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 pathology of malignant hypertension in dogs induced either purposely or inadvertently by the Goldblatt procedure has not been previously reported. Malignant hypertension was experimentally produced in beagle dogs by a modified Goldblatt procedure; in a single surgical procedure, one kidney was removed and the blood flow to the remaining kidney was reduced by 50%. A sudden onset of severe clinical signs developed within one to three weeks after surgery. The dogs were markedly depressed or in shock, were vomiting, and had either bloody feces or bloody diarrhea. Hematologic changes compatible with a diagnosis of microangiopathic hemolytic anemia consisted of hemolysis, thrombocytopenia, and the presence of burr cells and schistocytes. Some dogs had neutrophilia and slight to moderate increases in blood urea nitrogen and creatinine. At necropsy, there were gross hemorrhages in the heart, brain, urinary bladder, and gastrointestinal tract. Histologic findings consisted of multifocal parenchymal hemorrhage, fibrinoid necrosis of arterioles, medial smooth muscle hyperplasia, adventitial fibroplasia and mononuclear cell infiltrates, and microthrombi. The vascular clamp most likely protected the kidney from the systemic hypertension since the remaining kidney was largely not remarkable by light or electron microscopy. The dog appears to be a good model to study the pathology of malignant hypertension and microangiopathic hemolytic anemia.
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PMID:Experimentally induced malignant hypertension in beagle dogs. 376 16

To delineate the spectrum of clinical expressions of distal, type 1 renal tubular acidosis in children and to update progress in diagnosis, therapy, and prognosis, the medical records of 14 girls and 10 boys, seen over a 7 year period, who met the following criteria, were examined: persistent urinary pH more than 6, net acid excretion less than 70 microEq/min/1.73 m2, simultaneous serum total CO2 less than 17.5 mEq/1, and normal or mild impairment of the glomerular filtration rate. The mean age at diagnosis was 8 months. The presenting signs and symptoms were failure to thrive (50%), vomiting and/or diarrhea (37.5%), dehydration (12.5%), and poor feeding (8.3%). Mean values +/- SD of serum calcium (9.8 +/- 0.8 mg/dl), inorganic phosphate (5.6 +/- 0.8 mg/dl), and alkaline phosphatase (222.6 +/- 96.1 U/l) were normal. Hyperkalemia (serum potassium above 5.0 mEq/l) was present at diagnosis in 13 children. Type 4 renal tubular acidosis was ruled out by the inability to achieve a minimum urine pH. With a mean follow-up period of 28.1 +/- 25.3 months, after alkali therapy at 3.3-3.5 mEq/kg/day had been administered for at least 12 months, the growth parameters improved as follows: the percentile weight (mean +/- SD) increased from the initial 11.8 +/- 7.5 to the final 27.6 +/- 31.3 (p less than 0.003), and the length/height percentile increased from 11.5 +/- 7.3 to 29.7 +/- 24.2 (p less than 0.03). The relationship between urine calcium/creatinine ratio and serum total CO2 showed poor correlation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal tubular acidosis in children. Diagnosis, treatment and prognosis. 377 38

Seventy nine cases of sporadic, community acquired legionnaires' disease have been reviewed. Annual and seasonal variation in incidence was noted. The mean age of the patients was 53 years and 50 (63%) were male. Pre-existing chronic diseases were present in only 23 (29%), including two patients receiving immunosuppressive treatment. Common symptoms included unproductive cough, dyspnoea, chest pain, headache, confusion, nausea, vomiting, and diarrhoea. Respiratory symptoms were absent, however, in 17 (22%). Localising chest signs were present in 74 (95%) cases. Frequent laboratory findings included lymphopenia, high erythrocyte sedimentation rate, hyponatraemia, raised urea and creatinine concentrations, abnormal liver function, hypophosphataemia, hypoalbuminaemia, proteinuria, and haematuria. Thirteen patients died (16%), including nine of 20 who received assisted ventilation. The mortality rate in patients treated with erythromycin (11%) was lower than in those who received other antibiotics (23%), but this difference was not statistically significant. Of the features noted on admission, only a high plasma urea concentration was significantly associated with death. Sporadic community acquired legionnaires' disease is a not uncommon disorder, which with appropriate treatment has a prognosis similar to that of other forms of community acquired pneumonia.
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PMID:Legionnaires' disease: a review of 79 community acquired cases in Nottingham. 378 45

