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)

Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess. Charts of 100 inpatients with hypophosphatemia were reviewed and the patients divided into five groups on the basis of serum phosphate level: 18, 2.1 to 2.4 mg/dL; 49, 1.6 to 2.0 mg/dL; 20, 1.1 to 1.5 mg/dL; 12, 0.6 to 1.0 mg/dL; 1, 0.1 to 0.5 mg/dL. The effect of glucose ingestion on serum phosphate level was shown in one normal patient. Whenever carbohydrate was administered intravenously (45 cases), this was considered the primary cause of the hypophosphatemia. Other causes were as follows: diuretics, hyperalimentation, alcoholism, respiratory alkalosis, dialysis, insulin, corticosteroids, diabetic ketoacidosis, vomiting, phosphate-binding antacid, Gram-negative sepsis, primary hyperparathyroidism, saline, epinephrine, gastrointestinal malabsorption, and unknown. Hypophosphatemia in hospitalized patients may have multiple causes.
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PMID:Hypophosphatemia in hospitalized patients. 44 90

Chronic alcoholism is a frequently unrecognized cause of ketoacidosis in nondiabetic patients. Seven episodes of alcoholic ketoacidosis were observed in three patients. No consciousness disturbances were present. Semi-quantitative tests for ketones were strongly positive in urine, weakly positive in serum. The anion gap was between 25 and 41 mEq/l; serum lactate was between 0.9 and 9.0 mEq/l, and, in all cases, below the anion excess. Blood glucose ammonia was increased. Massive fatty liver was documented in all patients. All ketosis episodes followed an increase of alcohol ingestion associated with one to four week-starvation and vomiting; however, at the time of admission, alcohol was weakly increased in blood. In the four episodes where diagnosis was correct, ketoacidosis was rapidly corrected without insulin administration. In conclusion, in some nondiabetic subjects, the occurence of alcohol prolongated ingestion together with starvation and vomiting is responsible for ketoacidosis; because alcoholic ketoacidosis has often a mild clinical expression, its true prevalence is underestimated; insulin administration is not required.
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PMID:[Alcoholic ketoacidosis (author's transl)]. 53 15

Between Jan. 1, 1971 and June 30, 1976 the authors diagnosed tuberculous peritonitis in 17 patients. The basis for the diagnosis was a positive culture for Mycobacterium tuberculosis from the peritoneal fluid or nodules (nine patients) or the presence of caseating granulomas in biopsy specimens of the peritoneum (eight patients). Fifteen of the 17 patients were women. Eleven were North American Indians and eight of them suffered from alcoholism. The predominant symptoms of abdominal pain, progressive abdominal distension and vomiting, and abdominal tenderness on physical examination were present both in alcoholics and in nonalcoholics. However, only the former had demonstrable ascites. The mean time from admission to hospital until establishment of the diagnosis was 8.3 days in six nonalcoholics and 49 days in the alcoholics (P less than 0.01). The delay in making the diagnosis in the patients with alcoholism resulted from a tendency to attribute their fever to alcoholic hepatitis and the ascites to portal hypertension. The mean duration of hospitalization was 160.3 days for the alcoholics and only 41.5 days for the nonalcoholics. Two of the eight alcoholics died, one of hepatic failure and the other, 3 years after the diagnosis of tuberculous peritonitis was made, of miliary tuberculosis.
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PMID:Tuberculous peritonitis in Manitoba. 73 93

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

Three cases of benign pancreatic ascites have been added to 94 cases reviewed from the literature. Common characteristic of this syndrome were chronic alcoholism, intermittent abdominal pain, nausea, vomiting and considerable weight loss which occurred despite fluid accumulation. Markedly elevated protein and amylase levels in the ascitic fluid, hyperamylasemia and hypoalbuminemia were the major diagnostic clues as to the pancreatic origin of ascites. Predominant pathological findings were chronic pancreatitis with or without pseudocysts, pancreatic duct disruption, lesion which were considered to be the major pathogenic factor besides lymphatic obstruction by leaking pancreatic juice into the peritoneal cavity. Early laparotomy for diagnosis and treatment is essential. ERP might be of great value in diagnosis.
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PMID:Massive pancreatic ascites without carcinoma. Report of three cases. 84 74

