Inappropriate ADH Syndrome
Alcohol Dehydrogenase
Down Syndrome
Metabolic Syndrome X
Trazodone
Treating the syndrome of inappropriate ADH secretion with isotonic saline. (1/191)
It has been widely accepted that there is little use for saline treatment in the syndrome of inappropriate secretion of ADH (SIADH). However, having observed that most SIADH patients increased their plasma sodium (PNa) after 2 l isotonic saline over 24 h, we investigated whether urine osmolality or the sum of urinary sodium and potassium (UNa + K) predicted this response, in 17 consecutive patients with chronic SIADH. The initial measure of urinary sodium plus potassium (UNa + K t0) was weakly correlated to the change in PNa (DPNa) after infusion (r = -0.51; p < 0.05), while initial urine osmolality (UOSM t0) was a much better predictor (y = -0.024x + 12.90; r = -0.81; p < 0.001). The lack of predictive value for UNa + K t0 was probably because urine electrolyte concentrations were not maximal for the corresponding initial UOSM. This reflects differences in salt intake between the patients. The theoretical maximal value for UNa + K t0 (th max UNa + K t0) for a given USOM t0, was as good a predictor as UOSM t0 (th max UNa + K vs. DPNa: r = -0.81; p < 0.001). A theoretical model describing the effect of 2 l isotonic saline infusion on DPNa as a function of UNa + K, produced values comparable to those observed in our patients. Only 6/17 patients, those with UOSM > 530 mOsm/kg, had their hyponatraemia aggravated by 2 l isotonic saline. Many SIADH patients have lower UOSM; in most such patients, 2 l of isotonic saline will improve PNa. (+info)Hypertonic saline test for the investigation of posterior pituitary function. (2/191)
The hypertonic saline test is a useful technique for distinguishing partial diabetes insipidus from psychogenic polydipsia, and for the diagnosis of complex disorders of osmoreceptor and posterior pituitary function. However, there is little information concerning its use in childhood. The experience of using this test in five children (11 months to 18 years) who presented diagnostic problems is reported. In two patients, in whom water deprivation tests were equivocal or impractical, an inappropriately low antidiuretic hormone (ADH) concentration (< 1 pmol/l) was demonstrated in the presence of an adequate osmotic stimulus (plasma osmolality > 295 mosmol/kg). In two children--one presenting with adipsic hypernatraemia and the other with hyponatraemia complicating desmopressin treatment of partial diabetes insipidus--defects of osmoreceptor function were identified. Confirming a diagnosis of idiopathic syndrome of inappropriate ADH secretion (SIADH) was possible in a patient with no other evidence of pituitary dysfunction. The hypertonic saline test was well tolerated, easy to perform, and diagnostic in all cases. (+info)Hyponatraemia: biochemical and clinical perspectives. (3/191)
Hyponatraemia is a common bio-chemical abnormality, occurring in about 15% of hospital inpatients. It is often associated with severe illness and relatively poor outcome. Pathophysiologically, hyponatraemia may be spurious, dilutional, depletional or redistributional. Particularly difficult causes and concepts of hyponatraemia are the syndrome of inappropriate antidiuresis and the sick cell syndrome, which are discussed here in detail. Therapy should always be targeted at the underlying disease process. 'Hyponatraemic symptoms' are of doubtful importance, and may be more related to water overload and/or the causative disease, than to hyponatraemia per se. Artificial elevation of plasma sodium by saline infusion carries the risk of induction of osmotic demyelination (central pontine myelinolysis). (+info)Demeclocycline in the treatment of the syndrome of inappropriate antidiuretic hormone release: with measurement of plasma ADH. (4/191)
A patient with the syndrome of inappropriate antidiuretic hormone release (SIADH) following head injury and meningitis was studied during treatment with demeclocycline, a drug known to produce a reversible nephrogenic diabetes insipidus. No changes were observed during six days of demeclocycline 1200 mg/24 hr but urine output increased significantly, with the production of a dilute urine, when the dose was increased to 2400 mg/24 hr. The patient lost weight, and all biochemical features of the syndrome were rapidly corrected despite an unchanged fluid intake and despite the persistence of high plasma levels of ADH. The rise in serum sodium was accompanied by mild sodium retention, as measured by external balance and exchangeable sodium. A complication of treatment was the development of acute renal failure possibly induced by a nephrotoxic effect of high circulating levels of demeclocyline. On stopping demeclocyline renal function returned to normal and, after some delay, SIADH returned, and was still present 9 months after initial presentation. This confirms earlier reports of the efficacy of demeclocycline in SIADH; but the authors advise caution against increasing the dose above 1200 mg/24 hr. (+info)Syndrome of inappropriate secretion of antidiuretic hormone associated with idiopathic normal pressure hydrocephalus. (5/191)
