Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011991 (diarrhea)
 57,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-seven adult Nigerian patients with endoscopically proven active duodenal ulcers have received in a double-blind trial either the histamine H2 - receptor antagonist cimetidine 1g daily or placebo tablets of identical appearance for 4 weeks. Fifty-six per cent of the cimetidine patients and 18% of those receiving placebo had endoscopically completely healed ulcers and total pain relief at the completion of trial. This response amounted to clinical cure. An additional 19% of patients in the cimetidine group experienced clinical improvement either in endoscopic or symptomatic reassessment but not in both, thus leading to a disparity between clinical cure rate (56%), healing rate (69%), and pain relief (64%). Though therefore significantly better than placebo, this less favourable response to cimetidine in this study may be due to the short trial period, the disparity between healing and pain relief rates or to co-existing and persistent antroduodenitis in ulcer patients as shown on gastroduodenal mucosal biopsies taken at the time of the clinical investigation. There were no untoward clinical laboratory side effects with the exception of the one cimetidine patient who experienced diarrhoea and a small number who showed slight, asymptomatic rise in plasma creatinine level. Of particular interest to the reported occurrence of diarrhoea with cimetidine therapy is the finding in the bacteriological studies of intestinal aspirates and biochemistry estimations for indicanuria in the consenting patients which showed that orally administered cimetidine 1g daily for 4 weeks neither produced demonstratable alterations in the bacterial content of the small bowel not pathological indicanuria, thereby excluding bacterial overgrowth syndrome as a therapeutic hazard in the clinical application of cimetidine.
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PMID:A double-blind comparative study of cimetidine and placebo in adult Nigerian duodenal ulcer patients with special reference to gastroduodenal mucosal morphology and intestinal bacterial activity. 12 33

Summertime pneumonias in Philadelphia during 1976 were studied epidemiologically, and the epidemiologic, clinical, and laboratory features of pneumonia cases serologically positive for Legionnaires' disease were compared with features of serologically negative cases. Both groups were similar in many respects, but in patients with Legionnaires' disease diarrhea and neurologic findings were significantly more frequent (P = 0.01 and P = 0.05 respectively). A diagnosis of Legionnaires' disease was also suggested by an elevated serum creatinine phosphokinase level (P = 0.02) and the presence of occult blood in the urine with fewer than six erythrocytes per highpower field. Abnormalities in renal function tests or liver function tests were commoner in patients with Legionnaires' disease (P = 0.05). Radiographic features, however, could not be used to separate pneumonia cases. The high frequency of extrapulmonary manifestations involving the gastrointestinal tract, the central nervous system, kidneys, and liver suggests that Legionnaires' disease is a multisystemic disorder possibly caused by a toxin-producing organism.
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PMID:Summertime pneumonias in Philadelphia in 1976. An epidemiologic study. 43 38

A good tumoricidal activity of vindesine (VDS) has been reported in a variety of animal tumors and in human leukemias and lymphomas. We treated 22 patients who had received no prior chemotherapy and were suffering from a variety of malignant neoplasms with 0.5 mg/m2 to 3.0 mg/m2 VDS i. v. once or three times at weekly intervals and recorded the clinical, hematologic, and especially, neurological side effects. Clinically we observed fatigue in nine patients, paresthesias in seven, myalgias in three, vertigo and diarrhea in two, and skin pains, tinnitus, gastric pains, alopecia, and tremor in one patient each. There was no obvious dose-action relationship. Paravenous injection caused cellulitis similar to that seen with vincristine. No side effects were apparent in liver (SGPT) and renal (creatinine) function tests. Hematologically there was a clear trend toward leukopenia with higher doses of DVA and a mean increase in the thrombocyte count by 51 X 10(3)/mm3 was found (sign test: P greater than 0.05). The hemoglobin level did not change. Clinical neurological examination and monitoring by electroneurography revealed no changes in tensiometer performance, motor and sensory nerve conduction velocity, motor or sensory nerve action potential amplitudes, or H-reflex responses. There was dose-related diminution of the proprioceptive reflexes, especially in the lower extremities. Even with as little as 2.0 mg/m2 VDS i. v. at weekly intervals for 3 weeks Achilles and patellar tendon reflexes were diminished or absent in all patients.
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PMID:Vindesine. A clinical trial with special reference to neurological side effects. 45 81

