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)

Twelve patients with otherwise uncomplicated acute viral hepatitis (two were HBsAg-positive) developed renal failure. Apart from dehydration due to repeated vomiting in one patient, no factor responsible for precipitating renal failure could be identified. The clinical course was characterised by renal failure with plasma urea concentrations reaching maximum values of 26-69 mmol/l (175-416 mg/100 ml). Ten patients needed dialysis for up to two weeks. Seven patients recovered completely, while the other five died from sepsis. The types of renal failure were similar to those described in fulminant hepatic failure and cirrhosis--namely, functional renal failure in five patients and acute tubular necrosis in seven. Two of the patients with functional renal failure later developed tubular necrosis. The mechanism responsible for renal failure in acute viral hepatitis is uncertain, though endotoxaemia may contribute.
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PMID:Renal failure in otherwise uncomplicated acute viral hepatitis. 68 5

Tthe findings of 150 patients with proven primary hyperparathyroidism are reported. The purpose of the analysis was to find differences between the various clinical manifestations of the disease. Furthermore the occurrence of acute hyperparathyroid crisis in our series as well as in the literature are described. 65.8% of the patients were females, 34.2% were males. The leading symptom in 98 patients (group I) were kidney stones and in 23 patients (group II) cystic bone disease. Both manifestations of the disease occurred in only 7 patients (group III) and no symptoms related to the kidneys or to the bones occurred in 24 patients (group IV). Because of the difference of the clinical manifestations the additional data were analyzed for each group separately and compared with each other. There was no difference in the mean serum calcium levels for all four groups, however, patients of group I were on the average younger, the duration of the disease was longer and the weight of the parathyroid adenoma was lower compared to the other three groups. Data are presented regarding calcium excretion, phosphate clearance and tubular reabsorption of phosphate for each group. At operation single or multiple adenoma formation was present in 133 patients, whereas diffuse hyperplasia was found in 17 and carcinoma in 2 other patients. 46 of the adenomas were found in atypical anatomical localisation. This observation is responsible for the many unsuccessful or second explorations of the neck. The weight of the adenomas varied between 0.1 and 23.5 g. The most difficult diagnosis was that of diffuse hyperplasia. The success of the surgical intervention was usually established in over 80% of the cases within 24 to 48 hours after the operation with a significant fall of serum calcium. There is still no definite explanation for the variability of the clinical manifestations of primary hyperparathyroidism. Parathyroid hormone determinations on larger numbers of patients are not yet published. The assumption, that different hormones or peptide fragments are responsible for the different action on bone and kidney is discussed. In our series of 152 patients acute hyperparathyroid crisis occurred eight times. Our findings are compared to the other well documented cases in the literature. Main symptoms were nausea, vomiting abdominal pain and different states of cerebral dysfunction. Most of the patients had calcium levels over 16 mg/100 ml. Partial renal insufficiency with elevated blood urea and phosphate retention was found in ov er 50% of the cases. Overall mortality of all cases with acute parathyroid crisis is 52.5%. The pathogenesis of acute hyperparathyroidism and the implications of high calcium levels are discussed. According to our own experience hypercalcemia can be controlled with an intensive therapeutic program and emergency operation for acute parathyroid crisis is no longer necessary.
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PMID:[Primary hyperparathyroidism. An analysis of 152 patients with special references to acute life threatening complications (acute hyperparathyroidism)]. 79 28

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.
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PMID:The management of severe pre-eclampsia and eclampsia. 83 44

To determine the practicability of administering 15(S)-15-methyl-prostaglandin F2alpha-tromethamine (15(S)-15-Me-PGF2alpha) intra-amniotically for the induction of midtrimester abortion, initially 2.5 mg. of 15(S)-15-Me-PGF2alpha was administered to 20 physically healthy gravid women, and was repeated after 24 hours in those patients who had not aborted. Within 24 hours, 65% aborted, and within 36 hours, 95% aborted. Although 67% experienced emesis, no serious complications occurred. This abortion rate is similar to that obtained with the recommended dose schedule of the dosage of prostaglandin F2alpha approved by the Food and Drug Administration and those reported with intra-amniotic administration of either hypertonic saline or urea when augmented with high, continuous, intravenous infusions of oxytocin. While the study intra-amniotic dose schedule appeared to be practicable, large, comparative studies will be necessary to determine the most satisfactory dose schedule and whether this method is more acceptable than other available methods.
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PMID:Intra-amniotic administration of 15(S)-15-methyl-prostaglandin F2alpha for the induction of midtrimester abortion. 93 8

Urea cycle disorders and other hyperammonemic syndromes should be considered in the differential diagnosis in newborns with a history of severe vomiting, lethargy, and seizures, and in infants with feeding problems, episodic vomiting, and altered consciousness. Although the acute neonatal forms of urea cycle disorders are almost always lethal, several of the subacute forms of hyperammonemic syndromes respond favorably to early treatment.
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PMID:Congenital hyperammonemic syndromes. 95 43

An 18-year-old mentally and physically retarded boy, suffering from episodes of anorexia, vomiting, coma and convulsion which have been severer with advance in age, had periodic hyperammonemia, hyperlysinemia and homocitrullinuria. Blood cell arginase activity of the patient on normal diet was markedly reduced after an oral load of L-lysine. The oral loading tests of L-lysine revealed hyperammonemia, hyperlysinemia, hyperargininemia, hypercitrullinemia and homocitrullinuria. Etiology of metabolic error of our patient was discussed in reference to lysine-urea cycle.
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PMID:Clinical and biochemical studies on periodic hyperammonemia with hyperlysinemia and homocitrullinuria. 98 31

