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 Authors make a list of 17 cases of elevation of total CPK (creatine phosphokinase) in subjects with vomiting of different cause, supposing the exclusion of more kinowed causes be able to stir up the enzyme increase. The Authors place the above mentioned elevation in relation to muscular or traumatism on musculature delegate physiologically to vomiting. It is never observed any relation with entity of vomiting and elevation of CPK. The causes of elevation represent the 40% of examined subjects.
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PMID:[Elevation of the total blood CPK test in vomiting of various causes]. 52 89

The effect of simvastatin on serum total and HDL cholesterol and total triglyceride levels in 20 hypercholesterolemic patients on CAPD treatment was studied. The drug was given at the initial dose of 10 mg/day which was doubled up to 40 mg/day. Two non-compliant patients stopped the drug in the first week of treatment. One patient had vomiting and stopped simvastatin. One patients reduced the dose from 20 to 10 mg/day because of increase in CPK level. The study was completed in 16 patients. Serum cholesterol decreased from 318 +/- 39 to 208 +/- 34 mg/dl (p < 0.001), triglyceride from 317 +/- 129 to 278 +/- 160 mg/dl and HDL cholesterol from 43 +/- 13 to 35 +/- 11 mg/dl. The effective does was 10 mg/day in 4 cases, 20 mg/dl in 7 and 40 mg/dl in 5. In CAPD patients, simvastatin is safe and effective in lowering serum cholesterol. The clinical significance of the decrease in HDL cholesterol and its possible effect on clinical outcome are still unknown.
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PMID:Effect of simvastatin in CAPD patients with hypercholesterolemia. 136 17

A 74-year-old male was admitted to hospital with acute rhabdomyolysis and myoglobinuria due to hypokalemia. The hypokalemia resulted from diuretic treatment. He had no family history of myopathy, and no diarrhea and vomiting. The neurological examination revealed painful quadriplegia. The blood pressure was 160/74 mm Hg. Laboratory examination showed hypokalemic and hypochloremic metabolic alkalosis (serum K 1.5 mEq/l, serum Cl 89 mEq/l, base excess + 20.9, HCO3- 44.9 mmol/l, pH 7.563) and marked elevations of serum CPK, LDH, GOT, GPT and myoglobin. Endocrinological and renal functions were normal. Muscle biopsy revealed marked necrosis with remarkable phagocytosis and vacuolar degeneration. The cessation of diuretics and intravenous infusion of potassium chloride resulted in a marked improvement in clinical and laboratory findings. The diuretics-induced hypokalemic myopathy is rare in the literature.
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PMID:Marked hypokalemic rhabdomyolysis with myoglobinuria due to diuretic treatment. 175 65

Cocaine abuse is associated with a constellation of serious medical complications. An unrecognized and recently described complication of cocaine use is rhabdomyolysis with acute renal failure. We describe the first patient identified in our institution with this entity, admitted to the medical services with oliguric acute renal failure. Three days prior to admission the patient had a cocaine snorting binge. He presented with bilateral flank pain, gross hematuria, vomiting and chills. No history of crush injury, prolonged immobilization and or seizures was reported. On admission the vital signs were normal, physical exam revealed periorbital edema and marked soft tissue neck swelling. Lab values: Bun 120 mgs%, Creat. 10.7 mgs%, Na 132 meq/lt, Co2 13mq/lt, Cl, 103meq/lt, Co2 13meq/lt, Ca 5.3 mgs%, CPK 30,800 U/L with a MM fraction of 98%, LDH 600 U/L, SGOT 300 U/L. The urine was dark red with a ph of 6.5 and 100 rbc/hpf. The anti-GBM antibody and blood cultures were negative. An abdominal sonogram was normal. He received peritoneal dialysis and was discharged on his 14th hospital day with a CPK of 2,800 U/L and decreasing azotemia. Cocaine associated rhabdomyolysis has only been recently described in the literature (AJM April, 88). Acute myoglobinuric renal failure needs to be added to the growing list of medical complications of cocaine use.
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PMID:Cocaine and rhabdomyolysis: report of a case and review of the literature. 207 48