A 62-year-old man spread maneb on about 200 sq m of garden and subsequently was taken to the emergency clinic with complaints of oliguria, diarrhea, and hoarseness. Based on the clinicobiochemical data, he was found to have acute renal failure; the serum levels of BUN, creatinine, and potassium were 144.3 mg/dL, 14 mg/dL, and 5.8 mEq/L, respectively. The ST segment depression in V4-6, reciprocal ST segment elevation in V1-3, and inverted T waves in V5 and V6 were recorded on ECGs. Both the renal failure and the ECG abnormalities disappeared after hemodialysis. The possibility exists that the maneb caused the acute renal failure.
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PMID:Acute renal failure and maneb (manganous ethylenebis[dithiocarbamate]) exposure. 49 Aug 86

The absorption of oral methotrexate in syrup form has been compared in six patients with that of an identical IV dose (50 mg/m2). There was variable absorption amongst the group with respect to maximum levels achieved and the time taken to reach those levels. The area under the time-concentration curve was always smaller when the drug was given orally than after IV administration. A total of 33 patients receiving methotrexate for a variety of tumour types were followed for response to treatment and toxicity. A significantly longer methotrexate half-life (t1/2) was found in nine partial responders (9.2 +/- 1.6 h) than in the nonresponders (3.8 +/- 0.7 h). Severe methotrexate toxicity was not seen though occasional mucositis, conjunctivitis, and diarrhoea occurred in seven patients. The side effects could not be predicted from the dose, the bioavailability data, or the serum creatinine. Measurements of serum and urine methotrexate levels are useful in the assessment of absorption and bioavailability of the drug the prediction of tumour response.
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PMID:Bioavailability of methotrexate: implications for clinical use. 53 33

Haemofiltrate was administered into the duodenum of 5 ambulatory dogs through an implanted silastic catheter at a rate of 5-10 ml/min. None of the dogs presented signs of discomfort or suffered from regurgitation or diarrhoea. All 5 dogs had solid stools, enhanced diuresis and no change in body weight over a time period of 8 hours. Filtration rates between 5 and 10 ml/min were obtained in 7 dogs after connecting an Amicon in-line Ultrafilter with an external a.v. shunt. The intestinal recycling rate via the duodenal tube as a rule was 2 ml/min lower than the free flow ultrafiltration. Recirculation of autologous haemofiltrate in 5 uraemic dogs indicated unselective reabsorption of all electrolytes and small molecules. In 5 experiments with intestinal substitution of ultrafiltrate by a potassium-free Ringer's lactate solution, correction of acidosis and decrease in plasma potassium, creatinine and BUN was achieved.
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PMID:Intestinal recycling and substitution of haemofiltrate in dogs. 54 82

Twin male infant siblings who presented in Harrow, UK, with a Reye's-like syndrome associated with profound hypoglycaemia, vomiting, diarrhoea, coma and death in one child, with dicarboxylic aciduria, and similarities to Jamacian vomiting sickness (hypoglycin toxicity) have been shown to excrete large amounts of a previously unrecorded urinary organic acid. This has been identified as 5-hydroxyhexanoic acid by gas chromatography mass spectrometry using a synthesized standard. Concentrations observed were 340 and 330 mg g-1 creatinine in the two patients. The metabolic precursor of the urinary acid is suggested to be hex-4-enoic acid, a probable chemical toxin closely related to the active organic acid metabolite of hypoglycin. The possibility of omega - 1 oxidation of hexanoic acid to 5-hydroxyhexanoic acid in these and other patients with dicarbocylic aciduris is also discussed.
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PMID:Identification of 5-hydroxyhexanoic acid in the urine of twin siblings with a Reye's-like syndrome associated with dicarboxylic aciduria and hypoglycaemia and with similarities to Jamaican vomiting sickness. 57 58

