Plasmapheresis
Blood Group Incompatibility
Plasma Exchange
Immunoglobulins, Intravenous
Mushroom Poisoning
Purpura, Thrombotic Thrombocytopenic
Myasthenia Gravis
Cryoglobulins
Isoantibodies
Guillain-Barre Syndrome
ABO Blood-Group System
Ex vivo evaluation of a Taylor-Couette flow, immobilized heparinase I device for clinical application. (1/414)
Efficient and safe heparin anticoagulation has remained a problem for continuous renal replacement therapies and intermittent hemodialysis for patients with acute renal failure. To make heparin therapy safer for the patient with acute renal failure at high risk of bleeding, we have proposed regional heparinization of the circuit via an immobilized heparinase I filter. This study tested a device based on Taylor-Couette flow and simultaneous separation/reaction for efficacy and safety of heparin removal in a sheep model. Heparinase I was immobilized onto agarose beads via cyanogen bromide activation. The device, referred to as a vortex flow plasmapheretic reactor, consisted of two concentric cylinders, a priming volume of 45 ml, a microporous membrane for plasma separation, and an outer compartment where the immobilized heparinase I was fluidized separately from the blood cells. Manual white cell and platelet counts, hematocrit, total protein, and fibrinogen assays were performed. Heparin levels were indirectly measured via whole-blood recalcification times (WBRTs). The vortex flow plasmapheretic reactor maintained significantly higher heparin levels in the extracorporeal circuit than in the sheep (device inlet WBRTs were 1. 5 times the device outlet WBRTs) with no hemolysis. The reactor treatment did not effect any physiologically significant changes in complete blood cell counts, platelets, and protein levels for up to 2 hr of operation. Furthermore, gross necropsy and histopathology did not show any significant abnormalities in the kidney, liver, heart, brain, and spleen. (+info)"The FSGS factor:" enrichment and in vivo effect of activity from focal segmental glomerulosclerosis plasma. (2/414)
A circulating causative factor has been postulated in focal segmental glomerulosclerosis (FSGS). It has been shown that serum or plasma from some FSGS increases glomerular albumin permeability (Palb) in vitro. Palb greater than 0.5 (i.e., FS activity) is associated with recurrence after transplantation. Specimens from 15 FSGS patients were studied to document the presence of a permeability factor, to isolate this factor, to characterize its biochemical properties, and to show its effect in vivo. Total lipids were extracted by chloroform/methanol (2: 1); FS activity was absent from total lipid extract. Chylomicrons and lipoproteins were removed from the plasma with dextran sulfate, followed by sequential precipitation of proteins at 50 and 70% ammonium sulfate saturation. FS activity was retained in the 70% ammonium sulfate supernatant and exhibited a 100-fold purification. FS activity was lost after heating at 100 degrees C for 10 min or after protease digestion. Under nondenaturing conditions, electrophoresis of the FSGS 70% supernatant showed a prominent low molecular weight band that was not evident in the 70% supernatant from normal plasma. Dialysis and centrifugation-based membrane ultrafiltration of the FSGS factor indicated a molecular size between 30 and 50 kD. Injection of the 70% FSGS supernatant into rats caused a threefold increase in urine protein in collections from 6 to 24 h after injection. No increase in proteinuria occurred in rats injected with 70% supernatant from normal individuals. It is concluded that the FSGS factor is a low molecular weight protein with the potential to increase Palb in vitro and to cause proteinuria in vivo. (+info)The natural course of hepatitis C virus infection 18 years after an epidemic outbreak of non-A, non-B hepatitis in a plasmapheresis centre. (3/414)
BACKGROUND: The natural history of hepatitis C virus (HCV) infection is variable and factors determining the course of the illness are unclear. AIMS: To determine the natural course of HCV infection in a well characterised group of patients 18 years after an epidemic outbreak of non-A, non-B hepatitis at a plasmapheresis centre. METHODS: Between 1994 and 1996, 20 of 30 affected individuals were studied. HCV infection was confirmed using second and third generation ELISA test kits. HCV RNA was detected by a polymerase chain reaction (PCR) method and HCV genotyping was performed by analysing amplicons from the conserved 5'-non-translated region generated by nested PCR. Thirty two liver biopsies were carried out in 14 patients. RESULTS: HCV antibodies were detected in all subjects. Eighteen patients had abnormal liver enzymes and 17 were HCV RNA positive, all of whom were infected with genotype 1a. Ninety per cent of this cohort showed evidence of chronic HCV infection with 50% having progressive liver disease and 20% cirrhosis 18 years after acute onset of non-A, non-B hepatitis. Considerable variation in disease outcome occurred between individuals and no correlation with clinical features of the acute illness was found. CONCLUSIONS: Variability in the consequences of HCV infection in cases infected with the same virus suggests that host factors are important in determining disease outcome. The factors which determine differences in the natural history of the disease still remain to be elucidated. (+info)Pathogenesis and treatment of HTLV-I associated myelopathy. (4/414)
