Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 59 year old woman with insulin-dependent diabetes mellitus and chronic diarrhea was found to have mild steatorrhea, selective plasma IgA deficiency and adrenal insufficiency. Significant adrenal secretion of corticosteroids resulted only after prolonged stimulation with large doses of exogenous ACTH. Plasma ACTH levels were not elevated during clinical adrenal insufficiency or after metyrapone administration but did respond normally to vasopressin and insulin-induced hypoglycemia. These studies were interpreted as showing both primary adrenal insufficiency and impaired pituitary reserve for ACTH secretion in response to the feedback stimulus. No deficiency was found in secretion of other pituitary tropic hormones. Jejunal biopsy showed a lack of IgA-containing plasma cells. With cortisone replacement, diarrhea subsided and a malabsorption pattern on a film of the small bowel was no longer seen. IgA deficiency has been noted frequently with steatorrhea but rarely with diabetes and only once previously with adrenal insufficiency.
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PMID:Atypical adrenal insufficiency with failure of the pituitary feedback receptor. A case with associated diabetes mellitus and selective IgA deficiency with steatorrhea. 17 48

UNICEF promotes the use of a very effective, inexpensive treatment of dehydration in developing countries: oral rehydration therapy (ORT), which is oral administration of a solution with equimolar concentrations of sodium and glucose (osmolality of about 300 mosmol). The solution is isotonic with respect to total body water when it reaches the small intestine. It expands the extracellular fluid without changing serum osmolality, thus, brain edema does not occur. Further, metabolic degradation of glucose eventually releases free water. On the other hand, intravenous rehydration with saline solution can be lethal, causing excess free water to expand shrunken cells and, thereby, causing brain swelling, rupture of blood vessels and hemorrhage. Yet, physicians and other health workers in developed countries have been quite sow to accept ORT. Leading conditions of dehydration include insensible loss of water and heat through evaporation from the respiratory tract and skin (common in dry air, hot environment, and fever), sensible loss of water and heat through perspiration (common in hot, humid environment and with warm and absorbent clothing), and irritation of the intestinal mucosa by allergies, infections, toxins, and intolerance to some nutrients, resulting in diarrhea. Diarrhea is indeed the main cause of dehydration. Other causes of dehydration are: failure of the hypothalamus to secrete antidiuretic hormone (ADH), kidney unresponsiveness to ADH, diabetes mellitus, protein-rich nutrition, catabolic states, and brush-border lactase after weaning. Physiological changes in dehydration consist of rigidity of the connective tissue (vascular system and lungs) and intracellular fluid loss to the extracellular spaces, resulting in dry mucous membranes, shrunken muscle cells in the lips and the tongue, soft eyes, and adverse effects to the central nervous system. Children become dehydrated more readily than adults, but they tolerate it better.
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PMID:Water: mechanism of oral rehydration, water deficiency = deficiency in salt. 150 31

Plasma renin activity, plasma aldosterone and arginine-vasopressin concentrations were determined in five diarrhoeic and five healthy newborn calves. In animals suffering from diarrhoea these three parameters were 10-15 times higher than those observed in controls. These results suggest that the hormonal systems that control fluid and electrolyte homeostasis are highly stimulated by dehydration and salt depletion induced by faecal losses of water and sodium in calves affected with diarrhoea.
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PMID:Renin-aldosterone system and arginine vasopressin in diarrhoeic calves. 177 95

