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)

Septic shock may be defined as hypotension caused by bacteremia and accompanied by decreased peripheral blood flow, evidenced by oliguria. Clinically, a shaking chill is the warning signal. The immediate cause of hypotension is pooling of blood in the periphery, leading to decreased venous return: later, peripheral resistance falls and cardiac failure may occur. Irreversible shock is comparable to massive reactive hyperemia. Reticuloendothelial failure, histamine release, and toxic hypersensitivity may be factors in the pathogenesis of septic shock. Adrenal failure does not usually occur, but large doses of corticosteroid are employed therapeutically to counteract the effect of histamine release or hypersensitivity to endotoxin. The keys to successful therapy are time, antibiotics, vasopressors, cortisone and correction of acidosis.
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PMID:SEPTIC SHOCK. 1406 36

A 70-year-old obese, hypertensive woman taking angiotensin converting enzyme (ACE) inhibitors and chlorthalidone but with no history of corticosteroid treatment or hypothalamus-hypophyseal-adrenal disease, underwent nephrectomy and adrenalectomy under combined general and epidural anesthesia. Severe hypotension with oliguria developed during surgery and persisted during postoperative recovery, with anuria, metabolic acidosis, hyponatremia and hyperpotassemia. Although the symptoms were initially attributed to prior treatment with ACE inhibitors and diuretics together with combined anesthesia, the patient's lack of response to crystalloid, colloid and inotropic catecholamine therapy in the context of anuria, metabolic acidosis, hyponatremia and hyperpotassemia led us to consider a diagnosis of Addisonian crisis. Blood samples were taken to determine adrenocorticotropic hormone levels, and hydrocortisone treatment was started. The patient responded to treatment and cortisol levels fell, confirming the diagnosis of adrenal insufficiency. Compensatory endrocrine secretion of cortisol by the contralateral adrenal gland has been observed in patients undergoing nephrectomy and adrenalectomy for excision of a hypernephroma, and replacement therapy is therefore not recommended. Perioperative Addisonian crises have also been described in patients suffering great surgical stress, and severe hypotension has been observed in patients on long-term treatment with ACE inhibitors after induction of general anesthesia and after epidural anesthesia with local anesthetics. The combination of these factors made rapid diagnosis and start of appropriate therapy difficult.
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PMID:[Severe perioperative hypotension after nephrectomy with adrenalectomy]. 1460 83

Rhabdomyolysis is a syndrome characterized by muscle necrosis and the release of intracellular muscle contents into the systemic circulation. We hereby report a patient proved to be a case of unrecognized hypothyroidism presenting with rhabdomyolytic acute renal failure precipitated by the combined use of statin and fenofibrate. A 63-year-old woman was referred to our department because of fatigue, diffuse muscle pain and oliguria. On the basis of pathogenesis, clinical and laboratory examination the diagnoses of acute renal failure secondary to the statin-fibrate-derivative combination induced rhabdomyolysis and auto-immune thyroiditis induced hypothyroidism were made. Although saline, furosemide and sodium bicarbonate infusions enabled diuresis and have led to a rapid recovery of renal function and normalization of blood pressure in five days (creatinine level decreased from 4.5 mg/dl to 1.2 mg/dl), only thyroid replacement therapy (0,1 mg thyroxine) that begun after the exclusion of adrenal insufficiency resulted in complete resolution of rhabdomyolysis. This prompted the diagnosis of background, clinically silent rhabdomyolysis aggrevated by the statin-fibrate-derivative combination. To our knowledge this case illustrates the first example of rhabdomyolytic acute renal failure induced by a statin-fibrate-derivative combination with underlying hypothyroidism which was responsible for the basal clinically unobservable rhabdomyolysis.
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PMID:A case of rhabdomyolysis induced acute renal failure secondary to statin-fibrate-derivative combination and occult hypothyroidism. 1631 69

