin (TSB) as the definitive test for hyperbilirubinemia to guide phototherapy and escalation of care, including exchange transfusion. (medscape.com)
  • The presence of hyperbilirubinemia neurotoxicity risk factors lowers the threshold for treatment with phototherapy and the level at which care should be escalated," the authors wrote. (medscape.com)
  • Discontinuing phototherapy is an option when the TSB has decreased by at least 2 mg/dL below the hour-specific threshold at the initiation of phototherapy," and follow-up should be based on risk of rebound hyperbilirubinemia, according to the guidelines. (medscape.com)
  • What is the minimum duration of cycled phototherapy that is still effective in treating hyperbilirubinemia? (harvard.edu)
  • To standardize the use of phototherapy consistent with the American Academy of Pediatrics clinical practice guideline for the management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. (aap.org)
  • The intensity and spectral output of phototherapy devices is useful in predicting potential effectiveness in treating hyperbilirubinemia (group B recommendation). (aap.org)
  • Clinical trials have validated the efficacy of phototherapy in reducing excessive unconjugated hyperbilirubinemia, and its implementation has drastically curtailed the use of exchange transfusions. (aap.org)
  • This report standardizes the use of phototherapy consistent with the American Academy of Pediatrics clinical practice guideline for the management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. (aap.org)
  • Another treatment called exchange transfusion can be used in severe cases of hyperbilirubinemia. (healthychildren.org)
  • We conducted this study to investigate the risk factorsof severe hyperbilirubinemia in neonates undergoing exchange transfusion in Imam Reza Hospital Kermanshah, Iran. (ac.ir)
  • In this retrospective study , records of newborns with hyperbilirubinemia who were undergoing exchange transfusion to Imam Reza hospital in Kermanshah from of 2012 to 2016 were studied. (ac.ir)
  • Result: Out of 1970 cases of unconjugated hyperbilirubinemia 18(0.913%) required exchange transfusion. (journalcra.com)
  • Severe BWL was generally believed as a cause of significant hyperbilirubinemia in newborn babies. (ntu.edu.tw)
  • The aim was to determine the risk factors and treatment modalities of newborns with significant hyperbilirubinemia admitted from September 2011 to August 2013. (ijpediatrics.com)
  • One hundred and fifty newborns with significant hyperbilirubinemia, both inborn and outborn were included in the study. (ijpediatrics.com)
  • The presence of antenatal risk factors (P = 0.4), parity of the mother (P = 0.178) were not found to play a major role in development of significant hyperbilirubinemia. (ijpediatrics.com)
  • Significant hyperbilirubinemia was found to be more common in female babies, more than 37weeks of gestation, delivered vaginally, with birth weight of more than 2kgs, with ABO blood group incompatibility, admitted after 72hrs of life and with no identified antenatal risk factors. (ijpediatrics.com)
  • Pathak U, Chawla D, Kaur S, Jain S. Bilirubin nomogram for prediction of significant hyperbilirubinemia in north Indian neonates. (ijpediatrics.com)
  • Predictive ability of a predischarge hour-specific serum bilirubin for subsequent significant hyperbilirubinemia in healthy term and near-term newborns. (ijpediatrics.com)
  • The American Academy of Pediatrics established guidelines for the diagnosis and treatment of hyperbilirubinemia in newborns in 2004. (medscape.com)
  • These guidelines are based on the consensus of the American Academy of Pediatrics' Subcommittee on Hyperbilirubinemia. (medscape.com)
  • Universal screening for neonatal hyperbilirubinemia risk assessment is recommended by the American Academy of Pediatrics to reduce related morbidity . (bvsalud.org)
  • American academy of pediatrics, provisional committee for quality improvement and subcommittee on hyperbilirubinemia. (ijpediatrics.com)
  • The diagnosis of hyperbilirubinemia based on yellow discoloration of the skin and whiteness of eyes, idle in the child's movement and the lack of lactation. (journal-asia.education)
  • Orlistat treatment of unconjugated hyperbilirubinemia in Crigler-Najjar disease: a randomized controlled trial. (medscape.com)
  • Recurrent indirect hyperbilirubinemias in an infant can be caused by 2 autosomal recessive disorders- Gilbert syndrome and Crigler-Najjar syndrome. (pediatriconcall.com)
  • Since patients with Crigler-Najjar syndrome type II are much less likely to develop neurologic consequences than those with type I disease, 3 specific treatment for the hyperbilirubinemia may be unnecessary. (pediatriconcall.com)
