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)

This study is a description of a patient who exhibited diabetic ketosis associated with an alkalosis rather than acidosis and a review of eight previously reported cases. Precipitating factors for this syndrome are severe vomiting with loss of hydrogen, potassium, and chloride ions, and dehydration. The ingestion of alkali may also result in this mixed acid-base disturbance. Treatment consists primarily of replacement of potassium and chloride. All reported patients had received large doses of insulin for initial therapy; however, limited insulin (20 U) therapy in this patient almost completely reversed the metabolic abnormality with 12 hours.
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PMID:Mixed acid-base abnormalities in diabetes. 10 96

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

A four-month-old boy with beta-ketothiolase deficiency is described in this report. Presenting symptoms and signs were vomiting, irritability and acidotic respiration. Laboratory investigations revealed hyperglycinemia, metabolic acidosis and ketosis. Subsequent urinary GC-MS analysis of the patient's urine sample showed the typical pattern of beta-ketothiolase deficiency. Our experience with this case indicates that accurate diagnosis and early treatment of inborn errors might be lifesaving.
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PMID:Beta-ketothiolase deficiency. A case report. 150 29

A case of propionic acidemia is reported. The main features of this patient were recurrent vomiting, ketosis and occasional episodes of seizure. Serum concentrations of propionic acid and glycine were within the normal range. Blood ammonia was slightly elevated. Characteristic organic acids were present in the patient's urine. they were: 3-hydroxypropionic acid, propionylglycine, methyl-citric acid, tiglyglycine, 3-hydroxyvaleric acid, etc. The etiology, pathogenesis, clinical features, diagnosis, and treatment of propionic acidemia are briefly discussed.
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PMID:[Propionic acidemia: one case report]. 183 12

The metabolic response to human growth hormone (HGH) was studied in five obese subjects in the fed state and during prolonged (5-6 wk) starvation. In the fed state (three subjects), HGH induced an elevation in basal serum insulin concentration, a minimal increase in blood and urine ketone levels, and a marked reduction in urinary nitrogen and potassium excretion resulting in positive nitrogen and potassium balance. In prolonged fasting (four subjects), HGH administration resulted in a 2- to 3-fold increase in serum insulin which preceded a 50% elevation in blood glucose. Persistence of the lipolytic effects of HGH was indicated by a rise in free fatty acids and glycerol. The response differed markedly from the fed state in that blood beta-hydroxybutyrate and acetoacetate levels rose by 20-40%, resulting in total blood ketone acid concentrations of 10-12 mmoles/liter, ketonuria of 150-320 mmoles/day, and increased urinary potassium loss. The subjects complained of nausea, vomiting, weakness, and myalgias. Despite a 50% reduction in urea excretion during HGH administration, total nitrogen loss remained unchanged as urinary ammonia excretion rose by 50% and correlated directly with the degree of ketonuria. It is concluded that in prolonged starvation (a) HGH may have a direct insulinotropic effect on the beta cell independent of alterations in blood glucose concentration, (b) persistence of the lipolytic action of HGH results in severe exaggeration of starvation ketosis and interferes with its anticatabolic action by necessitating increased urinary ammonia loss, and (c) failure of HGH to reduce net protein catabolism in starvation suggests that this hormone does not have a prime regulatory role in conserving body protein stores during prolonged fasting.
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PMID:Metabolic response to human growth hormone during prolonged starvation. 554 Jan 76

1. Several investigators have found that the development of post-exercise ketosis is not counteracted by glucose ingestion. Post-exercise ketosis might therefore have more in common with diabetic ketoacidosis than with starvation ketosis. 2. The effects of ingesting 100 g of glucose, alanine or starch were therefore studied in subjects rendered hyperketonaemic by prolonged running on a low carbohydrate diet, or by 65 h of starvation. These substances were also ingested by normal post-prandial subjects. 3. The runners developed post-exercise ketosis (1.81 +/- S.D. 0.81 mmol/l), which was counteracted by alanine and glucose, but only minimally by starch. 4. Fasting caused a variable ketosis (2.19 +/- S.D. 1.63 mmol/l), also counteracted by glucose and less by starch, but alanine caused vomiting. 5. Glucose and alanine lowered the blood ketone body levels of the post-prandial subjects. 6. The rising ketone body levels in starvation and after exercise were accompanied by simultaneous increases in the plasma insulin/glucagon ratios; in both, glucose ingestion increased the ratio further, while alanine decreased it. 7. It is concluded that there is no essential difference between established post-exercise and starvation ketosis, and that the blood fuel-hormone changes do not correlate with the changes in blood ketone body concentrations.
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PMID:The effects of alanine, glucose and starch ingestion on the ketosis produced by exercise and by starvation. 705 Mar 44