Six new cases of psychogenic water intoxication are discussed in the light of 150 observations published in the literature since 1935. 87% of all patients were schizophrenic, and 13% had other psychoses and a variety of functional and organic psychopathies. Psychogenic polydipsia is a prerequisite of psychogenic water intoxication. Water intake either overrides an intact osmoregulation (46% of all cases) or, allied to an inadequate urinary dilutional capacity (54%), leads to a transitory, sometimes repeated, and (in 8% of all cases) lethal water intoxication and hypoosmolality. - The consequence of hypoosmolality is metabolic encephalopathy, with agitation, convulsions and coma as its most common symptoms. Profuse diuresis, enuresis and urinary retention, gastric dilatation, watery vomiting and watery diarrhea are diagnostically helpful symptoms of polydipsia typically denied by the patients. Hypoosmolality/hyponatremia are the hallmarks of water intoxication. However, fewer than 50% of all patients present with the expected maximal urinary dilution. Inadequate ADH activity and increased sensitivity of the renal tubule to antidiuretic hormone are the pathogenetic factors in this inappropriate urinary dilution, while psychosis, psychotropic drugs, diuretics, nicotine and alcohol withdrawal are possible causes and cofactors of polydipsia and inadequate urinary dilution. New aspects of treatment are discussed.
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PMID:[Psychogenic water intoxication]. 264 58

Drug-induced constipation is mostly caused by changes in gut motility, whilst diarrhoea is more frequently caused by an increase in intestinal fluid secretion. In both instances the drug has to reach the enteric nervous system or the enterocyte, either via the blood or from the lumen, in sufficient concentrations to affect the mediators that regulate motility and fluid transport. Diarrhoea and constipation are frequently mentioned as side-effects of drugs, and therapeutic agents for almost all organ systems have been implicated. However, both these side-effects are usually mild or moderate, and rarely necessitate interruption of drug treatment. An exception to this rule is the antibiotic-associated colitis seen in patients treated with antibiotics such as lincomycin or clindamycin; in principle almost all antibiotics may cause this severe and potentially life-threatening complication. Other rare forms of severe, drug-induced colitis and diarrhoea result from toxic or anaphylactic reactions against gold preparations, cytostatic agents and sulphonamides. Ischaemic colitis due to vascular complications has been described in some women taking oral contraceptives, and in patients treated with vasopressin or digitalis.
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PMID:Diarrhoea and constipation. 304 67

Energy expenditure, nitrogen excretion, and serum protein levels were studied from the time of hospital admission until 2 weeks after severe head injury in eight adolescents and four children with peak 24-hour Glasgow Coma Scale scores ranging from 3 to 8. The mean measured energy expenditure (MEE) was 1.3 times Harris and Benedict's predicted value for energy expenditure. Seventy percent of the patients achieved caloric balance (MEE X 1.2) by 4 to 14 days after injury, but balance was not consistently maintained. Five of the 12 patients had intermittent diarrhea, and two had increased gastric residuals. In five patients fluid restrictions were imposed due to either the syndrome of inappropriate secretion of antidiuretic hormone, pulmonary complications, or intracranial pressure complications. For the adolescents (aged 11 to 17 years) the mean calorie intake during the 1st week was 752 kcal/day and for the children (aged 2 to 5 years) it was 340 kcal/day. During the 2nd week the mean calorie intake for the adolescents was 1671 kcal/day and for the children was 691 kcal/day. Mean urinary nitrogen excretion was 307 mg/kg/day for the adolescents and 160 mg/kg/day for the children. The calculated mean nitrogen balance for the eight adolescents and the four younger children was -13.6 and -4.1, respectively. Mean albumin levels decreased from 2.9 gm/dl during the 1st week to 2.4 gm/dl during the 2nd week (normal 3.5 to 5.0 gm/dl). Mean total protein level during the 1st week was 5.4 gm/dl and increased to a mean of 6.0 gm/dl during the 2nd week (normal 6.0 to 7.8 gm/dl). Weight loss ranged from 2 to 26 lb during the 2-week period. From these studies it can be concluded that head injury in the child and adolescent induces a metabolic response that includes increased energy expenditure and decreased serum albumin levels similar to those observed for head-injured adults. Mean nitrogen excretion values are less than those in adults with a severe head injury.
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PMID:Nutritional support and measured energy expenditure of the child and adolescent with head injury. 311 94

