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)

The findings of 152 patients with proven primary hyperparathyroidism are reportedmthe purpose of the analysis was to find difference 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 an 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 sucess 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 ist 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 reposible 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 over 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 hypercalcenia 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 hyperparthyroidism. Analysis of 152 patients with special reference to acute life threatening complications (acute hyperparathyroidism)]. 20 39

A new derivative of ellipticine, hydroxy-9-methyl-2-ellipticinium acetate, was found to be a useful anti-tumor drug in advanced cancers which could not be treated any longer successfully by any other procedure. In our series of 100 patients, the best results were obtained with bone metastases from breast carcinomas and with anaplastic thyroid carcinomas. Most patients usually received a weekly perfusion of 80 mg/m2. The main characteristic of this drug is its lack of hematologic, and hepatic toxicity. No renal trouble was observed during the first year, but 2 deaths from renal insufficiency occured during the 18th and 15th month of treatment. The most frequent side effect consists of digestive troubles (nausea, vomiting) which rarely compelled to stop the treatment (4 times in 100 patients).
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PMID:[Hydroxy 9-methyl 2-ellipticinium acetate (NSC 264-137). Toxicologic study and therapeutic effect in 100 cancers (author's transl)]. 47 24

In 4 out of 9711 (= 1:2400) patients, lactice acidosis due to biguanides was diagnosed. Serum lactate concentration averaged 18.2 mmol/l and the pH value 6.87. All patients showed signs of renal insufficiency and three had congestive heart disease. In addition to treatment with biguanides, other factors might have contributed to the lactice acidosis in these patients: prolonged fasting, severe dehydration due to persistent vomiting, acute bronchopneumonia, and acute pyelonephritis. On addmission, two patients were in shock and all patients were semi-conscious or comatose. All patients were treated with bicarbonate and glucose/insulin. One patient was hemodialysed. Two of our four patients died. Oour four patients are compared with 179 patients in the literature with respect to mortality and prognosis of lactic acidosis due to biguanides.
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PMID:[Lactacidosis in biguanide therapy: diagnosis and therapy. 4 cases compared to 179 cases in the world literature]. 71 23

Description of 23 patients (21 women, 2 men) with an average age of 36.6 (19--68) years, who were hypokalemic during 6.5 years on the average (range 1/2--16 years). The cause of the potassium depletion was malnutrition (anorexia nervosa, vomiting) and/or abuse of laxatives and/or diuretics. With increasing duration of potassium depletion renal function deteriorated; in two cases terminal renal failure developed. Histology of the kidneys (9 cases) showed the picture of chronic abacterial interstitial nephritis. Urinalysis was negative or non-specific. The blood pressure levels were normal or low, hypertensive values being exceptional. Aside of hypokalemia a tendency to hyponatriemia, hypochloremia and metabolic alcalosis was observed, the latter turning into hypokalemic normochloremic acidosis with advancing renal insufficiency. Plasma renin activity and aldosterone concentration or excretion frequently were elevated, but no close correlation was found between these parameters or with the blood pressure. Bacterial infection of the urinary tract occured, if at all, in the late phase and seems to be complication rather than the cause of the kidney disease. The discussion of other possible pathogenetic factors leads to the conclusion that the term "chronic kaliopenic nephropathy" is justified. Some diagnostic and therapeutic consequences are mentioned.
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PMID:Chronic hypokalemic nephropathy: a clinical study. 73 56

The authors have studied 50 records of patients who had presented an acute attack of P. falciparum malaria. Both sexes were equally implied. Young people were predominant. The distribution of cases was about the same in the whole year. The fever decreases on the second day and increases on the third day (300/0). Among the classical signs: relative rarity of hepatomegalia (100/0), splenomegalia (10 0/0), jaundice (140/0), nervous symptoms (100/0). Vomiting is rather frequent (30 0/0). From the cardiovascular point of view a relative bradycardia is observed in 16 0/0 of the cases, and a relative tachycardia in 100/0 of the cases; hypotension in 100/0 of the cases. Electrocardiographic signs are observed in 360/0 of the cases; they are aspecific, concerning mainly ST-T anomalias (22 0/0) and a QT lengthening (200/0). The cardiothoracic ratio is higher than 0.5 in 320/0 of the cases. From the pulmonary point of view the authors have observed symptoms contemporary of the attack: two asthma attacks, three radiologic anomalias reminding of viral pneumopathias. The biological symptoms are mainly transitory functional renal insufficiency in 18 0/0 of the cases. Protection due to AS heterozygosis seems to be confirmed in this study. The efficiency of intravenous quinin treatment is certain.
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PMID:[50 cases of acute malaria: symptomatic study, especially cardiac]. 77 91