Five unusual cases of pneumomediastinum are described. In three the probable cause was thoraco-abdominal straining against a closed glottis during violent exercise, in criminal assault, or competitive sport. The resultant increase in intra-alveolar pressure produces an air leak which passes via the pulmonary interstitium into the mediastinum. It can then pass up into the neck to produce widespread subcutaneous emphysema and down through the diaphragmatic hiatuses to produce extraperitoneal emphysema. This may outline the lower surface of the diaphragm to stimulate intraperitoneal air, but it can also leak through the parietal peritoneum to result in actual intraperitoneal air. Therefore, in the patient who has been hospitalised after violent physical stress with or without blunt trauma, pneumomediastinum does not necessarily indicate tracheobronchial or oesophageal rupture and subdiaphragmatic air does not necessarily indicate bowel rupture. Probably any form of exercise in which the Valsalva manoeuvre is performed may cause pneumomediastinum, as may other causes of increased intra-alveolar pressure such as mechanical ventilation, bronchospasm, coughing and vomiting. Vomiting is a likely contributing cause in the pneumomediastinum of diabetic ketosis, of which a case is described. Another case is presented in which air passed in the opposite direction, from perforated extraperitoneal bowel up into the mediastinum.
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PMID:Air in unusual places: some causes and ramifications of pneumomediastinum. 707 35

A male infant who had vomiting and coma in the absence of ketoacidosis was initially thought to have dysautonomia because of abnormal responses to methacholine and histamine, as well as abnormal urinary catecholamine excretion. Following an episode of hyperammonemia, a liver biopsy was performed which revealed a partial deficiency of carbamyl phosphate synthetase activity. The patient was treated with a protein-restricted diet supplemented with a mixture of ketoacid analogues of the essential amino acids, which precipitated ketosis and acidosis. A primary deficiency of propionyl coenzyme A (CoA) carboxylase was subsequently demonstrated. Because disorders of propionate metabolism may not initially present with ketoacidosis, we recommend examination of both plasma and urine for metabolites of this pathway, as well as direct measurement of propionyl CoA carboxylase activity in peripheral blood leukocytes, before performing a liver biopsy to evaluate urea cycle enzyme activities, and particularly before adding keto acid/amino acid mixtures to a protein-restricted diet.
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PMID:Dysautonomia in an infant with secondary hyperammonemia due to propionyl coenzyme A carboxylase deficiency. 735 3

The aim of this work was to investigate the changes of cardiac performance by both electrocardiography (ECG) and echocardiography (ECHOc), in addition to anthropometric and hormonal variables before, during and after prolonged total fasting (TF) and re-feeding in an overweight adult man. Physical examination, laboratory and hormonal measurements, ultrasonographic study of body fat distribution, ECG and ECHOc study were performed before during and after 34 days of TF and after 17 days of isocaloric re-feeding. The subject was a 52-year old Caucasian who was overweight with increased abdominal fat content (BMI: 28.6; W/H ratio: 0.95) and increased levels of arterial systolic and diastolic blood pressure (SBP, DBP). HPLC measurements of urinary catecholamine levels (HPLC), ECHOc study of cardiac performance, ultrasonographic study of body fat distribution were performed. The subject starved for 34 days losing 22kg, but after that time he was compelled to re-feed because of nausea and severe vomiting. A marked ketosis (ketonuria > 1200mg/day) was already present after 6 days of TF. After 17 days of TF norepinephrine (NE) and epinephrine (EPI) urinary levels showed a two-fold and nine-fold increase respectively, but they became undetectable at the end of TF. After 17 days of re-feeding catecholamine urinary levels were similar to those measured after 17 days of TF. After both TF and 17-day isocaloric re-feeding we found a decrease of visceral fat content and W/H ratio reached the normal values for age-matched subjects (W/H ratio after TF: 0.80, after re-feeding: 0.80).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:34-day total fast in an adult man. 771 90

We describe two children with deficiency of short-chain L-3-hydroxyacyl-CoA dehydrogenase, a new disorder of the mitochondrial beta-oxidation of straight-chain fatty acids. The patients presented with fasting-induced vomiting, and ketosis and low blood glucose, features typical of ketotic hypoglycemia were documented in one. Enzyme assays were performed in cultured skin fibroblasts. In whole fibroblast preparations there was reduced enzyme activity but high residual activity due to the presence of a nonmitochondrial enzyme. In isolated fibroblast mitochondria the residual enzyme activities were 5 and 6% of the normal controls. Activity in an obligate heterozygote was intermediate, suggesting that this is an autosomal recessive disorder.
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PMID:Mitochondrial short-chain L-3-hydroxyacyl-coenzyme A dehydrogenase deficiency: a new defect of fatty acid oxidation. 882 8


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