Tiazofurin (2-B-D-Ribofuranosylthiazole-4-Carboxamide: NSC 286193) is a nucleoside antimetabolite that acts as a potent inhibitor of IMP dehydrogenase resulting in a guanine nucleotide deprivation. Recent in vivo biochemical observations in rats bearing hepatoma suggested a correlation between depletion of guanine nucleotides and antitumor effect. The present phase I trial utilized a weekly x 3 bolus infusion schedule, repeated every 5 weeks. Biochemical measurements of GTP and dGTP were performed in patients at each dose level. Twelve patients received 16 courses of the drug in doses ranging from 1100 to 2050 mg/m2 weekly x 3. The dose limiting toxicities were pericarditis and clinical symptoms suggestive of a more generalized serositis (chest and abdominal pain). Other toxicities included reversible elevations in CPK (MM band only) and SGOT, nausea, vomiting, and arthralgias. Neurotoxic effects were generally mild, including headaches, anxiety, and malaise. Only 1 of 6 patients evaluated for tiazofurin's biochemical activity showed a sustained depletion of guanine nucleotide pools. No antitumor activity was observed. The maximally tolerated dose of tiazofurin on this intermittent weekly x 3 schedule was 1650 mg/m2. Toxicity and the overall lack of biochemical and biologic effect at clinically achievable doses may preclude further clinical evaluation of this drug on a weekly schedule. The toxicities observed in our study were similar to those reported for phase I investigations using a considerably higher dose intensity with daily x 5 schedules.
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PMID:Phase I trial and biochemical evaluation of tiazofurin administered on a weekly schedule. 234 2

Four patients had trichinosis after consuming raw home-butchered pork. The patients had fever, myalgias, periorbital edema, and conjunctivitis. All of the patients had nausea, vomiting, or diarrhea (corresponding to the intestinal phase of the infection) seven to ten days before the onset of fever and myalgias. Laboratory findings included eosinophilia, elevated serum CPK and aldolase values, and seroconversion of Trichinella serology one month after onset of myalgias. The patients were treated with mebendazole and prednisone and recovered uneventfully.
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PMID:Common-source outbreak of trichinosis associated with eating raw home-butchered pork. 304 86

To investigate possible undesirable effects due to the intravenous administration of a reagent of a xenogenic nature (monoclonal antibody 225-28S) in man, a toxicologic study was carried out on 85 patients with metastatic cutaneous melanoma. Two reagents were tested in this study: purified monoclonal antibody (MoAb) 225-28S and its F(ab')2 fragment. Purified MoAb was labelled with 131I and F(ab')2 fragment with 131I, or 123I, or 111In or 99Tc. The quantity of MoAb or F(ab')2 injected ranged from 14 to 750 micrograms, and the specific activity from 37.0 to 2116.4 MBq/mg. The total radioactivity injected varied from 25.9 to 891.7 MBq/mg. In addition to a careful clinical examination, the following tests were done to monitor possible adverse effects: blood glucose, azotemia, RBC, WBC, platelet count, serum creatinine, creatinine clearance, plasma electrolyte levels, serum proteins, albumin/globulin ratio, serum bilirubin, SGOT, SGPT, gamma GT, and CPK. These tests were done before the injection and on days 7 and 14. No patient experienced adverse general effects like fever, nausea, vomiting or allergic reactions. None of the aforementioned hematometric and biochemical tests showed significant variations compared with the initial values. It is concluded that a single injection of these reagents at the dosages tested is completely atoxic.
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PMID:Anti-melanoma monoclonal antibody 225-28S: evaluation of toxicity in man. 335 62