  • Several inherited disorders can also produce unconjugated hyperbilirubinemia, including Gilbert syndrome, Crigler-Najjar syndromes type I and II, and inherited disorders causing hemolytic anemia. (statpearls.com)
  • We speak of pathological hyperbilirubinemia in the case of a specific increase in the level of conjugated and unconjugated bilirubin. (wikilectures.eu)
  • MOC reflex measurement has the potential to form part of the audiologic evaluation of newborns with hyperbilirubinemia in the future. (vivosonic.com)
  • We also discuss the management of severe hyperbilirubinaemia including the prevention of kernicterus, and highlight future directions for research. (nih.gov)
  • It presents early in life with unconjugated hyperbilirubinemia and kernicterus, but some patients may not have neurologic signs until later in life. (pediatriconcall.com)
  • Kernicterus is brain damage caused by unconjugated bilirubin deposition in basal ganglia and brain stem nuclei, caused by either acute or chronic hyperbilirubinemia. (msdmanuals.com)
  • In newborns, unconjugated hyperbilirubinemia is very common, and increased bilirubin (unconjugated) levels can cause life-threatening kernicterus. (statpearls.com)
  • However, newborns who are slightly premature and are breastfeeding, especially if discharged early from the hospital, must be monitored closely for hyperbilirubinemia because they can develop kernicterus if the bilirubin level becomes very high. (diseases-conditions.org)
  • The most common causes of severe hyperbilirubinemia including: unknown causes (42.2%, n=38), ABO incompatibility (27.8%, n=25), and sepsis (12.2%, n=11). (ac.ir)
  • According to the results, major risk factors for the occurrence of severe hyperbilirubinemia in neonates were birth weight less than 2,500 gram, gestational age below 37 weeks, age less than 5 days, and weight loss more than 10% of birth weight at the time of admission. (ac.ir)
  • However, the guidelines recommend against oral supplementation with water or dextrose water to prevent hyperbilirubinemia. (medscape.com)
  • There are ways we can help prevent hyperbilirubinemia, starting with good prenatal care and breastfeeding support,' Dr. Kemper said. (healthychildren.org)
  • The new thresholds, outlined in the complete guidelines, are based on gestational age , hyperbilirubinemia neurotoxicity risk factors, and the age of the infant in hours. (medscape.com)
  • Controlling for potential confounders including gestational age, these findings persisted with betamethasone-exposed neonates 1.6 times more likely to have hypoglycemia (aOR 1.60, 95% CI 1.24-2.07) and 3.2 times more likely to have hyperbilirubinemia (aOR 3.23, 95% CI 2.92-3.58). (elsevierpure.com)
  • Totally 222 newborns, aged ≥35 weeks of gestational age and hospitalized in neonatal unit with indirect hyperbilirubinemia, were investigated. (jceionline.org)
  • The current revision, published in Pediatrics, updates and replaces the 2004 AAP clinical practice guidelines for the management and prevention of hyperbilirubinemia in newborns of at least 35 weeks' gestation. (medscape.com)
  • Hereditary hyperbilirubinemia refers to the condition where levels of bilirubin are elevated, for reasons that can be attributed to a metabolic disorder. (wikipedia.org)
  • It's important for hospitals and clinicians caring for newborns to have plans in place to prevent the serious complications of hyperbilirubinemia, including measuring bilirubin on all newborns prior to discharge,' said Alex R. Kemper, MD, MPH, MS, FAAP, chair of the guideline authoring committee. (healthychildren.org)
  • Conjugated hyperbilirubinemia is defined as direct reacting bilirubin of >1.0 mg/dL (>17 µmol/L) if the total serum bilirubin is ≤5 mg/dL, or >20% of total serum bilirubin when the total bilirubin is >5 mg/dL. (mhmedical.com)
  • Thus, we sought to examine the association between antenatal betamethasone exposure and neonatal hypoglycemia and hyperbilirubinemia. (elsevierpure.com)
  • Conclusions: Antenatal betamethasone was associated with neonatal hypoglycemia and hyperbilirubinemia. (elsevierpure.com)
  • Transient familial hyperbilirubinemia is a metabolic disorder that is passed down through families. (medlineplus.gov)
  • Transient familial hyperbilirubinemia is an inherited disorder. (medlineplus.gov)
  • Physiological hyperbilirubinemia is characterized by a transient increase in unconjugated bilirubin. (wikilectures.eu)
  • Neurotoxicity is the major consequence of neonatal hyperbilirubinemia. (msdmanuals.com)
  • Gilbert syndrome has a broad differential diagnosis because numerous causes of unconjugated hyperbilirubinemia must be considered. (medscape.com)
  • A technical report, ' Diagnosis and Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation ,' also will be published. (healthychildren.org)
