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)

Some aspects of typhoid fever in 77 children are discussed. There were 48 boys and 29 girls and their ages ranged from 1 month to 12 years. The patients were treated with chloramphenicol 100 mg/kg/d during the first 2 weeks and with either amoxycillin (100 mg/kg/d) or ampicillin (200 mg/kg/d) during the third week. The average duration of fever was 5.2 days. There was 1 relapse and 1 child, a baby aged 1 month, died. The correct diagnosis was not suspected by the referring doctor in 38% of the patients. On admission the commonest complaints were fever, abdominal pain, diarrhoea, headache and vomiting. The commonest findings on examination were tenderness or distension of the abdomen, apathy or delirium, rhonchi or crepitations, liver enlargement and meningism. There was anaemia (Hb less than 10 g/dl) in 23% and lymphopenia (less than 1500/microliter) in 43% of the patients. The differential white blood cell count revealed 5% or more unsegmented neutrophils in 32% of the patients, while 25% had 10% or more band cells. Two patients (sisters) failed to respond after 15 and 16 days of therapy with chloramphenicol and ampicillin because of resistant Salmonella typhi and were successfully treated with co-trimoxazole. Practitioners caring for black patients should always be on the alert for typhoid fever; some patients may not respond to chloramphenicol or amoxicillin. During the acute phase milk feeds are best replaced by soya products because of abdominal distension or aggravation of diarrhoea by milk.
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PMID:[Aspects of typhoid fever in children]. 376 9

Two types of bilateral amygdalar lesions were performed successively. The first operation, involving the dorsomedial part, produced aphagia and subsequent hypophagia, vomiting and apathy. Consequently the body weight was reduced. After a few weeks partial recovery occurred. The second operation, involving the lateral part of the amygdaloid complex, produced hyperphagia, increase of body weight and restoration of general arousal. These results indicate the existence of two antagonistic systems: excitatory in the dorsomedial amygdala and inhibitory in the lateral amygdala. Damage of the inhibitory system reverses almost completely the syndrome produced by an initial lesion of the excitatory system.
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PMID:The normalizing effect of lateral amygdalar lesions upon the dorsomedial amygdalar syndrome in dogs. 451 16

Congenital methylmalonic acidaemia (MMA-aemia) was diagnosed in an 8-month-old girl who presented with severe metabolic acidosis, hypoglycaemia and hyperglycinaemia. Vomiting, failure to thrive and apathy first appeared when breast feeding was replaced by a cows' milk formula at the age of 3 months. The patient, unresponsive to OH-Cbl therapy, was successfully treated with dietary protein restriction and with Shohl's solution. Aged 4 years 9 months, she is in good health. Studies in cultured fibroblasts revealed a defect of the MMA-CoA mutase apoenzyme. Mutase activity in cell extracts was barely detectable both with and without added coenzyme (Ado-Cbl). Addition of OH-Cbl to the culture medium improved overall propionate metabolism in intact fibroblasts but had no effect on mutase activity in cell extracts. These observations point to the presence of a very labile mutant enzyme, suggesting that the patient reported here may be suffering from yet another variant of MMA-aemia.
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PMID:Methylmalonic acidaemia due to mutase apoenzyme defect: responsive to vitamin B12 in intact fibroblasts but not in vivo. 613 33

