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)

A 3-yr-old boy was investigated for numerous episodes of fatigue, irritability, pallor, and sweating, which began at 11 mo of age, when he had an episode of symptomatic hypoglycemia with ketonuria. He had euphoria, mental confusion, drowsiness, nausea, and vomiting 1-5 hr after oral administration of glycerol in doses of 0.5-1.0gm/kg. Orally administered MCT (1 gm/kg) had similar effects. On one occasion, oral glycerol also provoked hypoglycemia, as had a 16 1/2 hr fast. Intravenously administered glycerol (0.09 gm/kg) induced an immediate loss of consciousness from which he recovered spontaneously after 30 min; there were no changes in blood glucose values. Intravenously administered fructose (0.25 gm/kg) was tolerated normally. Leukocytes showed normal activities for FDPase, glycerol kinase, and glycerol phosphate dehydrogenase. The restriction of dietary intake of fat has been associated with a marked improvement in physical and mental activities. These observations suggest a unique, yet undifined intolerance to glycerol, which suggest caution in the diagnostic use of glycerol in the investigation of hypoglycemia as well as in the therapy of increased intracranial or intraocular pressure.
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PMID:Glycerol intolerance in a child with intermittent hypoglycemia. 16 54

A 3 1/2 year old boy presented with a history of vomiting and generalized oedema. Biochemically proven protein losing enteropathy was associated with huge gastric fundal rugae on barium examination. Gastroscopy confirmed the barium findings but biopsy material demonstrated normal mucosa. The condition regressed on a high protein diet. Cytomegalovirus (CMV) was found in the urine after the illness had subsided.
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PMID:A case of hypertrophic protein losing gastropathy. 22 55

A 3 1/2-year-old girl with a huge optic glioma was reported. On February 26, 1978, she was hospitalized for signs of increased intracranial pressure, namely headache, vomiting and consciousness disturbance. Before admission she did not complain of her visual disturbance. A huge mass lesion in the subfrontal-suprasellar region was found by neuroradiological examination. The operation was performed on March 7, 1978, and the tumor arising from the right optic nerve, about 170 grams in weight, was totally removed in piecemeals. Histopathological diagnosis was pilocytic astrocytoma. Immediately after operation diabetes insipidus and hypernatremia developed, but two months later these symptoms disappeared. Post-operative CT scan demonstrated no mass lesion in the subfrontal-suprasellar region. After radiation therapy, she was discharged with slight left hemiparesis on August 31, 1978. Though her right eye was blind, visual acuity remained 0.2 in the left eye. No other neurologic deficits could be found.
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PMID:[Giant optic glioma--case report (author's transl)]. 49 74

A 3-month-old male infant had two episodes of fever, projectile vomiting, dehydration, generalized fine tremors and gross metabloic ketoacidosis. Methylmalonic acid was found in high concentration in both serum and urine, although the concentration of serum vitamin B12 was normal. A therapeutic trial of vitamin B12, administered parenterally, reduced greatly the methylmalonic aciduria. The patient has since been given vitamin B12 supplements continuously, initially 1 mg intramuscularly every other day, then 15 mg/d orally, and the protein in his diet was subsequently restricted. The most effected control of the methylmalonic aciduria was achieved with the combined regimen of oral vitamin therapy and dietary protein restriction. His physical and intellectual development have progressed normally and he has survived several acute respiratory tract infections without recurrence of metabolic acidosis.
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PMID:Methylmalonic acidemia controlled with oral administration of vitamin B12. 95 84

A 3-year-old Chow Chow was examined because of a 2-week history of vomiting and anorexia after administration of 200 mg of ibuprofen. Peritoneal effusion and free gas within the peritoneal cavity were observed on radiography of the abdomen. A full-thickness perforation of the pyloric antrum and pylorus were detected during exploratory laparotomy, and a Billroth-I gastroduodenostomy was performed successfully.
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PMID:Gastric perforation associated with administration of ibuprofen in a dog. 845 96