A study involving 115 women was conducted to determine the effectiveness of doses of PGR2alpha (prostaglandin F2alpha) and urea for 2nd trimester abortions. 2.5-20 mg of PGF2alpha was combined with 80 gm of urea to induced abortion, with 10 mg being the optimal dose. Only 2 patients had not aborted after 36 hours and only 6 patients required a 2nd injection at 24 hours; laminaria tents did not shorten abortal times. For 33 multiparous patients the mean abortal time was 14.3 hours and for 82 nulliparous women, the mean abortal time was 16.4 hours. 30% of the women had the placenta removed operatively using intravenous sedation. Vomiting occurred in 19 women, nausea in 4 women, 8 became febrile, 2 received blood transfusions for hemorrhage, and 2 had a 4-cm cervical laceration
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PMID:Intra-amniotic prostaglandin F2alpha and urea for midtrimester abortion. 100 22

4-Pentenoic acid, an analog of hypoglycin which is believed to cause Jamaican vomiting sickness, was administered intraperitoneally to rats in an attempt to produce the features of Reye's syndrome in rats. Mean ammonia levels in plasma were found to be elevated approximately four-fold after injection of 200 mg/kg pentenoic acid in fed rats. Pentenoic acid caused hypoglycemia in fasted rats and hyperglycemia in fed rats. In chronic experiments rats were injected intraperitoneally every 4 hr with 50 mg/kg body weight of pentenoic acid for 10 doses, followed by a single dose of 200 mg/kg. The livers of the treated group were enlarged and yellow and showed extensive fatty degeneration. The blood-urea-nitrogen (BUN) was significantly higher and the free fatty acids (FFA's) significantly lower in these rats. This study shows that pentenoic acid administered to rats produces findings similar to those of Reye's syndrome and Jamaican vomiting sickness.
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PMID:Production of the features of Reye's syndrome in rats with 4-pentenoic acid. 112 19

Lysinuric protein intolerance (LPI), an autosomal recessive defect of diamino acid transport, is characterized chemically by renal hyperdiaminoaciduria, especially lysinuria, and by impaired formation of urea with hyperammonemia after protein ingestion. Our 20 patients thrived during breast-feeding, but ingestion of cow's milk caused diarrhea and vomiting. When able to select their diet, they rejected all protein-rich foods. They were short staturated and had weak atrophic muscles, osteoporosis, hepatomegaly and often splenomegaly. Four patients were mentally retarded. Fifteen patients had leukocyte counts below 4,000/mm3, and 17 patients had platelet counts below 150,000/mm3. Serum lactate dehydrogenase activity was constantly increased, and transaminase and aldolase activities were often increased. In the infants' livers, changes were only revealed by electron microscopy: increased and vesicular smooth endoplasmic reticulum, and abundance of glycogen particles in the hepatocytes. In the older patients, light microscopy demonstrated clearly limited areas where hepatocytes had large pale cytoplasm and small pyknotic nuclei. The diamino acids lysine, arginine and ornithine had plasma concentrations only one-third to one-half the normal mean; the renal clearances were clearly increased. Oral diamino acid loading tests suggested impaired intestinal absorption. Urea is built in the liver through transformation of ornithine to arginine, and cleavage of arginine to ornithine and urea. The addition of ornithine to an intravenous I-alanine loading prevented the hyperammonemia and normalized the urea production. Therefore, the diet has been supplemented with arginine, and more protein has been added. This therapy has lead to a remarkable catch-up growth in some patients. The pathophysiology of LPI is explained. Because of defective intestinal absorption and incrased renal loss, the diamino acids have a low plasma concentration. Their transport from plasma to hepatocytes is also impaired, and the liver becomes deficient in ornithine. This retards the urea cycle, and leads to postprandial hyperammonemia and protein aversion. The presence of the transport defect in the hepatocytes distinguishes LPI from other hyperdibasicaminoacidurias.
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PMID:Lysinuric protein intolerance. 115 80

The effectiveness of levamisole hydrochloride as a microfilaricidal agent when used 3 weeks after thiacetarsamide sodium therapy for canine dirofilariasis, was studied in 6 experimental dogs and 20 clinical cases. The drug, when administered orally in gelatine capsules daily, cleared microfilariae from the circulation in the experimental dogs in 7 to 11 days. A dose rate of 10mg/kg appeared as effective as 15mg/kg. In the clinical group 70% of dogs had zero microfilarial counts after 4 to 8 doses at 10mg/kg daily. Vomiting, diarrhoea and inappetence were observed in some animals, but were not a significant problem. Elevations in plasma GPT and AP levels were recorded during the administration of levamisole in some dogs while GOT levels rose in 1 dog only. Urea and creatinine levels were unaffected in all dogs. The only haematological parameter affected was the eosinophil count which rose during levamisole administration. All levamisole-treated animals, were successfully commenced on daily DEC, as a prophylactic measure, while an anaphylactic-type reaction occurred when this drug was administered to 1 of the 2 control animals.
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PMID:Levamisole as a microfilaricidal agent in the control of canine dirofilariasis. 116 38


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