Since 1972, telecobalt irradiation plus intrathecal methotrexate (ITMTX) has been successfully replaced in Jena by intrathecal colloidal radioactive gold (198Au) plus ITMTX for meningosis prophylaxis in leukemia. Seventy-three children with acute lymphocytic leukemia (ALL) were given 1.24-4.89 mCi (45.8-181 MBq) of colloidal 198Au IT after successful initiation of remission. During cytostatic therapy, the following relapses occurred: meningosis leucaemica, five patients (6.8%); bone-marrow relapse and the meningosis leucaemica, one patient; and bone-marrow relapse, 20 patients (27.4%). In 18 children, combination chemotherapy was terminated after two and a half or three years of treatment. After that time, one meningeal relapse and six bone-marrow relapses occurred. Within the first 24 hours after application of radioactive gold, headaches, vomiting, and fever occurred in less than 10% of the children. An apathy syndrome, leukecephalopathy, or severe infections, were not observed in a single case. Radioactive gold spreads in the subarachnoid space and is phagocytized by the arachnoidea. The tumoricide effect extends selectively over the space of distribution of the latent meningosis leucaemia. The cerebral parenchyma remains unaffected by radiation. Thus, radioactive gold may be preferable to telecobalt irradiation in preventing central nervous system leukemia.
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PMID:Meningosis prophylaxis with intrathecal 198Au-colloid and methotrexate in childhood acute lymphocytic leukemia. 627 5

We report the first case of lysinuric protein intolerance observed in Germany. A girl of Turkish ancestry suffered from severe dehydration at the age of 6 months after changing from breast milk to cow milk. Because of a microcytic hypochromic anaemia and erythrophagocytosis in the bone marrow a hematologic disease (Farquar's disease) was suspected. The definite diagnosis of lysinuric protein intolerance was eventually clarified by the following laboratory and clinical data: increased urinary excretion and low plasma concentration of lysine, arginine and ornithine, apathy, vomiting, diarrhea and hyperammonemia after an oral protein load, high serum LDH-activity, ferritinemia, and increased urinary excretion of orotic acid. Under therapy with citrullin and a low-protein diet the metabolic situation remained stable, even during infections. The bone marrow findings have been reported only in one further case of lysinuric protein intolerance.
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PMID:[Lysinuric protein intolerance]. 642 Jun 70

Since our last report on valproate (VPA)-related hepatotoxicity in 1988, 8 other children have died of VPA-associated liver failure in Germany and Switzerland. We compared the clinical course of these children with that of 6 children with a reversible outcome of severe hepatotoxicity related to VPA. Thirty-five percent of patients with fatal liver failure were normally developed, 23.5% were receiving VPA monotherapy, and 35.3% were aged < or = 2 years. The initial clinical symptoms of VPA-related hepatotoxicity were nausea, vomiting, apathy or coma, and increasing seizures in more than 50% of patients, in combination with febrile infections at onset of symptoms. As compared with the series of German patients reported in 1988, one third of the fatalities occurred after the first 6 months of therapy as compared with 6% in the 1988 series. Clinical symptoms and laboratory findings were the same in patients with reversible and with fatal outcome. Early or immediate withdrawal of VPA after the first signs of VPA-associated hepatotoxicity may be responsible for the increased number of children who recovered after VPA-related severe liver failure. The pathogenesis of liver failure during VPA treatment remains unknown; metabolic defects and cofactors such as polypharmacy or infections have become increasingly likely to contribute by depleting intracellular CoA. Worldwide, 132 patients have died of VPA-associated liver failure and/or pancreatitis. Because a group at risk for fatalities with VPA cannot be defined precisely, patients treated with VPA and their families must be made well aware of the clinical symptoms of hepatotoxicity such as apathy, vomiting, or increased seizure frequency, especially in the presence of febrile infections. Laboratory tests and clinical controls during the first 6 months of therapy should not be neglected.
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PMID:Severe hepatotoxicity during valproate therapy: an update and report of eight new fatalities. 792 43

Intussusception, the invagination of a portion of the intestine into an adjacent segment, is the most common cause of intestinal obstruction in post neonatal children. Most cases are idiopathic, but in about 2-12% the intussusception evolves secondary to an underlying abnormality. Classically, there is sudden onset of attacks of screaming, accompanied by pallor, vomiting, and irritability in a previously health child. Some gradually become weaker and lethargic. We evaluated variations in presenting symptoms and outcome as related to age and time until admission. There were incidence peaks in the spring and autumn. 48% developed irritability, while 42% were described as apathetic. These results emphasize the importance of awareness that apathy can be a major presenting symptom. The younger the child, the greater the rate of success of reduction by hydrostatic pressure. In those admitted within 24 hours of onset, the rate of reduction was twice that in those admitted later. Awareness of atypical symptoms and early diagnosis may affect treatment and improve prognosis.
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PMID:[Intussusception in infants]. 792 13