A 79-year-old woman suffering from urinary incontinence and unsteady gait was diagnosed as having idiopathic normal pressure hydrocephalus (NPH) with hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The concentration of antidiuretic hormone was high while the plasma osmolality was low in the presence of concentrated urine during the episodes of hyponatremia. Magnetic resonance imaging (MRI) of the head showed enlargement of the third and lateral ventricles. After ventriculoperitoneal shunt surgery, the symptoms of NPH and hyponatremia improved. It may be possibly explained that mechanical pressure on the hypothalamus from the third ventricle is responsible for hyponatremia. (+info)Severe hyponatremia caused by hypothalamic adrenal insufficiency. (6/191)
A 60-year-old woman was admitted with severe hyponatremia. Basal values of adrenocorticotropic hormone (ACTH), thyroid hormone and cortisol were normal on admission. Impairment of water diuresis was observed by water loading test. Initially, we diagnosed her condition as the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). By provocation test, we finally confirmed that the hyponatremia was caused by hypothalamic adrenal insufficiency. The basal values of ACTH and cortisol might not be sufficient to exclude the possibility of adrenal insufficiency. Therefore, it is necessary to evaluate adrenal function by provocation test or to re-evaluate it after recovery from hyponatremia. (+info)Premenstrual attacks of acute intermittent porphyria: hormonal and metabolic aspects - a case report. (7/191)
We report the case of a 38-year-old woman with acute intermittent porphyria (AIP). Following the observation of an acute AIP attack in the patient's father, the diagnosis was established after genetic and biochemical examinations. At the age of 29, eight months after delivery of her first and only child, the patient was hospitalized due to a first proven attack of AIP. In the following years she suffered several premenstrual AIP attacks, with clinical symptoms ranging from abdominal pain to paralysis. One attack was accompanied by an increased urinary catecholamine output, strongly indicating adrenergic hyperactivity. The precipitation of acute episodes by secretion of gonadotrophins and a severe hyponatraemia due to a syndrome of inappropriate anti-diuretic hormone secretion indicated hypothalamic involvement in the pathogenesis of AIP. This patient has experienced an evolution of treatment regimens. At first, acute attacks were treated by i.v. hypertonic glucose. Afterwards propranolol was instituted as a maintenance therapy. Later on, i.v. injections of haem arginate were very successful in resolving acute AIP episodes. However, until therapy with an LHRH analogue was started, the patient continued to suffer premenstrual AIP attacks. These LHRH analogues cause hypothalamic inhibition of gonadotrophin secretion, with stabilization of endogenous ovarian steroid production at a low level, and therefore may be effective in preventing acute exacerbations of this disease. Since this patient went on a fixed regimen of an LHRH analogue combined with the lowest dose oestrogen patch her quality of life has improved substantially and she has not required hospitalization, now for over 3 years. (+info)Osmoregulation of vasopressin secretion in patients with the syndrome of inappropriate antidiuresis associated with central nervous system disorders. (8/191)
To clarify the characteristics of vasopressin (AVP) secretion in patients with the syndrome of inappropriate antidiuresis (SIAD) related to central nervous system disorders, we examined the response of AVP secretion to osmotic stimulus by hypertonic saline infusion and analyzed the possible causative factors in six patients with SIAD associated with head trauma or cerebral infarction. Hyponatremia developed after head trauma in four patients and cerebral infarction in two patients. In all patients the clinical state and laboratory findings fulfilled the criteria for SIAD, which was supported by either nonsuppressible plasma AVP levels or effectiveness of treatments with water restriction, demeclocycline, nonpeptide V2 AVP antagonist or diphenylhydantoin. Although patterns of plasma AVP response to the osmotic stimulus varied, plasma AVP concentrations neither increased nor decreased to undetectable levels with a rise in plasma osmolality. In one patient, plasma AVP levels responded to increasing plasma osmolality when plasma osmolality normalized; in which the threshold and the sensitivity of osmostat were normal. In two other patients, AVP secretion responded to plasma osmolality after the treatment. The changes in AVP secretion were not due to nonosmotic stimuli for AVP release. In conclusion, this study shows that patients with SIAD and central nervous system disorders may have persistent AVP secretion with a loss of hypotonic suppression such as found in patients with adrenal insufficiency or depletional hyponatremia in central nervous system disorders, indicating that careful evaluation is necessary to determine the relationship between persistent AVP secretion and the pathogenesis of hyponatremic disorders. (+info)Inappropriate Antidiuretic Hormone (ADH) Syndrome, also known as the Syndrome of Inappropriate Antidiuresis (SIAD), is a condition characterized by the excessive release or action of antidiuretic hormone (ADH) leading to an imbalance of water and electrolytes in the body.