Fifteen patients with advanced malignancy were treated with escalating doses of recombinant beta ser 17 interferon (IFN). Doses ranging from 0.006 to 500 X 10(6) units/m2 were administered according to a dosage escalation scheme by iv push twice weekly (starting 1 week after an initial dose) for a planned minimum of 5 weeks, to be continued as a function of response. Toxic effects were broad in scope but generally low in grade. They included fever, malaise, leukopenia, proteinuria, nausea/vomiting, diarrhea, and mild elevations of serum transaminases and creatinine. In one patient, transient hypotension with bradycardia ensued. Malaise and fever increased somewhat with increasing dose. Doses of up to 500 X 10(6) units/m2 were tolerated without severe toxicity. A maximum tolerated dose was not defined. IFN pharmacokinetics followed a biphasic decay curve, with a distribution phase alpha-half-life of 9 minutes and an elimination phase beta-half-life of 103 minutes. Anti-IFN antibodies by the ELISA technique were present in seven of 15 patients. Presence of antibody did not correlate with toxicity or response. 2',5'-Adenylate synthetase levels were increased 2 and 24 hours after the initial dose, with a trend toward higher increments with higher doses. Minimal anti-tumor responses were seen in two patients with melanoma.
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PMID:Phase I study of recombinant beta ser 17 interferon in the treatment of cancer. 379 Dec 49

The clinical, pathomorphological and serological features of acute canine leptospirosis are evaluated and the IgM- and IgG-specific ELISA for leptospirosis serology in dogs is assessed. The clinical syndrome of acute canine leptospirosis was characterized by depression, anorexia, vomiting and often haemorrhagic diarrhoea. In addition, jaundice, uraemia, elevated creatinine and alkaline phosphatase were observed in the majority of the dogs. In pups invagination of the intestines was a noteworthy finding. The clinical signs and the post-mortem findings were rather non-specific so that the clinical and post-mortem diagnosis had to be confirmed serologically. In acute clinical cases of canine leptospirosis a high anti-leptospiral IgM titre, ranging from 160 in pups to 10240 in adults, was always present, whereas the anti-leptospiral IgG titre and the agglutination titre usually were negative or low. Dogs died from leptospirosis in spite of a high anti-leptospiral IgM titre. Only two dogs having, at the first examination, a high IgM titre in conjunction with a high IgG titre survived an acute infection. The possible role of IgM and IgG in the pathogenesis of an acute leptospiral infection is discussed. Different serological patterns in reference dogs, which were not suffering from acute leptospirosis, are presented.
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PMID:Clinical, pathological and serological features of spontaneous canine leptospirosis. An evaluation of the IgM- and IgG-specific ELISA. 379 34

From April 1982 through February 1984, 29 patients with pancreatic cancer were treated with ifosfamide (1.25-1.5 g/m2 on days 1-5) + N-acetylcysteine (NAC) 2 g p.o. every 6 h on days 1-7 every 3 weeks. In responding patients without serious toxicity, subsequent courses of ifosfamide were escalated every 3 weeks by 0.25 g/m2 per day to a maximum of 2 g/m2 per day, with escalation of NAC to 12 g/day. Patients with KPS less than 50, serum creatinine or bilirubin greater than 2 mg/d 1, or obstructive uropathy were ineligible. The median age was 54 (range 36-78), median KPS 70, and median pretreatment weight loss 9 kg. Toxicity included nausea, vomiting, moderate myelosuppression, and occasional mental confusion. Hematuria (greater than 11 RBC/HPF) developed in only 1/29 courses (17 patients) of ifosfamide at greater than or equal to 1.75 g/m2 per day, and in 7/52 courses (27 patients) overall (13%). Of 27 evaluable patients 6 responded (22%), including 1 with complete response. The median survival was 6 months. Based upon these results, we are currently evaluating ifosfamide + 5-fluorouracil in pancreatic cancer.
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PMID:Ifosfamide chemotherapy for pancreatic carcinoma. 381 19

The chronic toxicity of potassium clavulanate (CVA-K) and BRL28500 were evaluated using dogs in 26-week intravenous administration studies followed by a 5-week off-dose period. The doses for CVA-K and BRL28500 were 10, 20, 50 and 100 mg/kg (p.f.a.), and 80, 160, 320 and 800 mg/kg (p.f.a.) respectively. There were no deaths in either of the groups. For general condition, dogs dosed with CVA-K at 100 mg/kg showed reddening of the skin and mucous membranes, shaking of the head, facial oedema, a decrease in food intake and a reduction in body weight. Also some dogs of the same group showed decreased spontaneous activity, emaciation and signs of dehydration. In the BRL28500 treatment groups, there was reddening of the skin and mucous membranes, vomiting and salivation at 800 mg/kg. Urinalysis of dogs dosed with CVA-K showed occasional dark yellow coloration of the urine. There was also a very weak and equivocal response or positive reaction for protein, occult blood, and urine sugar in some animals at 100 mg/kg. Some dogs dosed with BRL28500 also showed either a very weak and equivocal response or slight positive reaction for occult blood at 320 mg/kg and above, and dark yellow coloration of the urine at 800 mg/kg. Haematological examination of the CVA-K groups showed increases in leukocyte count and platelet count at the highest dose of 100 mg/kg. No haematological abnormalities were noted in any of the BRL28500 groups. Serum biochemical studies of dogs dosed with CVA-K revealed a decrease in total protein at 50 mg/kg and above, and increases in Al-P, total bilirubin, GPT, BUN and creatinine at 100 mg/kg. In the BRL28500 treatment groups, there were increases in total cholesterol and triglyceride at 160 mg/kg and above. In dogs dosed with CVA-K there was an increase in liver weight at 100 mg/kg. Histopathological examination showed a ground glass-like appearance of the hepatocyte cytoplasm and also altered distribution of PAS positive material at 50 mg/kg and above. In the BRL28500 groups, there was an increase in liver weight at 320 mg/kg and above. There were the same ground glass-like appearance in hepatocytes and altered distribution of PAS positive material at 800 mg/kg. In view of the above results, the maximum non-effect dose levels in the present studies were considered to be 20 mg/kg for CVA-K and 80 mg/kg for BRL28500.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Chronic intravenous toxicity studies of potassium clavulanate and BRL28500 in dogs]. 382 May 67

