Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 14 year old boy was admitted for vomiting, anorexia, flank pain and leukocyturia/hematuria. Shortly after admission, he developed anuria and acute renal failure so that hemodialysis had to be started. Pre- and post-renal causes were excluded. There were no signs of acute glomerulonephritis; liver enzymes were normal. The 123Iodine-Hippuran scan showed a shock kidney pattern lacking tubular clearance. Renal biopsy revealed an interstitial nephritis with edema and a mixed cellular infiltration. History was empty for nephrotoxic agents except for mushroom ingestion: Five days before admission the boy ate Cortinarius speciocissimus mushrooms, the toxine of which is known to be nephrotoxic, causing irreversible renal failure in severe cases (Orellanus Syndrome). Renal function did not improve much and renal transplantation was performed after 14 months on hemodialysis. In interstitial nephritis of unknown etiology the possibility of mushroom poisoning should be considered.
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PMID:[Terminal renal failure caused by interstitial nephritis following mushroom poisoning by Cortinarius speciocissimus]. 361 24

Nephrogenic diabetes insipidus usually presents with polyuria, polydipsia, fever, vomiting, dehydration and failure to thrive. However, in infancy polyuria may be absent because of dehydration and reduced glomerular filtration rate. In 2 cases the main presenting feature was hypotonia, with marked head lag. Family studies confirmed the X-linked mode of inheritance of the disease; in case 1 the disease appeared to have arisen as a new mutation in the mother, and in case 2 the carrier status was traced back to the great-grandmother. Pitfalls in the diagnosis and detection of the carriers are discussed. Treatment with thiazide diuretics and prostaglandin synthesis inhibitors is effective in reducing urine volumes and polydipsia. The early detection of the disease and adequate management may prevent such complications as megacystis, mega-ureter and hydronephrosis, with resulting renal failure. Mental and physical retardation may also be avoided.
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PMID:Nephrogenic diabetes insipidus presenting with infantile hypotonia. A report of 2 cases. 373 62

An autopsy case of clostridial gas gangrene occurring in a 54-year-old man with colon adenocarcinoma, liver cirrhosis, and diabetes mellitus is reported. The patient died 4 days after the onset of symptoms with episodes of vomiting and abdominal pain. Gangrene of both hips and perineum, hemolysis, renal failure, and disseminated intravascular coagulation were the dominant clinical features. Clostridium septicum was isolated from the subcutaneous tissue fluid. Adenocarcinoma of the ascending colon with ulceration found at autopsy was supposed to be an entry of the organism. Histologically, lesions of subcutaneous tissue and muscles were characterized by the absence of inflammatory infiltrates in spite of extensive necrosis. A summary of 35 cases of gas gangrene hospitalized to the Osaka University Hospital for the past 16 years indicates that clostridial gas gangrene patients with underlying diseases such as malignant neoplasm, diabetes, liver cirrhosis or immunodeficiency have a relatively poor prognosis.
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PMID:A case of nontraumatic clostridial gas gangrene occurring in a patient with colon adenocarcinoma, liver cirrhosis, and diabetes mellitus. 373 9

Acute iron poisoning is most common in children below the age of 5 years. While there is no doubt that it may be fatal, recent surveys show that death occurs in only a very small percentage of cases and that iron salts are responsible for a small minority of fatalities due to overdosage with drugs. Similarly, the proportion of severe cases seems to have fallen over the last thirty years, possibly due to earlier and more aggressive treatment but more probably due to an increase in the number of minor exposures reported. Iron salts are directly toxic to the gastrointestinal tract causing vomiting, diarrhoea, abdominal pain and occasionally significant blood loss. They also cause metabolic acidosis by interfering with intermediary metabolism and producing shock and reduced tissue perfusion. The clinical course of acute iron poisoning is divided into 4 phases. Features of acute gastrointestinal irritation dominate the period up to 6 hours after ingestion and most patients do not develop other features or progress beyond this stage. Rarely, blood loss may be sufficient to cause hypotension. Severe poisoning is characterised by impairment of consciousness, convulsions and metabolic acidosis. The second phase, 6 to 12 hours after ingestion, is one of remission of features. Phase 3 comprises the period 12 to 48 hours from ingestion and is reached only by a small minority of patients. Recurrence or development of shock, and metabolic acidosis are usual and renal failure and features of extensive hepatocellular necrosis may develop. The last (fourth) phase, 2 to 6 weeks after ingestion, is only likely to develop in young children and is characterised by recurrence of vomiting due to gastric or duodenal stenosis caused by healing of iron-induced mucosal ulcers. Acute iron poisoning in humans has not been adequately studied and is unlikely to be so now because of the infrequent and sporadic occurrence of cases. The evidence for many conventional aspects of management is therefore unsatisfactory. Assessment of severity of poisoning is an essential prerequisite to optimum management but is difficult. The amount of elemental iron ingested is unacceptable since it is seldom known with accuracy and absorption is unpredictable because of vomiting and diarrhoea. The commonly encountered clinical features are also unreliable although it is generally accepted that coma, shock and metabolic acidosis indicate severe poisoning.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Management of acute iron poisoning. 378 42