Single dose toxicity studies of T-3761 were carried out in mice, rats and dogs, and the following results were obtained. 1. The approximate lethal dose of T-3761 were more than 5,000 mg/kg for mice and rats, more than 2,000 mg/kg for dogs with oral administration, and more than 5,000 mg/kg for mice and rats with subcutaneous injection. LD50 values with intravenous injection were 783 mg/kg for male mice, 832 mg/kg for female mice, 341 mg/kg for male rats, and 403 mg/kg for female rats. Two dogs given 200 mg/kg did not die but one of the two treated with 400 mg/kg died after intravenous injection. The approximate lethal dose for dog was 400 mg/kg. 2. Neither abnormal symptoms and macroscopic findings nor deaths were observed in mice and rats treated orally. Granuloma around precipitates of T-3761 at the injection site was seen in mice and rats injected subcutaneously. Slight increase of white blood cell count, serum GOT, CPK and urea nitrogen were transiently found in dogs treated orally. Neither abnormal macroscopic findings nor deaths were observed in dogs treated orally. 3. Decreased motor activity and irregular breathing were observed in mice and rats injected intravenously. In dying animals, tonic or clonic convulsions were observed. Vomiting, hyperemia of ophthalmic mucosa, edema of face, decrease of motor activity, salivation and decrease in body temperature were observed in dogs injected intravenously. At higher doses, scream and tachypnea were observed while injecting. Hematological examinations disclosed that increases in red blood cell count, white blood cell count, hematocrit and hemoglobin were found transiently. In biochemical examinations, increases in serum GOT, GPT, urea nitrogen and creatinine were found transiently. One dog intravenously injected 400 mg/kg, showed tonic convulsion and died.
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PMID:[Single administration toxicity studies of T-3761 in mice, rats and dogs]. 766 80

A 39-year-old female presented to the Emergency Department during the fourth day of menstruation and within 2 hours of the onset of chest pain associated with dyspnea, diaphoresis, and emesis. An electrocardiogram showed acute inferior myocardial infarction and serial CPK enzyme levels peaked at 958 IU/L with 9% MB fraction. Along with aspirin and intravenous nitroglycerin, the patient was given thrombolytic therapy consisting of tPA with an initial bolus of 35 units, followed by 65 units infused within 60 minutes together with heparin 5000 units intravenous bolus, and 1000 units/hour maintenance infusion for 5 days. The menses were prolonged 1 day longer than her usual 5 days; however, there was no increase in the amount of bleeding during any day. The hemoglobin dropped from 12.5 G/dl to 11.3 G/dl in the first 6 hours, but remained stable thereafter. This initial drop in hemoglobin was considered a dilutional effect of 1.5 L of normal saline the patient received intravenously during that period. Although no available guidelines exist regarding the safety of thrombolytic agents during active menstruation, this case report and a few others reported in the literature suggest that normal menstruation is not a contraindication to thrombolytic therapy during acute myocardial infarction.
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PMID:Is thrombolytic therapy safe during active menstruation? 767 27

The authors report a case of post-traumatic rhabdomyolysis in a victim of a car accident who, after having being initially examined at an emergency ward, was sent home having been requested to return for a control visit a few days later. The patient did not attend the control visit on the appointed day but returned to the same emergency ward eight days after the accident suffering from vomiting, general malaise and violent pain in the left forearm that appeared swollen. Anamnesis revealed a severe condition of rhabdomyolysis with dehydration, pale red urine and general signs of marked renal insufficiency. Tests showed marked myoglobinemia and myoglobinuria, very high CPK, azotemia, creatinemia, transaminase and high diastasemia. Given the disappearance of peripheral pulse and the severe neurovascular impairment of the left forearm caused by edematous compression, it was decided to proceed to surgical decompression using extensive longitudinal fasciotomy under supraclavicular anesthesia. After surgery peripheral pulse returned to normal, as was confirmed by Doppler. After adequate hydration while renal insufficiency lasted, hemodialysis was commenced immediately and repeated during the following days. Given that all the tests had improved and results were virtually within the norm, the patient was transferred to the medical ward after eight days for continuation of therapy. It is important to underline the importance of possible signs, such as oleguria, dark urine, swelling and edemas of the limbs, in injured patients. If renal insufficiency occurs, it is important to commence early hemodialysis. On day 23 the patient was again transferred to the intensive care ward because he presented epigastric pain and vomiting. CAT showed acute pancreatitis which resolved leading to full recovery after 20 days.
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PMID:[Traumatic rhabdomyolysis. A clinical case]. 901 71


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