Two patients with central pontine myelinolysis are described. Both were middle aged women presenting with a history of protracted vomiting and drowsiness. Hyponatraemia (serum sodium 96 to 100 mmol/L) was a feature in both patients. No underlying malignancy, alcoholism, malnutrition or other serious disease was identified. Correction of electrolyte abnormalities was accompanied by deterioration in level of consciousness and development of a neurological syndrome characterized by quadriparesis, dysphasia and mutism. Death followed and histopathological examination confirmed classical myelinolysis in the central pons and extensive similar, though not identical, lesions in the cerebral hemispheres in both cases. The pathophysiological basis of the lesions is likely to be a special metabolic susceptibility of oligodendroglial cells in areas where neurones, glial cells and myelin sheaths lie in close proximity to one another.
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PMID:Central pontine myelinolysis. Two cases with associated electrolyte disturbance. 94 40

Health workers took blood examples from 130 9-70 year old patients with liver cirrhosis admitted to the Department of Gastroenterology at BYL Nair Hospital in Bombay, India, between January 1990 and February 1992. Since patients with liver cirrhosis tend to undergo many blood transfusions in emergency situations, because of vomiting blood, researchers wanted to determine whether an association exists between HIV infection and liver cirrhosis. Laboratory personnel tested the samples for anti-HIV antibodies using first the ELISA and then confirming positive samples with the Western Blot (WB) test. The ELISA revealed 11 positive samples (5 were WB positive; 4 were WB negative, and 2 had indeterminate results) and the WB confirmed 5 HIV positive cases (all being 20 to 50 year old males). Thus, the HIV seroprevalence was 3.8% among the liver cirrhosis cases. 1 HIV-positive patient had earlier engaged in homosexual intercourse, 2 others had had multiple sexual partners. 4 HIV=positive patients had chronic alcoholism. 1 HIV-positive patient suffered from extensive intra abdominal tuberculosis and died during his hospital stay. None of the HIV-positive patients had earlier undergone a blood transfusion. The researchers called for more studies to confirm a relationship between HIV infection and liver cirrhosis with or without alcoholism.
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PMID:HIV infection in patients of liver cirrhosis. 139 3

Boerhaave's-syndrome is a rare illness, usually caused when sudden intense vomiting leads to a spontaneous rupture of the healthy esophagus. Alcoholism and neurological diseases are considered to be the main predisposing factors. Because the complaint is so rare the casuistic of Boerhaave's-syndrome is described in connection with pyloric stenosis. In order to confirm the diagnosis the following practice is recommended: During gastrografin swallowing the pylorus should be examined in order to remedy the possible cause of the complaint when the operative therapy is carried out.
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PMID:[Boerhaave syndrome in pyloric hyperplasia]. 147 45

Overall 69 patients with sensitive traits of character not reaching the degree of psychopathy, suffering from stage II chronic alcoholism were examined on a clinical basis. In the given patients' group, alcoholism manifested itself atypically. The initial lack of the protective nauseous and vomiting reflex and high tolerance, relative preservation of the quantitative control, no amnesia during drunkenness, temporal break between the formation of compulsive addiction and the abstinent syndrome, manifestation of compulsive addiction only in a state of alcoholic intoxication were recorded. At the same time attention should be drawn to the frequently occurring depressive forms of drunkenness, early appearance of the asthenic state, the lack of marked personality changes by the alcoholic type, relative preservation of a critical attitude towards the disease, and to the abortive abstinent syndrome, characterized sometimes by an elevated attitude of mind resembling the hypomaniacal state. Alcoholism tends towards a moderate progredient course, which is often not realized because of the influence of psychic trauma and in that case alcoholism takes a malignant course.
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PMID:[Characteristics of chronic alcoholism in patients with sensitive premorbid states]. 164 30

The term "microvesicular steatosis of the liver" refers to a variant form of hepatic fat accumulation whose histologic features contrast with the much more common macrovesicular steatosis. Microvesicular steatosis of the liver was originally described in association with conditions who share a number of biochemical and a limited number of clinical features: acute fatty liver of pregnancy, Reye's syndrome, Jamaican vomiting sickness, sodium valproate toxicity, high-dose tetracycline toxicity and certain congenital defects of urea cycle enzymes; they were thought to constitute an entity of "microvesicular fat diseases". In recent years the disease has been described in a wide variety of conditions: alcoholism, toxicity of several medications, delta hepatitis in South America and Central Africa, sudden childhood death, congenital defects of fatty acid beta oxidation, cholesterol ester storage disease, Wolman disease and Alpers syndrome. Not much is known regarding the pathogenesis of microvesicular steatosis but in many instances the primary defect could be a mitochondrial lesion, and inhibition of the mitochondrial beta oxidation of fatty acids has been the most frequently implicated defect. The different conditions associated with microvesicular steatosis are heterogenous in many aspects. Maintaining the concept of "microvesicular fat diseases" as a unique entity seems no longer justified.
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PMID:Microvesicular steatosis of the liver. 217


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