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

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

Seven patients, 4 girls and 3 boys, aged 3 to 12 years /X = 7.14/ affected by haemorrhagic fever with renal syndrome /HFRS/., were hospitalized at the University Children's Hospital in Belgrade during the last two years /January 1988-January 1990/. The diagnosis was established on the basis of clinical features, epidemiological data and autopsy findings in one patient while in the others the diagnosis of HFRS was confirmed serologically by indirect immunoflorescence tests on Vero E 6 cells. A significant increase in antibody titre against Hantaan virus was found in all serologically tested patients. Three of them had also significant increase of antibody titre against Soeul and one against Puumale virus. In four patients the disease appeared as family outbreak at the end of January 1988 while the others were sporadical cases. All patients but one mentioned contact with rodents at home or in fields. The predominant slynical symptom were: sudden onset of febrile condition with headache, generalized malaise, myalgia, abdominal pain, vomiting, diarrhoea, oliguria and oedema. All patients had haematuria and only one had other severe haemorrhagic manifestations. Four patients were hypertensive. Two patients had renal insufficiency, but only one required haemodialysis. Five patients recovered after 2 to 8 weeks without sequellae, one patient was still /7 months after the beginning of the disease/ in mild renal insufficiency and one patient died. Autopsy findings showed tubular necrosis in the kidney, myocarditis, massive pneumonia with hydrothorax and jejunal haemorrhagia.
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PMID:[Hemorrhagic fever with renal syndrome in children]. 168 34

Recently introduced chloroquine resistant malaria has altered the clinical picture and complicated the overall management of malaria. 113 adults with proved malaria admitted at Harare Central Hospital, Zimbabwe, were evaluated to determine the incidence, nature, relationship to morbidity and mortality and response to treatment of the complications due to malaria. 47.7 pc (52 of 109) patients had relatively chloroquine resistant malaria. 87.4 pc (99 of 113) had complications whose percentage frequency of occurrence were: Anaemia 51.2 pc, diarrhoea and/or vomiting 42.2 pc, cerebral malaria +/- fits 39.2 pc, renal insufficiency +/- hyperkalaemia 26.4 pc, hypoglycaemia 15.6 pc, jaundice 15.2 pc, neuro-psychiatric 15.0 pc, shock 10.6 pc, concurrent sepsis 8.9 pc, pulmonary oedema 3.5 pc and hyperpyrexia 1.7 pc. Multiple complications in the same patient were common. The combination of cerebral malaria and renal insufficiency had the worst mortality (p less than 0.001). All patients dialysed, however, survived. Non-iron deficiency anaemia, 91.7 pc (51 of 55) and diarrhoea and/or vomiting, were common, worsened morbidity but not mortality (p = 0.555). A seriously-ill patient with malaria should be suspected of having complications and chloroquine resistance and should be referred promptly to a centre with facilities for dialysis. Anti-malaria drugs should be mixed in a dextrose solution and iron supplements should not be given routinely.
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PMID:Complications of seasonal adult malaria at a central hospital. 209 79

We undertook a phase I trial using fixed-dose cisplatin, escalating doses of etoposide, and reinfusion of previously obtained autologous bone marrow in 29 relapsed or refractory small cell and non-small-cell lung cancer patients. Median age was 59 years (range of 38-68 years). Three patients had small-cell and 26 patients had non-small-cell lung cancer. Patients received i.v. cisplatin 200 mg/m2 over 5 days and i.v. etoposide 600 mg/m2/day for 3 days (total of 1,800 mg/m2) that was escalated to 800, 1,000, 1,200, 1,400, and 1,600 mg/m2/day for 3 days (total of 2,400-4,800 mg/m2). Cryopreserved autologous bone marrow was thawed and reinfused through a central venous catheter the second day after the completion of chemotherapy. Toxicities included nausea, vomiting, alopecia, high-tone hearing loss, mucositis, diarrhea, renal insufficiency, metabolic acidosis, and severe myelosuppression. The duration of neutropenia (less than 500 neutrophils/microliter) ranged from 5 to 22 days (median of 11 days) and the duration of severe thrombocytopenia (platelets of less than 20,000/microliters untransfused) ranged from 2 to 19 days (median of 9 days). Reversible renal insufficiency (peak serum creatinines of 6.7, 6.6, 4.3, and 3.5 mg/dl) occurred in four patients who completed the therapy. In three patients, death occurred within 4 weeks of chemotherapy and marrow reinfusion. Three complete and 12 partial remissions (range of 1+(-)22+ months, median of 3 months) were observed. No response was noted in eight patients and tumor progression within 1 month of transplant occurred in two patients. The maximally tolerated dose of etoposide was 1,400 mg/m2/day (total of 4,200 mg/m2), since two of three patients developed life-threatening diarrhea at the 1,600 mg/m2/day (total of 4,800 mg/m2) dose. The encouraging antitumor effects of this regimen suggest that this approach may be useful therapy for lung cancer and other tumors sensitive to VP-16 and cisplatin.
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PMID:Phase I trial of high-dose etoposide, high-dose cisplatin, and reinfusion of autologous bone marrow for lung cancer. 215 15


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