That HTLV-I is not a latent infection is indicated by the detection of mRNA in the peripheral blood and CNS of patients with HTLV-I infection and by the persisting humoral and cellular immune responses. Indeed the frequency of anti-HTLV CTL is extremely high. The reduction in anti-TAX CTL frequency following reduction in proviral load suggests that removal of viral antigen may result in a reduced inflammatory response at least in peripheral blood and although the clinical data should be interpreted with caution, perhaps in the CNS. Patients with more advanced disease, and possibly fixed deficits may not benefit from either anti-inflammatory or antiretroviral treatment. The patients with most to gain are those with least deficit in whom early diagnosis and treatment will depend on raising awareness of HTLV-I beyond the neurological community. Many patients with HAM first present to a urologist or gynaecologist with bladder dysfunction or may have been seen in the genitourinary clinical with impotence or positive treponemal serology, which in the older patient is often the result of childhood infection with Treponema pallidum pertenue. Investigation of these patients should include HTLV-I serology and further investigation of HTLV-I positive patients should include proviral load measurements as well as markers of inflammation. Treatments whether antiviral or anti-inflammatory should be assessed for their effect on both as well as a clinical response. (+info)Acquired factor VIII inhibitor in a non-hemophilic patient with chronic hepatitis C viral infection. (5/414)
Production of coagulation factor VIII inhibitor is rarely encountered in non-hemophilic patients. A 63-year-old Japanese male suffered from severe bleeding tendency caused by this inhibitor. Although he did not have malignancy or collagen disease, he had chronic hepatitis C virus (HCV) infection. Although HCV is known to induce production of various autoimmune antibodies, this may be the first report of a case with both acquired factor VIII inhibitor and HCV infection. (+info)Calcinosis cutis and intestinal pseudoobstruction in a patient with adult onset Still's disease associated with recurrent relapses of disordered coagulopathy. (6/414)
Adult onset Still's disease (AOSD) is a systemic inflammatory disorder of unknown origin, characterized by a typical spiking fever, evanescent salmon-colored rash, polyarthralgia, and myalgia. Calcinosis cutis and gastrointestinal involvement have rarely been noted in AOSD. We herein describe a 54-year-old woman who demonstrated repeated disseminated intravascular coagulation (DIC), and adult respiratory distress syndrome (ARDS), associated with AOSD. The patient also revealed a remarkable degree of digital calcinosis cutis and intestinal pseudoobstruction. A connective tissue disease, such as systemic sclerosis, might have been the underlying factor in the latter two symptoms. (+info)Systemic lupus erythematosus demonstrating serum anti-GM1 antibody, with sudden onset of drop foot as the initial presentation. (7/414)
In systemic lupus erythematosus (SLE), peripheral neuropathies are relatively uncommon and rarely present as the initial symptom. We herein describe a 61-year-old woman who developed a sudden onset of drop foot, which was indistinguishable from Guillain-Barre syndrome based on the clinical symptoms alone. Antibodies against ganglioside GM1 were detected in the serum, while no antibodies to Campylobacter jejuni were observed. An electrophysiological study showed axonal impairment rather than demyelination. A pathological examination of a sural nerve biopsy specimen and further laboratory examinations suggested the observed peripheral neuropathies to have arisen due to lupus vasculitis. The serological activities of SLE responded well to treatment with corticosteroids, mizoribine and immunoadsorption therapies, however, the drop foot symptoms did not change remarkably. (+info)Role of plasmalogens in the enhanced resistance of LDL to copper-induced oxidation after LDL apheresis. (8/414)