The incidence of hyponatremia in 34 patients following administration of high-dose L-phenylalanine mustard (L-PAM) and dianhydrogalactitol (DAG) was determined. Two consecutive daily levels of 133 mEq/l or less were observed in 12 patients. These episodes coincided with the advent of diarrhea about 10-12 days after drug administration. The hyponatremia was not due to the syndrome of inappropriate antidiuretic hormone secretion.
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PMID:L-phenylalanine mustard-dianhydrogalactitol and hyponatremia. 315 41

Administration of vincristine resulted in a hyponatremic state and concurrent elevation of the plasma immunoreactive arginine8-vasopressin (IR-AVP) level in rats. Development of the vincristine-induced hyponatremia and hypoosmolality was accompanied by a loss in weight, a decreased water intake and a large reduction in the daily urine sodium excretion. The cause of the sodium loss is thought to be the diarrhea observed during vincristine treatment. Hematocrit and serum urea nitrogen levels were increased. It is concluded that the condition differs from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH): the increase in plasma IR-AVP concentration may be associated with dehydration due to vincristine toxicity.
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PMID:Hyponatremia and increased secretion of vasopressin induced by vincristine administration in rat. 342 63

Spontaneous bacterial peritonitis (SBP), a fascinating disease that had been reported perhaps 50 times in varying guises over the preceding century, suddenly burst forth in the 1960s and was recognized in clusters of cases almost simultaneously in Paris, London, and West Haven, Connecticut. The spectrum of the disease has broadened. Initially, it was associated almost exclusively with alcoholic cirrhosis, but it has now been found in association with posthepatitic cirrhosis, cryptogenic cirrhosis, chronic active liver disease, and, occasionally, in biliary cirrhosis and cardiac cirrhosis. Recently, it has been reported in alcoholic hepatitis and acute viral hepatitis. It occurs occasionally in malignant ascites and in pancreatitis in the absence of cirrhosis. It is surprisingly common in disseminated lupus, in which it occurs relatively more commonly than in alcoholic cirrhosis. A similar syndrome, primary peritonitis, occurs frequently in children with nephrotic ascites. The clinical pattern of SBP has broadened. Initially it consisted of abdominal pain, fever, rebound tenderness, hypoactive bowel sounds, hypotension, encephalopathy, and cloudy ascites with large numbers of polymorphonuclear leukocytes in ascitic fluid. Each and every symptom, sign, and laboratory abnormality may be absent; indeed, the syndrome can be completely silent. Initially, the causative bacteria appeared to be almost exclusively enteric, but now the list of bacteria isolated in cases of SBP looks like a bacteriology textbook. Anaerobes are rare. Multiple organisms usually suggest nonspontaneous origin such as perforation or vasopressin induction. The differentiation between spontaneous and nonspontaneous bacterial peritonitis is crucial in the differential diagnosis. The great majority of cases of SBP develop in the hospital, 80% more than one week after admission. It is therefore a nosocomial disease that may be precipitated by procedure-induced bacteremia, gastrointestinal bleeding, or diarrhea, and it tends to occur in patients with low ascitic fluid protein (complement) concentrations and severe portal-systemic shunting.
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PMID:Spontaneous bacterial peritonitis: variant syndromes. 368 33

Several physiological variables were measured after endotoxin administration in the rat to examine the relationship between these variables. Rats responded to endotoxin with a biphasic body temperature response, an initial decrease and a subsequent increase in body temperature. Plasma vasopressin and oxytocin levels increased markedly after endotoxin administration. Diarrhea occurred in some animals. There was a strong negative correlation between increase in body temperature and base-line body temperature, and weak correlations between body weight and plasma vasopressin release and between base-line body temperature and minimum body temperature reached. Plasma vasopressin and oxytocin levels were correlated if samples from all time points were analyzed together, whereas they were not correlated if data from each time point were analyzed separately or if total peptide release for each rat was evaluated. These data suggest similar regulation for the release of vasopressin and oxytocin, that is, release by a common stimulus, but the magnitude of release of vasopressin and oxytocin appears to be independent, probably reflecting differences in synthesis and storage of these two peptides.
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PMID:Characteristics of body temperature, vasopressin, and oxytocin responses to endotoxin in the rat. 382 4


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