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)

Two children are described who suffered from episodes of metabolic acidosis and progressive mental and motor deterioration. The patients showed periodic elevation of blood lactate, pyruvate and alanine, which was accompanied by vomiting, hypotonia or convulsions. The concentrations of lactate and pyruvate in cerebrospinal fluid were found to be increased. Liver biopsies revealed a decrease in pyruvate carboxylase activity and normal pyruvate decarboxylase activity. No inhibitor of TPP-ATP phosphoryl transferase was detected in urine from the patients. These findings suggest that congenital lactic acidosis due to pyruvate carboxylase deficiency is probably a different disease entity from Leigh's encephalomyelopathy. A possible mechanism of brain damage caused by a defect in pyruvate carboxylase is postulated.
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PMID:Congenital lactic acidosis due to pyruvate carboxylase deficiency: absence of an inhibitor of TPP-ATP phosphoryl transferase. 20 66

Three case histories of patients with large tumors in the posterior fossa who were operated on in a sitting position subsequently developed 1 or more symptoms referable to the temporoparietooccipital regions of the brain 24 to 48 hours postoperatively. Initially, it was believed that such symptoms were due to a stimulation of the association pathways causing firing of remote association areas (See Ch. 4). Subsequent studies of the rotation of blood vessels of the brain in the developing embryo and a review of the anatomical location of the arteries supplying the temporoparietooccipital region led to the conclusion that some compromise of the posterior cerebral artery was responsible for the symptoms. The symptomatology in these brain tumor patients was not unlike that seen in the cosmonauts and astronauts in space flight, designated as "motion sickness" in the space literature. A suggestion was made as to clarification of the definitions. This author advocated that the term "motion sickness" be confined to those symptoms of dizziness, nausea, and vomiting, due to involvement of the peripheral end organ, the inner ear. "Space sickness" might include these symptoms but also might have the addition of disorientation or the inversion of image in space and formed or unformed hallucinations. These relate to the temporoparietooccipital area, the midtemporal, and the occipital regions. In such instances, there must be central involvement or a stimulation of this interpretive cortex of the brain. The remote symptoms from the supratentorial cotex were believed to be due to hypoxia related to the posterior cerebral artery compromise, resulting in delayed "luxury perfusion" and the development of local lactic acidosis. Transaxial transmission of force with an uncal tentorial herniation causing compression of the posterior cerebral artery was suggested as a mechanism responsible for the vascular compression.
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PMID:Remote cerebral hemisphere symptoms from surgically treated patients with posterior fossa brain tumors; vascular factors: a basis for a theory concerning space sickness. 56 32

In 4 out of 9711 (= 1:2400) patients, lactice acidosis due to biguanides was diagnosed. Serum lactate concentration averaged 18.2 mmol/l and the pH value 6.87. All patients showed signs of renal insufficiency and three had congestive heart disease. In addition to treatment with biguanides, other factors might have contributed to the lactice acidosis in these patients: prolonged fasting, severe dehydration due to persistent vomiting, acute bronchopneumonia, and acute pyelonephritis. On addmission, two patients were in shock and all patients were semi-conscious or comatose. All patients were treated with bicarbonate and glucose/insulin. One patient was hemodialysed. Two of our four patients died. Oour four patients are compared with 179 patients in the literature with respect to mortality and prognosis of lactic acidosis due to biguanides.
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PMID:[Lactacidosis in biguanide therapy: diagnosis and therapy. 4 cases compared to 179 cases in the world literature]. 71 23

The case is reported of a non-diabetic young woman who attempted suicide by ingesting 2,500 mg of phenformin. The most marked clinical and laboratory findings during the first 24 hrs included nausea, vomiting, anxiety, agitation, polydipsia, polyuria, increased appetite, tachycardia, tachypnea, persistent lactic acidosis, hypoglycemia and hypokalemia. Treatment at the ICU 10 hrs after ingestion of the overdose was essentially symptomatic and included measures to correct acidosis and hypoglycemia. The patient recovered completely.
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PMID:Acute self-poisoning with phenformin. 102 Jun 9

A case of lactic acidosis associated with phenformin therapy for diabetes mellitus is reported, and 34 previously reported cases of lactic acidosis associated with phenformin therapy are reviewed to determine if any predisposing factors to lactic acidosis were apparent. Observations of sex, age, duration of diabetes, pathologic conditions, dosage, duration of phenformin therapy and the onset of symptoms preceding lactic acidosis were made. Renal impairment, urinary tract infections, hepatic impairment, ethanol ingestion and poorly controlled congestive heart failure were found to be predisposing factors to lactic acidosis. The appearance of a syndrome of impending lactic acidosis consisted of anorexia, nausea, vomiting with abdominal pain or lethargy.
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PMID:Phenformin-associated lactic acidosis; a review. 114 21