Extracorporeal reduction of plasma low density lipoproteins (LDLs) by LDL apheresis was shown to attenuate the proatherogenic influences of LDL, such as impairment of vasodilation and increased monocyte adhesion to the endothelium. In 16 patients with familial hypercholesterolemia, we analyzed whether LDL apheresis by the heparin precipitation procedure affected the oxidative resistance of LDL. Plasma LDL cholesterol concentrations were reduced by 65% after the apheresis. The lag time of copper-mediated LDL oxidation was increased from 103 to 117 minutes (P<0.0005). The LDL contents of alpha-tocopherol and beta-carotene, as well as the ratio of monounsaturated to polyunsaturated fatty acids in LDL, were not altered. However, the LDL apheresis induced a 15% increase in the LDL contents of plasmalogen phospholipids (P<0.0005), a class of ether phospholipids that were recently shown to prevent lipid oxidation. The phosphatidylcholine (PC) to lysoPC ratio was elevated by 16% after the apheresis (P<0.0005). The percent increase in LDL plasmalogen phospholipids showed a close association with the increased lag time after apheresis (P<0.0005). The LDL plasmalogen contents of the blood samples from patients and from normolipidemic donors were also positively related to the lag time (P<0.005). In vitro loading of LDL with plasmalogen phospholipids resulted in a prolongation of the lag time and an increase in the PC/lysoPC ratio. In conclusion, the rapid rise in LDL contents of plasmalogen phospholipids most probably causes the increase in lag time after LDL apheresis. Plasmalogens appear to play an important role in the oxidation resistance of LDL in vivo. (+info)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 or toxins, is then removed and replaced with fresh plasma or a plasma substitute. The remaining blood cells are mixed with the new plasma and returned to the body. This process is also known as therapeutic plasma exchange (TPE). It's used to treat various medical conditions including certain autoimmune diseases, poisonings, and neurological disorders.
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.
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.
Intravenous Immunoglobulins (IVIG) are a preparation of antibodies, specifically immunoglobulins, that are derived from the plasma of healthy donors. They are administered intravenously to provide passive immunity and help boost the immune system's response in individuals with weakened or compromised immune systems. IVIG can be used for various medical conditions such as primary immunodeficiency disorders, secondary immunodeficiencies, autoimmune diseases, and some infectious diseases. The administration of IVIG can help prevent infections, reduce the severity and frequency of infections, and manage the symptoms of certain autoimmune disorders. It is important to note that while IVIG provides temporary immunity, it does not replace a person's own immune system.
Mushroom poisoning refers to the adverse health effects that occur after ingesting toxic mushrooms. These effects can range from mild gastrointestinal symptoms like nausea, vomiting, and diarrhea, to severe neurological and systemic reactions, including hallucinations, organ failure, and even death in serious cases. The severity of the poisoning depends on several factors, including the type and amount of toxic mushroom consumed, the age and health status of the individual, and the time elapsed between ingestion and medical treatment. It is crucial to seek immediate medical attention if mushroom poisoning is suspected, as some symptoms may not appear until several hours or days after consumption, and delays in treatment can lead to more severe outcomes.
Thrombotic thrombocytopenic purpura (TTP) is a rare but serious blood disorder. It's characterized by the formation of small blood clots throughout the body, which can lead to serious complications such as low platelet count (thrombocytopenia), hemolytic anemia, neurological symptoms, and kidney damage.
The term "purpura" refers to the purple-colored spots on the skin that result from bleeding under the skin. In TTP, these spots are caused by the rupture of red blood cells that have been damaged by the abnormal clotting process.
TTP is often caused by a deficiency or inhibitor of ADAMTS13, a protein in the blood that helps to regulate the formation of blood clots. This deficiency or inhibitor can lead to the formation of large clots called microthrombi, which can block small blood vessels throughout the body and cause tissue damage.
TTP is a medical emergency that requires prompt treatment with plasma exchange therapy, which involves removing and replacing the patient's plasma to restore normal levels of ADAMTS13 and prevent further clotting. Other treatments may include corticosteroids, immunosuppressive drugs, and rituximab.
Myasthenia Gravis is a long-term autoimmune neuromuscular disorder that leads to muscle weakness. It occurs when communication between nerves and muscles is disrupted at the nerve endings, resulting in fewer impulses being transmitted to activate the muscles. This results in muscle weakness and rapid fatigue. The condition can affect any voluntary muscle, but it most commonly affects muscles of the eyes, face, throat, and limbs. Symptoms may include drooping eyelids (ptosis), double vision (diplopia), difficulty swallowing, slurred speech, and weakness in the arms and legs. The severity of symptoms can vary greatly from person to person, ranging from mild to life-threatening.