A recent survey found that approximately 4% of very low birth weight infants in Japan were treated with glucocorticoids postnatally for circulatory collapse thought to be caused by late-onset adrenal insufficiency. We identified 11 preterm infants with clinical signs compatible with this diagnosis (hypotension, oliguria, hyponatremia, lung edema, and increased demand for oxygen treatment) and matched them for gestational age with 11 infants without such signs. Blood samples were obtained for cortisol and its precursors from the patient group before the administration of hydrocortisone, and from the control group during the same postnatal week. All samples were analyzed using a gas chromatography-mass spectrometry system. Cortisol concentrations did not differ between the two groups (6.6 +/- 4.5 vs 3.4 +/- 2.7 microg/dL); however, the total concentration of precursors in the pathway to cortisol production was significantly higher in the patient group (72.2 +/- 50.3 vs 25.0 +/- 28.5 microg/dL; p < 0.05). We conclude that the clinical picture of late-onset adrenal insufficiency in preterm infants is not a result of an absolute deficiency of cortisol production, but may be a result of a limited ability to synthesize sufficient cortisol for the degree of clinical stress.
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PMID:Comparison of serum cortisol concentrations in preterm infants with or without late-onset circulatory collapse due to adrenal insufficiency of prematurity. 1852 Mar 32

Late-onset circulatory dysfunction (LCD) is a phenomenon specific to premature infants and is characterized by sudden onset of hyponatremia, hypotension, oliguria and non-physiological weight gain, without an obvious cause, in premature infants after stabilization of circulation and respiration. The cause of LCD is not clear, but adrenal insufficiency in premature infants is a severe syndrome because steroid replacement therapy is often essential to treat the symptoms. We report a rare case of a premature infant who developed an LCD crisis the day after thyroxine replacement therapy. The female infant was born at 25 weeks of gestational age, weighing 672 g, and appeared to have hypothyroidism, with free T4 of 0.19 ng/dl and elevated TSH levels of 26.3 microIU/ml at Day 14. She developed an LCD crisis the day after starting thyroxine treatment. She received steroid replacement therapy for 4 weeks and her adrenal function progressively recovered. She also needed thyroxine supplementation for 13 weeks, which maintained her thyroid function as euthyroid. Because she exhibited cortisol insufficiency and thyroid hormone insufficiency, the antecedent thyroid hormone replacement may be responsible for the onset of LCD. We must consider monitoring adrenal function when starting thyroxine therapy in premature infants with hypothyroxinemia.
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PMID:Late-onset circulatory dysfunction after thyroid hormone treatment in an extremely low birth weight infant. 2043 99

Late-onset glucocorticoid-responsive circulatory collapse (LGCC) in infants is characterized by sudden onset of hypotension and/or oliguria, which is resistant to volume expanders and inotropes but responds rapidly to intravenous glucocorticoids. LGCC occurs after the first week of life mainly in relatively stable very low birth weight (VLBW) infants. In Japan, the incidence of LGCC is reported to be 8%. Relative adrenal insufficiency (AI) is considered the most likely cause of LGCC, but its detailed pathophysiology remains unclear. Intrinsic and extrinsic factors may affect the pathophysiological mechanism. LGCC should be recognized as one of the high-risk complications in VLBW infants and managed promptly and properly, because if it is not, it may cause life-long neurological problems. To diagnose relative AI, an accurate evaluation of adrenal function is necessary; however, the interpretation of basal serum cortisol levels is difficult in preterm infants after 7 days of life. To recognize LGCC, it is recommended that blood pressure and urine volume be carefully monitored, even outside of the transitional period. If no underlying causes are documented or volume expansion and inotropic support fail, intravenous hydrocortisone should be initiated, and an additional dose of hydrocortisone is required when the response is inadequate. There are few reports to verify or characterize LGCC and this phenomenon has not been recognized worldwide to date. This review summarizes the current knowledge about LGCC in premature infants and evaluates the most significant new findings regarding its pathophysiology, treatment, and prognosis.
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PMID:Late-onset glucocorticoid-responsive circulatory collapse in premature infants. 3156 21