We describe the full history and postmortem findings in one of the first identified cases of mitochondrial encephalomyopathy with stroke-like episodes (MELAS). To clarify diagnostic criteria, we analyzed 69 reported cases. The syndrome should be suspected by the following three invariant criteria: (1) stroke-like episode before age 40 yr; (2) encephalopathy characterized by seizures, dementia, or both; and (3) lactic acidosis, ragged-red fibers (RRF), or both. The diagnosis may be considered secure if there are also at least two of the following: normal early development, recurrent headache, or recurrent vomiting. There are incomplete syndromes in relatives of patients with the full syndrome and incomplete syndromes might also be encountered in sporadic cases. Some MELAS patients have features of the Kearns-Sayre syndrome (KSS) or myoclonic epilepsy with ragged-red fibers (MERRF), but none had the full KSS syndrome. In partial or confusing cases, analysis of mitochondrial DNA (mtDNA) may point to the correct diagnosis; however, not all patients with clinical MELAS have had the typical mtDNA point mutation and some patients with the mutation have clinical syndromes other than MELAS.
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PMID:Melas: an original case and clinical criteria for diagnosis. 142

A 9-year-old girl and an 11-year-old boy had ptosis, progressive external ophthalmoplegia, pigmentary retinopathy, and sensorineural hearing loss. The girl had diabetes mellitus and the boy had hypoparathyroidism. Both children also developed recurrent vomiting and cerebral infarcts with lactic acidosis. Muscle biopsy specimens showed ragged-red fibers and Southern analysis demonstrated a distinct heteroplasmic deletion of muscle mitochondrial DNA in each patient but no evidence of the point mutation in the transfer RNALeu(UUR) gene recently identified in mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS). These 2 children had combined features of Kearns-Sayre syndrome and MELAS, suggesting that mitochondrial DNA deletions occasionally can have pleomorphic clinical expression.
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PMID:Deletion of mitochondrial DNA in patients with combined features of Kearns-Sayre and MELAS syndromes. 189 71

We report a 14-year-old boy with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) who presented repeated episodes of abdominal pain and vomiting since the age of 8 years. In addition, he developed strokelike episodes with myoclonic seizures and transient hemiplegia on three occasions. At the age of 14-1/12-years, he also developed epilepsia partialis continua persisting for 10 days, which was associated with myoclonic seizures synchronized with spike discharges at the right central area. Laboratory examination disclosed increased levels of lactate and pyruvate in serum and CSF and low density areas in the bilateral temporal regions on CT scan. Muscle biopsy showed scattered ragged-red fibers. The enzyme activities (pyruvate dehydrogenase complex, pyruvate carboxylase, phosphoenol pyruvate carboxykinase, and cytochrome c oxidase) and the rates of decarboxylation of [3-14C]pyruvate in cultured skin fibroblasts were within normal ranges.
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PMID:[A case with MELAS associated with epilepsia partialis continua]. 189 96

A case of 25-year-old woman with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) was reported. She had short stature, episodic vomiting with headache, several episodes with homonymous hemianopsia, progressive intellectual decline, generalized convulsion, muscular atrophy, sensory disturbance on the left side of the body, and primary amenorrhea. Lactate, pyruvate and the lactate to pyruvate ratio were elevated in the serum and cerebrospinal fluid. Muscle biopsy revealed ragged-red fibers. On electron microscopy there were subsarcolemmal aggregations of abnormal mitochondria with proliferation of crista and inclusions. Activities of the respiratory chain enzymes of the muscle mitochondria were normal. She showed a failure of GH response to arginine and levodopa and delayed response of serum GH to growth hormone releasing factor (GRF). She also showed decreased gonadotropin levels and delayed response of the hormone to LH-RH. In this case, a dysfunction of the hypothalamo-pituitary axis may be related to the short stature and primary amenorrhea. It is suggested that the hypothalamo-pituitary hypofunction may be one of the characteristic features in MELAS.
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PMID:[Mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) associated with hypothalamo-pituitary hypofunction--a case report]. 206 Feb 43

A 12 year old girl with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke like episodes (MELAS) is reported. After a normal childhood, at 9 years of age she developed generalized and hemilateralized seizures. Posteriorly, these episodes became more frequent and were accompanied by headache, homonimous hemianopsia, ataxia, vomiting, photophobia, left hemiparesis, slurred speech and even convulsive status. Laboratory tests evidenced lactic acidosis, brain lucencies at CT Scan and ragged skeletal muscle fibers at muscle biopsy.
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PMID:[Mitochondrial encephalomyopathy, lactic acidosis and features of cerebrovascular disorders]. 207 86


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