In a 10-day study, carbenicillin indanyl sodium cured urinary-tract infections in 22 of 30 patients (ages, 24-91). In 3 of the remaining patients the treatment was a failure; in 3 others the drug had to be discontinued because of diarrhea and vomiting; and in 2 instances it induced overgrowth of Candida albicans in the urine. Carbenicillin was lethal to Pseudomonas aeruginosa in all 9 cases, to Proteus mirabilis in all 6 cases, and to enterococcus in all 3 cases. A trimethoprim/sulfamethoxazole combination cured urinary-tract infections in 18 of 30 other patients (ages, 28-91), but failed in 3. In 3 patients it gave rise to a skin rash; in 2 to elevation of blood urea nitrogen and creatinine levels; in 1 to neutropenia; and in 1 to overgrowth of Candida albicans in the urine. Reinfection occurred in 2 patients. Carbenicillin indanyl sodium was more effective than the sulfonamide/trimethoprim combination.
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PMID:Relative efficacy of carbenicillin indanyl sodium and of trimethoprim/sulfamethoxazole in urinary-tract infections. 58 78

In 1148 cases the serum digoxin concentration (SDC) was correlated with the extracardiac signs of digitalis intoxication. There is a considerably overlap of SDC levels of patients with and without extracardiac signs of toxicity even though the mean SDC's of these two groups differ significantly. An increasing percentage of clinical intoxicated patients with increasing SDC levels was found at digoxin concentrations of 2.0 ng/ml and higher. At lower SDC levels patients with and without extracardiac signs of digitalis intoxication did not differ significantly in their mean SDC but in mean age and in mean creatinine concentration indicating that at least part of the symptoms in these patients might be due to a more severe illness. We could show that many of the extracardiac signs of digitalis intoxication are also seen in patients with impaired kidney function at low SDC levels and may lead to a wrong diagnosis. The most common complaint in patients with SDC's of 2.0 ng/ml and more is nausea (39.4%), followed by tiredness (30.4%), dizzyness (23.7%), vomiting (23.1%), headache (16.0%), visual disturbances (13,5%), colour (yellow) seeing (6;7%), diarrhea (4.2%) and severe neuro-psychiatric disturbances (3.8%). In patients with digitalis-induced arrhythmias the sequence of symptoms is the same only with a somewhat higher percentage rate. Only about one half of the patients with digitalis-induced arrhythmias and SDC values up to 2.5 ng/ml showed also extracardiac signs of intoxication. Therefore these signs are not to be taken as early symptoms of digitalis intoxication. Divided into subgroups (patients with/without digitalis-induced arrhythmias, patients with SDC values of more/less than 2.0 ng/ml) the patients with and without extracardiac signs of digitalis toxicity are compared with each other in regard to: mean body height and weight, concentration of digoxin, potassium and creatinine, digoxin dosage and mean age. The greatest differences were found between patients with combined cardiac and extracardiac signs of intoxication and patients with neither cardiac nor extracardiac signs of intoxication: These intoxicated patients are of significantly higher mean age and lower body weight, their mean concentration of digoxin and creatinine and the digoxin dosage administered are significantly greater, but there is no significant difference in potassium concentration. An important group of patients, namely the elderly with impaired kidney function, are especially prone to develop digitalis intoxication. In this group, however, the extracardial symptoms are of little benefit in the diagnosis of digitalis intoxication. In these patients rhythm disturbances and intoxication-like symptoms are frequently caused by other reasons. In most cases the SDC value can clarify the diagnosis without withdrawal of the drug.
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PMID:[Digitalis intoxication: specifity and significance of cardiac and extracardiac symptoms. part II. Patients with extracardiac symptoms of digitalis intoxications (author's transl)]. 85 53

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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