Comprehensive data on 30 patients with propionic acidaemia, diagnosed by selective screening for inborn errors of metabolism, are presented. The most valuable diagnostic metabolites found were methylcitric-, 3-hydroxypropionic-, and 2-methyl-3-oxovaleric acids. Hyperlysinaemia and hyperlysinuria are also characteristic findings in this disease. The metabolic pattern found in propionic acidaemia is discussed extensively as are enzymatic findings. Residual activity of propionyl-CoA carboxylase is neither a predictive marker for severity nor for outcome of the disease. Propionate fixation assays were less reliable for confirmation of propionic acidaemia and of no prognostic value. Clinical presentation of the disease is discussed in detail. Besides the well-known unspecific findings (poor appetite, feeding difficulties, vomiting, dehydration, weight loss, muscular hypotonia, dyspnoea, somnolence, apathy, convulsion, coma, severe metabolic acidosis, hyperammonaemia) various skin abnormalities have been detected in about 50% of all patients. In 27% "dermatitis acidemica" was found.
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PMID:Propionic acidaemia: clinical, biochemical and therapeutic aspects. Experience in 30 patients. 795 90

Between 1989 and 1992, 22 Bernese mountain dogs (18 females and four males) aged between two and seven years, which had been suffering for some weeks from weight loss, anorexia, apathy, vomiting, polydipsia and polyuria, were examined. All of them had high blood urea nitrogen and serum creatinine concentrations, and many had hyperphosphataemia, hypercholesterolaemia, hypoproteinaemia and nonregenerative anaemia. All the dogs had very high protein: creatinine ratios in the urine, and macroproteinuria was identified by sodium dodecyl sulphate gel electrophoresis. The immunofluorescent titres against Borrelia burgdorferi, measured in 19 of the dogs, ranged between 256 and 32,768. In all cases, membrano-proliferative glomerulonephritis with concomitant interstitial nephritis was diagnosed. From an analysis of the dogs' pedigree it was concluded that the glomerulonephritis of these Bernese mountain dogs was inherited as an autosomal recessive trait and that its expression was influenced by a second gene locus with a sex-linked dominance exchange.
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PMID:A new familial glomerulonephropathy in Bernese mountain dogs. 803 71

Portal hypertension caused by primary hypoplasia of the portal vein was diagnosed in 42 dogs. The portal hypertension was manifested by the presence of multiple portosystemic collateral vessels. The main clinical signs were retarded growth or weight loss, apathy, intermittent diarrhoea and vomiting, anorexia, abdominal distension and polydipsia. Major findings at physical examination were ascites in 23 dogs and neurological signs in 16 dogs. The dogs had increased activities of liver enzymes in plasma and increased fasting levels of total bile acids and ammonia; in many of the dogs the packed red cell volume, total serum protein and albumin were low. Gross inspection of the portal vein revealed a patent but underdeveloped extrahepatic vein in 13 of the dogs. Microscopic examination of the liver revealed hypoplasia of the intrahepatic portal veins in all the dogs, and this was associated with minor arteriolar proliferation and absence of fibrosis in 12 of them, with moderate to marked arteriolar proliferation often combined with ductular proliferation in 13, and with marked portal fibrosis (formerly described as hepatoportal fibrosis) with a varying number of arteriolar and bile ductular structures in 17 of the dogs. The disease affected mainly young dogs, and was most likely to have been of congenital origin.
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PMID:Portal hypertension associated with primary hypoplasia of the hepatic portal vein in dogs. 856 Jul


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