An adult Keeshond had clinical signs associated with hypercalcemia, including inappetence, polyuria, polydipsia, and vomiting. Blood biochemical findings and urinary clearance studies were consistent with a diagnosis of primary hyperparathyroidism. Histomorphometric analysis of trabecular bone in an iliac crest biopsy indicated increased bone remodeling activity. Surgical exploration of the neck revealed an oval mass, which was removed by blunt dissection. Histologic diagnosis was parathyroid gland adenoma. The dog died because of renal failure on the eighth postoperative day. This report defines primary hyperparathyroidism in the dog, thus facilitating diagnosis for the veterinary clinician.
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PMID:Primary hyperparathyroidism in a dog: biochemical, bone histomorphometric, and pathologic findings. 380 43

In a 26-year-old patient admitted to the emergency ward with acute abdomen, all the symptoms--nausea, vomiting, indeterminate abdominal pain, constipation, renal failure, polyuria and polydipsia--could be explained by calcium intoxication syndrome. Investigation revealed generalized sarcoidosis. Under medical treatment with prednisone all the pathologic findings rapidly regressed. The pathogenesis of hypercalcemia in sarcoidosis, and particularly the disorder of vitamin D metabolism with raised levels of 1,25-dihydroxycholecalciferol, are discussed.
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PMID:[Acute hypercalcemia syndrome in sarcoidosis]. 384 Sep 13

Mitomycin was approved for marketing by the Food and Drug Administration in 1974 for use in gastric and pancreatic carcinomas when combined with other chemotherapeutic agents. Since then, mitomycin has been used extensively in combination chemotherapy for a variety of tumors, particularly in the past seven years. However, the contribution of this agent to the various drug regimens has not been adequately defined. Clear evidence of the drug's activity as a single agent has been seen in the intravesical treatment of superficial bladder carcinoma. Common toxicities include anorexia, vomiting, and myelosuppression. Less common, but potentially lethal, toxicities in the form of fibrosing alveolitis and microangiopathic hemolytic anemia with renal failure are being reported with increasing frequency. These potentially severe adverse effects, coupled with the still undefined role of mitomycin in systemic cancer chemotherapy, suggest that selection of this drug for other than investigational use should be made with care.
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PMID:Mitomycin: ten years after approval for marketing. 388 63

We treated a patient with idiopathic fatty liver of pregnancy and a subsequent uncomplicated pregnancy. She experienced general fatigue, nausea, vomiting and jaundice, and renal failure occurred in the third trimester of her first pregnancy. Liver biopsy revealed swollen hepatocytes with microvesicular changes in the cytoplasm. A diagnosis of idiopathic fatty liver of pregnancy was made. Following delivery of a dead fetus, she recovered completely and was discharged on the 30th hospital day. Eighteen months later, she became pregnant again and was delivered of a healthy male baby in the 39th week of gestation. Total bilirubin and transaminase levels were normal, and renal function tests revealed no significant changes during the course of the pregnancy. However, cholinesterase activity increased progressively from the 7th month, thereby suggesting a predisposition to idiopathic fatty liver of pregnancy.
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PMID:Idiopathic fatty liver of pregnancy with a subsequent uncomplicated pregnancy and a progressive increase in serum cholinesterase activity during the third trimester. A case report. 395 27

Although the highly toxic nature of castor bean (Ricinus communis) is well recognized, reports of human toxicity in the English medical literature are scarce. The potentially lethal doses reported for children and adults are three beans and four to eight beans respectively. Recent experience with two cases provides added insight into the expected course of toxicity. In both cases, repeated vomiting, diarrhea, and transiently elevated serum creatinine occurred. Dehydration was much more pronounced in the second case. Both patients recovered uneventfully. Other reported manifestations of castor bean toxicity, such as hepatic necrosis, renal failure, erythrocyte hemolysis, convulsions, and shock, did not occur.
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PMID:Castor bean poisoning. 396 68

Acute hemolysis as a reaction to rifampicin is extremely rare; case reports number less than 15. We recently evaluated a 65-year-old Cambodian refugee who self-regulated the use of rifampicin and isoniazid for pulmonary tuberculosis. Fifteen minutes after a single discontinuous oral dose, he developed flank pain, chills, rigors, vomiting, diarrhea, fever, and brown turbid urine. Laboratory tests at presentation showed acute intravascular hemolysis. Nonoliguric renal failure ensured, and he was transferred to our institution 2 days later. The patient was group A, Rh (D) positive, P1 negative with a cold autoantibody and cold anti-P1 alloantibody. The direct antiglobulin test was negative at the time of transfer. To evaluate the hemolysis, studies were done to test for rifampicin- or isoniazid-dependent antibodies. Rifampicin-dependent antibodies were detected in the antiglobulin phase with broad spectrum anti-human globulin, monospecific anti-gamma chain, and anti-complement antisera. Agglutination titers did not change after dithiothreitol reduction of the patient's serum. We conclude that this patient developed rifampicin-dependent IgG antibodies with complement-fixing capability. The presence of rifampicin-dependent antibodies should be suspected in a patient with hemolysis and/or renal failure taking rifampicin.
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PMID:Acute hemolysis and renal failure with rifampicin-dependent antibodies after discontinuous administration. 398 5


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