The disorder is caused by an abnormal immune system response that produces antibodies against the acetylcholine receptors in the postsynaptic membrane of the neuromuscular junction. These antibodies block or destroy the receptors, which leads to a decrease in the number of available receptors for nerve impulses to activate the muscle fibers.
Myasthenia Gravis can be treated with medications that improve communication between nerves and muscles, such as cholinesterase inhibitors, immunosuppressants, and plasmapheresis or intravenous immunoglobulin (IVIG) to remove the harmful antibodies from the blood. With proper treatment, many people with Myasthenia Gravis can lead normal or nearly normal lives.
Cryoglobulins are immunoglobulins (a type of antibody) that precipitate or become insoluble at reduced temperatures, typically below 37°C (98.6°F), and re-dissolve when rewarmed. They can be found in various clinical conditions such as infections, inflammatory diseases, and lymphoproliferative disorders.
The presence of cryoglobulins in the blood can lead to a variety of symptoms, including purpura (a type of skin rash), arthralgias (joint pain), neuropathy (nerve damage), and glomerulonephritis (kidney inflammation). The diagnosis of cryoglobulinemia is made by detecting the presence of cryoglobulins in the serum, which requires special handling and processing of the blood sample. Treatment of cryoglobulinemia depends on the underlying cause and may include medications such as corticosteroids, immunosuppressive agents, or targeted therapies.
Isoantibodies are antibodies produced by the immune system that recognize and react to antigens (markers) found on the cells or tissues of another individual of the same species. These antigens are typically proteins or carbohydrates present on the surface of red blood cells, but they can also be found on other cell types.
Isoantibodies are formed when an individual is exposed to foreign antigens, usually through blood transfusions, pregnancy, or tissue transplantation. The exposure triggers the immune system to produce specific antibodies against these antigens, which can cause a harmful immune response if the individual receives another transfusion or transplant from the same donor in the future.
There are two main types of isoantibodies:
1. Agglutinins: These are IgM antibodies that cause red blood cells to clump together (agglutinate) when mixed with the corresponding antigen. They develop rapidly after exposure and can cause immediate transfusion reactions or hemolytic disease of the newborn in pregnant women.
2. Hemolysins: These are IgG antibodies that destroy red blood cells by causing their membranes to become more permeable, leading to lysis (bursting) of the cells and release of hemoglobin into the plasma. They take longer to develop but can cause delayed transfusion reactions or hemolytic disease of the newborn in pregnant women.
Isoantibodies are detected through blood tests, such as the crossmatch test, which determines compatibility between a donor's and recipient's blood before transfusions or transplants.
Guillain-Barré syndrome (GBS) is a rare autoimmune disorder in which the body's immune system mistakenly attacks the peripheral nervous system, leading to muscle weakness, tingling sensations, and sometimes paralysis. The peripheral nervous system includes the nerves that control our movements and transmit signals from our skin, muscles, and joints to our brain.
The onset of GBS usually occurs after a viral or bacterial infection, such as respiratory or gastrointestinal infections, or following surgery, vaccinations, or other immune system triggers. The exact cause of the immune response that leads to GBS is not fully understood.
GBS typically progresses rapidly over days or weeks, with symptoms reaching their peak within 2-4 weeks after onset. Most people with GBS experience muscle weakness that starts in the lower limbs and spreads upward to the upper body, arms, and face. In severe cases, the diaphragm and chest muscles may become weakened, leading to difficulty breathing and requiring mechanical ventilation.
The diagnosis of GBS is based on clinical symptoms, nerve conduction studies, and sometimes cerebrospinal fluid analysis. Treatment typically involves supportive care, such as pain management, physical therapy, and respiratory support if necessary. In addition, plasma exchange (plasmapheresis) or intravenous immunoglobulin (IVIG) may be used to reduce the severity of symptoms and speed up recovery.
While most people with GBS recover completely or with minimal residual symptoms, some may experience long-term disability or require ongoing medical care. The prognosis for GBS varies depending on the severity of the illness and the individual's age and overall health.
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.
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