  • After diagnosis of hyperbilirubinemia, the patients were divided into three groups according to age (1-3), (4-7) and (7-9) days. (journal-asia.education)
  • ABSTRACT This study aimed to understand the reasons for late presentation of cases of severe neonatal hyperbilirubinaemia. (who.int)
  • Najib K, Saki F, Hemmati F, Inaloo S. Incidence, risk factors and causes of severe neonatal hyperbilirubinemia in South of Iran (Fars Province). (ijpediatrics.com)
  • Smith JR, Donze A, Schuller L. An evidence-based review of hyperbilirubinemia in the late preterm infant, with implications for practice: management, follow-up, and breastfeeding support. (medscape.com)
  • The ' Clinical Practice Guideline Revision: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation ,' published in the September 2022 Pediatrics, incorporates new research findings on risk-assessment and treatment. (healthychildren.org)
  • Clinical Practice Guideline Revision: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. (harvard.edu)
  • 2017. Mice with hyperbilirubinemia due to Gilbert's syndrome polymorphism are resistant to hepatic steatosis by decreased serine 73 phosphorylation of PPAR alpha. (nih.gov)
  • This activity describes the pathophysiology and management of unconjugated hyperbilirubinemia. (statpearls.com)
  • A 7-month-old boy was referred for recurrent indirect hyperbilirubinemia since day 6 of life. (pediatriconcall.com)
  • Depending on the form of bilirubin present in serum, hyperbilirubinemia can be further classified as unconjugated (indirect) or conjugated (direct). (statpearls.com)
  • The aim of this study was to investigate characteristics of neonates hospitalized to Neonatal Unit due to indirect hyperbilirubinemia and to determine risk factors for indirect hyperbilirubinemia. (jceionline.org)
  • 2021. Potential of therapeutic bile acids in the treatment of neonatal Hyperbilirubinemia. (nih.gov)
  • Explain how to differentiate unconjugated hyperbilirubinemia from conjugated hyperbilirubinemia. (statpearls.com)
  • It is also important to differentiate between physiological and pathological hyperbilirubinemia. (wikilectures.eu)
  • Clofibrate for the treatment of hyperbilirubinemia in neonates born at term: a double-blind controlled study (author's transl). (pediatriconcall.com)
  • Identify the several causes of unconjugated hyperbilirubinemia and summarize the available treatment options. (statpearls.com)
  • Neonates have physiologically increased bilirubin production and immature bilirubin metabolism, and present hyperbilirubinemia in association with genetic and or epigenetic factors. (elsevierpure.com)
  • Neonatal hyperbilirubinemia results from a readiness for the bilirubin production in neonates and limited their ability to excrete it. (journal-asia.education)
  • Hyperbilirubinemia is a common condition that affects approximately 60% of term newborn and 80% pre-term (premature) babies in the first week of birth. (mfine.co)
  • To evaluate medial olivocochlear efferent system of babies with hyperbilirubinemia with normal auditory brain stem responses. (vivosonic.com)
  • 0.05) in serum cystatin-C in neonatal hyperbilirubinemia as compared with healthy group. (journal-asia.education)
  • Risk of hyperbilirubinemia. (msdmanuals.com)
  • Statistical analysis revealed that maximal body weight loss is the only independent risk factor for the development of neonatal hyperbilirubinemia. (elsevierpure.com)
  • Bili Check vs JM-103 in identifying neonates not at risk of hyperbilirubinaemia. (ijpediatrics.com)
  • Hyperbilirubinaemia in appendicitis: the diagnostic value for prediction of appendicitis and appendiceal perforation. (springermedizin.de)
  • Unconjugated hyperbilirubinemia is a condition defined as elevated serum or plasma bilirubin (unconjugated) levels above the reference range of the laboratory. (statpearls.com)
  • Hyperbilirubinemia is a condition defined as elevated serum or plasma bilirubin levels above the reference range of the laboratory, and it is due to disorders of bilirubin metabolism. (statpearls.com)
  • Hyperbilirubinemia" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
  • We analyzed 280 neonates with BWL rate reaching the predictive value (4.5%, 7.5%, and 8% on the first, second, third day after birth, respectively) for subsequent hyperbilirubinemia after 72 hours after birth. (ntu.edu.tw)
  • See Chapter 99 for a discussion of unconjugated hyperbilirubinemia and Chapters 62 and 63 for rapid "on-call" assessment and management. (mhmedical.com)
  • The guideline updates and replaces the 2004 AAP clinical practice guideline for the management and prevention of hyperbilirubinemia. (healthychildren.org)
  • Practice parameter: management of hyperbilirubinemia in the healthy term newborn. (ijpediatrics.com)

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