Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HFRS-related oliguria brings about hyperactivity of the system hypothalamus-hypophysis-adrenals and hyperfunction of the pancreas; glucose, urea and creatinine plasma levels are elevated. Prednisolone treatment leads to diminution of ACTH and cortisol levels, elevation of glucose, insulin and C-peptide concentrations in plasma compared to prednisolone-untreated patients, producing insignificant effect on plasma levels of STH, vasopressin, aldosterone, area and creatinine. Therefore, a course administration of glucocorticoids to HFRS patients is justified only in severe collapses and hypopituitary coma confirmed by the laboratory methods.
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PMID:[Effect of glucocorticoid hormones on the status of the hypothalamo-hypophyseal-adrenal system and endocrine function of the pancreas in patients with hemorrhagic fever with renal syndrome]. 197 53

A syndrome of periodic catecholamine and prostaglandin E2 discharge is described in 2 patients aged 17 and 3 years. They had recurrent attacks of vomiting, hypertension and psychotic depression for several years with a fixed periodicity. At initiation of the attack, plasma ACTH, AVP, norepinephrine and prostaglandin E2 were markedly elevated, whereas dopamine was undetectable. This resulted in hypercortisolemia, hyponatremia and oliguria, which were completely normalized when the attack subsided. Dopaminergic inhibition by metoclopramide injection induced a sustained rise in plasma bicyclo-prostaglandin E2 in the patients, a transient rise in 4 controls, and no response in 8 control children. The 4 control responders had significantly higher plasma norepinephrine levels and aldosterone responses than the non-responders (P less than 0.001). There was a linear correlation between peak values of bicyclo-prostaglandin E2 and basal norepinephrine levels (r = 0.990, P less than 0.001). The patients released bicyclo-prostaglandin E2 and aldosterone more easily than the control responders in terms of plasma norepinephrine and dopamine levels. Treatment of the patient with clonidine was partially effective, whereas administration of indomethacin completely suppressed recurrence of the attacks for 1 year. These results suggest the etiologic possibility that the patients have a decreased dopaminergic inhibition of prostaglandin E2-mediated norepinephrine secretion, which causes periodic discharge of norepinephrine and concomitant release of ACTH and AVP.
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PMID:Recurrent attacks of vomiting, hypertension and psychotic depression: a syndrome of periodic catecholamine and prostaglandin discharge. 283 85

162 children with infantile spasms were treated with ACTH at the Children's Hospital, Helsinki, and at the Aurora Hospital, Helsinki, during 1960--76. In a large proportion (37%) of the children the treatment caused pronounced side effects, and the mortality was 4.9%. The most common complications were infections: septic infections, pneumonias, and urinary and gastrointestinal infections. Other side effects were arterial hypertension (11), osteoporosis (2), hypokalaemic alkalosis (2), and other marked electrolyte disturbances (10). In children necropsy showed fresh intracerebral haemorrhages. Four children developed oliguria and hyperkalaemia during and after withdrawal of ACTH. One of them had tubular necrosis confirmed by renal biopsy. Infections were significantly more common with large doses (120 units) of ACTH than with small ones (40 units). It is concluded that side effects, even severe ones, are more common during treatment than had been assumed. Careful watch is important before and after treatment. The benefit of very high dosages should also be reconsidered.
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PMID:ACTH therapy in infantile spasms: side effects. 625 50

In vitro secretion of glycocorticoids by adrenal glands pooled from several control mice was compared with that of glands removed from animals following injections of either ACTH or endotoxin. Both substances prevent glycocorticoid synthesis stimulated in vitro with ACTH. Cholesterol content of adrenal glands under these conditions was nearly depleted, indicating maximal response to ACTH or endotoxin prior to their removal for the in vitro tests. In an effort to account physiologically for the manner in which endotoxin suppresses or prevents the rise in urinary nitrogen excreted in response to ACTH, blood non-protein nitrogen levels (NPN) were determined. The following experimental conditions resulted in increased urinary nitrogen excretion but did not alter blood NPN: cortisone given alone or at the same time as endotoxin; ACTH alone; dichloroisoproterenol (DCI) given concurrently with endotoxin; and lactalbumin digest injected intraperitoneally. Increases (2- to 3-fold) in blood NPN were observed when endotoxin was given alone, concurrently with ACTH, or 3 hours prior to cortisone, DCI, or lactalbumin digest. Urinary nitrogen excretion showed no change under these conditions. The elevation in blood NPN in endotoxin-poisoned mice was found to be due almost entirely to urea nitrogen and not to amino acid nitrogen or to other nitrogenous wastes. Blood clearance of mulin, phenol red excretion, and urea elimination were each determined in control and in endotoxin-poisoned mice. The latter mice showed impaired renal function. Treatment with diuretics (diuril and aminophylline) failed to alter oliguria or elevated blood NPN. Hydergine treatment was also without effect. Total carcass NPN and urinary nitrogen excretion data were combined to give a picture of total protein catabolized by mice under different experimental conditions. Cortisone injected at the same time as endotoxin or 3 hours later resulted in the same increase in total NPN. However, in the former case all the extra nitrogen appeared in the urine while in the latter it remained in the carcass. ACTH given alone or concurrently with endotoxin produced large increases in total NPN but less in poisoned mice. This suggests that endotoxin suppresses adrenal response to ACTH. Urea injected into normal mice was recovered quantitatively in urine while in endotoxin-poisoned mice it was partitioned between carcass and urine. Elevation of carcass NPN by means of urea injections failed to alter the lethality of an LD(70) dose of endotoxin.
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PMID:EFFECTS OF BACTERIAL ENDOTOXINS ON METABOLISM : IV. RENAL FUNCTION AND ADRENOCORTICAL ACTIVITY AS FACTORS IN THE NITROGEN EXCRETION ASSAY FOR ENDOTOXIN. 1986 6