ADH is a hormone produced by the pituitary gland that helps regulate water balance in the body by controlling the amount of urine produced by the kidneys. In normal conditions, ADH levels increase in response to dehydration or decreased blood volume, causing the kidneys to retain water and decrease urine output.
However, in Inappropriate ADH Syndrome, there is an overproduction or inappropriate release of ADH, even when the body does not need it. This can lead to a condition called hyponatremia, which is low sodium levels in the blood. Hyponatremia can cause symptoms such as headache, confusion, seizures, and in severe cases, coma or death.
Inappropriate ADH Syndrome can be caused by various factors, including certain medications, brain tumors, lung diseases, and other medical conditions that affect the production or release of ADH. It is important to diagnose and treat Inappropriate ADH Syndrome promptly to prevent serious complications from hyponatremia. Treatment typically involves addressing the underlying cause and adjusting fluid intake and electrolyte levels as needed.
A syndrome, in medical terms, is a set of symptoms that collectively indicate or characterize a disease, disorder, or underlying pathological process. It's essentially a collection of signs and/or symptoms that frequently occur together and can suggest a particular cause or condition, even though the exact physiological mechanisms might not be fully understood.
For example, Down syndrome is characterized by specific physical features, cognitive delays, and other developmental issues resulting from an extra copy of chromosome 21. Similarly, metabolic syndromes like diabetes mellitus type 2 involve a group of risk factors such as obesity, high blood pressure, high blood sugar, and abnormal cholesterol or triglyceride levels that collectively increase the risk of heart disease, stroke, and diabetes.
It's important to note that a syndrome is not a specific diagnosis; rather, it's a pattern of symptoms that can help guide further diagnostic evaluation and management.
Alcohol dehydrogenase (ADH) is a group of enzymes responsible for catalyzing the oxidation of alcohols to aldehydes or ketones, and reducing equivalents such as NAD+ to NADH. In humans, ADH plays a crucial role in the metabolism of ethanol, converting it into acetaldehyde, which is then further metabolized by aldehyde dehydrogenase (ALDH) into acetate. This process helps to detoxify and eliminate ethanol from the body. Additionally, ADH enzymes are also involved in the metabolism of other alcohols, such as methanol and ethylene glycol, which can be toxic if allowed to accumulate in the body.
Down syndrome is a genetic disorder caused by the presence of all or part of a third copy of chromosome 21. It is characterized by intellectual and developmental disabilities, distinctive facial features, and sometimes physical growth delays and health problems. The condition affects approximately one in every 700 babies born in the United States.
Individuals with Down syndrome have varying degrees of cognitive impairment, ranging from mild to moderate or severe. They may also have delayed development, including late walking and talking, and may require additional support and education services throughout their lives.
People with Down syndrome are at increased risk for certain health conditions, such as congenital heart defects, respiratory infections, hearing loss, vision problems, gastrointestinal issues, and thyroid disorders. However, many individuals with Down syndrome live healthy and fulfilling lives with appropriate medical care and support.
The condition is named after John Langdon Down, an English physician who first described the syndrome in 1866.