Pentamidine, recently released for clinical use, is effective in therapy for the hemolymphatic stage of Gambian trypanosomiasis, antimony-resistant leishmaniasis, and Pneumocystis carinii pneumonia. The mechanism of action is unclear and may differ for different organisms. Trypanosomes actively transport pentamidine intracellularly, and the drug may then interfere with DNA biosynthetics. However, pentamidine appears to kill nonreplicating P. carinii. The mechanism of killing is unexplained. The pharmacokinetics of pentamidine has been incompletely studied in humans. The estimated volume of distribution is 3 liters/kg. Levels in plasma of pentamidine range from 0.3-1.4 microgram/ml after standard 4 mg/kg dosing, with no appreciable increase in drug levels on successive dosing and no correlation between levels and creatinine clearance or adverse reactions. The drug appears to be concentrated in the kidney and excreted in the urine, with levels detectable six to eight weeks after cessation of therapy. Immediate adverse reactions have included hypotension, nausea, and vomiting. Local pain or abscess formation at an injection site, mild azotemia, leukopenia, abnormal findings from liver function tests, and hypoglycemia may also occur.
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PMID:Pentamidine: a review. 390 42

Carboplatin has been developed for clinical trials as a less nephrotoxic, less emetogenic analog of cisplatin. In preclinical tumor models it was less potent than the parent compound on a molar basis, but reduced toxicity allowed comparable antitumor doses to be given. In phase I studies its dose-limiting toxicities were reversible myelosuppression, especially thrombocytopenia. Leucopenia and anemia occurred to a lesser degree. Other reported toxicities included nausea, vomiting, malaise, myalgia, arthralgia, ototoxicity, hypomagnesemia, and proteinuria. Nausea and vomiting occurred frequently, but was much less severe than that observed with cisplatin. The incidence of serum creatinine elevations was low. The increase was usually reversible and occurred only in association with administration of aminoglycosides, or abnormal pretreatment renal function. Recommended phase II doses by schedule are: bolus every 4 weeks, 400-500 mg/m2 (560 mg/m2 in children); 24 hour continuous infusion every 4 weeks, 320-400 mg/m2; weekly bolus for 4 consecutive weeks with 2 weeks rest, 100-125 mg/m2 (175 mg/m2 in children); bolus for 5 consecutive days every 4 weeks, 77-95 mg/m2. Objective responses were observed during these phase I studies in adult patients (head and neck, breast, renal carcinomas) and children (osteosarcoma, brain stem lesions). In addition to phase II evaluations in all major tumor types, plans for phase III studies in selected tumors are underway.
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PMID:Results of NCI-sponsored phase I trials with carboplatin. 391 Feb 21

5-Formyl-tetrahydrofolate [citrovorum factor (CF)] is commonly used for preventing or reversing toxicity due to treatment with high-dose methotrexate (HDMTX). In vivo, CF is converted to 5-methyltetrahydrofolate (MTHF) and then to the 5,10-methylene tetrahydrofolate, which is the active coenzyme involved in thymidine synthesis. In this study, MTHF was used for protection from toxicity following larger doses of MTX than previously studied, doses which could not be tolerated without effective "rescue." Fifteen patients were given 18 courses of MTX in escalating doses (1-24 g) followed by MTHF. The toxic effects observed included: leukopenia, thrombocytopenia, mucositis, nausea, vomiting, and elevation of serum creatinine and serum transaminase. The side effects were reversible and all patients recovered fully. "Matched pairs" comparison of CF and MTHF rescue in five patients showed no difference in rescue efficacy between the two agents. Since ten of the treatments consisted of 12 and 24 g of MTX, doses potentially fatal without rescue, MTHF is an effective agent for prevention of MTX toxicity.
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PMID:Rescue from high-dose methotrexate with 5-methyltetrahydrofolate. 394 89


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