A 3-month-old girl was admitted to the hospital because of hypotonia and frequent vomiting. She had severe metabolic acidosis and her liver function was abnormal. Hepatomegaly and rapidly progressive liver failure developed, and she died at 4 months of age. Two half-siblings from a different mother had died in infancy of an undiagnosed myopathy. The liver was fatty and hepatocytes were filled with large and small lipid droplets. Other tissues were morphologically normal. The respiratory chain enzymes containing subunits encoded by mitochondrial DNA were markedly decreased in liver, partially decreased in muscle, but normal in other tissues. Southern blot analysis showed 90% depletion of mitochondrial DNA in liver, 53% depletion in muscle, and normal amounts in other tissues. This is the second case of fatal infantile liver failure associated with mitochondrial DNA depletion. This pathogenetic mechanism should be considered in infants with multiple respiratory chain defects and variable tissue expression.
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PMID:Fatal infantile liver failure associated with mitochondrial DNA depletion. 144 52

A 3-week-old boy presented with repeated episodes of vomiting and constipation. At laparotomy a jejunal diverticulum arising from its antimesenteric border and extending retroperitoneally was found. The narrow neck of diverticulum caused a situation similar to a Richter's hernia. The fundus of diverticulum was attached to the upper pole of left kidney. A retroperitoneal jejunal diverticulum is a new addition to the cause of neonatal intestinal obstruction.
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PMID:Retroperitoneal jejunal diverticulum: cause of intestinal obstruction. 146 85

A 2.5 kg female neonate, born after a normal 39-week pregnancy to Arab parents (1st degree cousins), developed unremitting vomiting of gastric contents, not bile-stained. Barium study demonstrated a grossly distended stomach with complete obstruction of the outlet. At laparotomy, pyloric atresia and a heterotopic pancreas located subserosally on the antrum of the stomach were diagnosed. A 3-cm gap was measured between the occluded antrum and the duodenum. Transmesocolic gastrojejunostomy was performed, and oral feeding was started 5 days later. Pyloric atresia and heterotopic pancreas are both rare congenital malformations. To the best of our knowledge, the combination of pyloric atresia and heterotopic pancreas has not previously been reported.
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PMID:[Heterotopic pancreas and pyloric atresia]. 186 19

A 3 year old boy who had glutaric aciduria diagnosed at 22 months of age was admitted with a history of lethargy, vomiting, and fever. He had been receiving glucose polymers as part of his dietary management. He was severely hypernatraemic, but after resuscitation and rehydration made a good recovery. The possible aetiology of his hypernatraemia is discussed.
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PMID:Glucose polymer regimens and hypernatraemia. 224 22

Apart from the classic distal renal tubular acidosis (RTA), the proximal RTA, and a few cases of distal RTA and renal bicarbonate wasting we know only 2 cases of infantile transient distal RTA with bicarbonate wasting. A 3 month-old male patient is admitted because of deficient suction, vomiting and dehydration. Despite a strong metabolic acidosis (pH 7,09, bicarbonate 8,6 mMol/l, chloride 110 meq/l) the urine is constantly alkaline; clinically the disease manifests itself in the form of an alkali-resistant RTA. Accompanying troubles such as inner ear deafness, G6PDH deficiency, hyperparathyroidism and vitamin D intoxication are to be excluded. A bicarbonate study carried out with care so as to prevent extracellular fluid expansion reveals the lack of excretion of titratable acid (-2.4 to +4.7 mueq/min/1.73 m2), an reduced excretion of ammonium (5 to 24.8 mueq/min/1.73 m2) with regard to GFR (42.4 ml/min/1.73 m2), and a constant loss of bicarbonate (FE HCO3- about 10%) covering most of the bicarbonate plasma concentration, which results in a constantly negative net acid excretion. Even with alkalosis there is no urine minus blood pCO2 increase. The renal excretion of gamma GT is significantly reduced. On substitution with high quantities of bicarbonate (10 meq/kg BW/day) the defect heals up at the age of 13 months. The pathogenesis of this disease is not quite clear, but is similar to that of the Lightwood infantile RTA. The acidification defect may be explained by a deficient hydrogen ions--secretion in the distal tubule; as for kinetics, it is not in the proximal tubule that the bicarbonate wasting occurs but it may be due to increased sodium delivery to the distal nephron.
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PMID:[Infantile transitory distal renal tubular acidosis with bicarbonate loss]. 286 14


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