Metabolic syndrome, also known as Syndrome X, is a cluster of conditions that increase the risk of heart disease, stroke, and diabetes. It is not a single disease but a group of risk factors that often co-occur. According to the American Heart Association and the National Heart, Lung, and Blood Institute, a person has metabolic syndrome if they have any three of the following five conditions:
1. Abdominal obesity (waist circumference of 40 inches or more in men, and 35 inches or more in women)
2. Triglyceride level of 150 milligrams per deciliter of blood (mg/dL) or greater
3. HDL cholesterol level of less than 40 mg/dL in men or less than 50 mg/dL in women
4. Systolic blood pressure of 130 millimeters of mercury (mmHg) or greater, or diastolic blood pressure of 85 mmHg or greater
5. Fasting glucose level of 100 mg/dL or greater
Metabolic syndrome is thought to be caused by a combination of genetic and lifestyle factors, such as physical inactivity and a diet high in refined carbohydrates and unhealthy fats. Treatment typically involves making lifestyle changes, such as eating a healthy diet, getting regular exercise, and losing weight if necessary. In some cases, medication may also be needed to manage individual components of the syndrome, such as high blood pressure or high cholesterol.
Trazodone is an antidepressant medication that belongs to the class of drugs called serotonin antagonist and reuptake inhibitors (SARIs). It works by increasing the levels of the neurotransmitter serotonin in the brain, which helps to improve mood and reduce symptoms of depression.
Trazodone is primarily used to treat major depressive disorder, but it may also be prescribed for anxiety, insomnia, and other conditions. The medication comes in various forms, including tablets and an extended-release formulation, and is typically taken orally one to three times a day. Common side effects of trazodone include dizziness, dry mouth, and sedation.
It's important to note that trazodone can interact with other medications and substances, so it's essential to inform your healthcare provider about all the drugs you are taking before starting treatment. Additionally, trazodone may increase the risk of suicidal thoughts or behavior in some people, particularly during the initial stages of treatment, so close monitoring is necessary.
Bromthymol Blue is a pH indicator dye that is commonly used in laboratory settings to determine the acidity or alkalinity of a solution. It is a blue, water-soluble compound that turns yellow in acidic solutions with a pH below 6.0 and can turn green, blue, or purple in solutions with a pH between 6.0 and 7.6, depending on the concentration of hydrogen ions present. At a pH above 7.6, Bromthymol Blue turns bright blue-green.
The chemical formula for Bromthymol Blue is C27H35BrClO5S. It has a molecular weight of 609.64 g/mol and a structural formula that includes a thymol blue core with bromine and chlorine atoms attached to it, along with a sulfonate group that makes the compound water-soluble.
Bromthymol Blue is often used in medical and biological research to measure pH changes in bodily fluids such as urine or blood. It can also be used in environmental testing to monitor water quality and detect acid rain, for example. In addition, Bromthymol Blue has been used in educational settings to teach students about pH and chemical indicators.
Second-generation antidepressants (SGAs) are a class of medications used primarily for the treatment of depression, although they are also used for other psychiatric and medical conditions. They are called "second-generation" because they were developed after the first generation of antidepressants, which include tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs).
SGAs are also known as atypical antidepressants or novel antidepressants. They work by affecting the levels of neurotransmitters in the brain, such as serotonin, norepinephrine, and dopamine. However, they have a different chemical structure and mechanism of action than first-generation antidepressants.
Some examples of second-generation antidepressants include:
* Selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine (Prozac), sertraline (Zoloft), and citalopram (Celexa)
* Serotonin-norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine (Effexor) and duloxetine (Cymbalta)
* Norepinephrine and dopamine reuptake inhibitors (NDRIs) such as bupropion (Wellbutrin)
* Atypical antidepressants such as mirtazapine (Remeron), trazodone, and vortioxetine (Brintellix)
SGAs are generally considered to have a more favorable side effect profile than first-generation antidepressants. They are less likely to cause anticholinergic effects such as dry mouth, constipation, and blurred vision, and they are less likely to cause cardiac conduction abnormalities or orthostatic hypotension. However, SGAs may still cause side effects such as nausea, insomnia, sexual dysfunction, and weight gain.
It's important to note that the choice of antidepressant medication should be individualized based on the patient's specific symptoms, medical history, and other factors. It may take some trial and error to find the most effective and well-tolerated medication for a given patient.