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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two infants with lethargy, vomiting, convulsions, coma and marked metabolic acidosis were found to have very high concentrations of methylmalonic acid in their serum and urine. In vitro studies of fibroblasts demonstrated that the infants had different variants of methylmalonic acidemia.Vitamin B(12) was given in two different forms at 1 month of age and at 12 months of age. Each trial continued for 4 months but neither infant showed a clinical or biochemical response.In both infants hyperglycinemia, neutropenia and thrombocytopenia developed during acute metabolic crises only. Hypoglycemia was found in patient 2. Hyperammonemia was severe in patient 2 during acute crises but never appeared in patient 1. When clinically well, both infants continued to excrete abnormal amounts of methylmalonic acid in the urine and both had persistent compensated metabolic acidosis.Marked hyperuricemia developed in patient 1 at 18 months of age and led to progressive renal failure. Allopurinol therapy was necessary to keep the uric acid concentration within the normal range. Renal function returned to normal, as indicated by a marked increase in the renal clearance of creatinine and uric acid.Patient 1 is physically and mentally retarded, and has moderate hypotonia, hepatomegaly and persistent vomiting. Patient 2 has developed normally.The urine concentrations of methylmalonic acid in the four parents were normal.
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PMID:Methylmalonic acidemia: 6 years' clinical experience with two variants unresponsive to vitamin B12 therapy. 3 17

Clinical observations were made on 95 serologically or virologically confirmed dengue fever cases during an epidemic in a rural area of Indonesia in December 1976. The age distribution was similar to that observed in patients with dengue hemorrhagic fever in Jakarta, a highly endemic urban area. The observed disease ranged in severity from undifferentiated fever to shock and death. The majority of patients had acute onset of fever with nausea, vomiting, headache, and abdominal pain. Hepatomegaly was observed in only 19% of the patients. A positive tourniquet test was the most frequently observed hemorrhagic manifestation, but epistaxis was observed in 20% and hematemesis in 6% of the patients. Dengue shock syndrome was observed in 37% of the patients. There were four deaths, three of which were confirmed as due to dengue infection by virus isolation. The data suggest that one, and possibly two, of the fatal cases with virus isolation were primary infections, based on the results of hemagglutination-inhibition test using all four dengue antigens.
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PMID:Epidemic dengue hemorrhagic fever in rural Indonesia. II. Clinical studies. 46 92

The varied presentation and clinical features of classical galactosaemia are illustrated by the case histories of seven babies born in Western Australia since January, 1962, and of two babies born in South Australia in whom diagnosis was made as a result of adding galactosaemia to the Guthrie screening programme in October, 1974. All were shown to have a severe deficiency of galactose-1-phosphate uridyl transferase in their red blood cells. We compare our findings with those in 10 galactosaemic babies born in Victoria over a similar period, and show that in both groups these were two main modes of onset: acute and insidious. Jaundice and Escherichia coli infection were prominent in the 13 babies with an acute onset of galactosaemia, while poor weight gain, intermittent vomiting and cataracts were features of the five babies with an insidious onset. An enlarged liver was usually found in both groups. We discuss the various approaches to neonatal screening of galactosaemia in the light of experience in Massachusetts and South Australia. The use of cord blood can be expected to lead to diagnosis before babies with acute onset become ill, while the use of blood collected at five days for the Guthrie test avoids the collection of another routine sample for a relatively rare disorder. The result of red cell transferase assays of parents and siblings of our patients are discussed in relation to their implication for genetic counselling. The relevance of antenatal diagnosis to the prevention of possible intrauterine damage to an affected fetus is pointed out.
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PMID:Galactosaemia: case for neonatal screening illustrated by recent Australian experience. 73 9

Twenty infants and young children with hereditary fructose intolerance (HFI) were admitted to hospital. None was diagnosed at admission. Referals were for vomiting of unknown aetiology (16X), pyloric stenosis or hiatus hernia (5X), toxic condition (3X), and hepatomegaly of unknown origin (5X). Feeding difficulties (20X), vomiting (18X), and failure to thrive (16X) were leading symptoms. The most frequent clinical findings were hepatomegaly (18X), pallor (14X), haemorrhages (13X). Ascites, oliguria, tachypnoea, fever, splenomegaly and rickets were less frequent. Laboratory findings were indicative of disturbed hepatic and renal tubular function and also of disturbed intermediary metabolism (hypokaliaemia, hypophosphataemia). However, hypoglycaemia was found in only 4 out of 15 patients tested. Differential diagnosis after hospital admission centered on metabolic disorders such as glycogenoses, galactosaemia, tyrosinosis, or Wilson's disease. Hepatitis, toxic hepatosis, liver tumour, intrauterine infection and sepsis were also considered. Eleven children had first ingested fructose within the first 6 weeks of life. The diagnosis was usually established only many weeks or months after first fructose intake and appearance of symptoms. This documents how difficult the diagnosis of this disease can be both in practice and in hospital. The course was severe in 11 children and lethal in 4. In only 5 patients was the course mild. The 16 survivors are doing well under fructose-exclusion diet. Irreversible visual impairment after intraocular haemorrhage occurred once. In each case HFI could have been suspected immediately, had a detailed nutritional history been taken. Practising paediatricians should know the composition of commonly used infant formulae. They should never prescribe sugared condensed milk for intractable vomiting prior to excluding HFI. Solution for intravenous infusion containing fructose and sorbitol are life-threatening for undiagnosed HFI patients.
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PMID:Hereditary fructose intolerance in early childhood: a major diagnostic challenge. Survey of 20 symptomatic cases. 73

Clinical data on 24 civilian patients hospitalized for malaria in The New York Hospital were analyzed. Of 16 patients infected with Plasmodium falciparum, 14 acquired the disease in West Africa. Only three of the 24 had taken recommended courses of prophylaxis. Diagnosis was invariably, and often dangerously, delayed because physicians often made diagnoses of viral syndromes or used antibiotics; only one patient had a blood smear taken by a personal physician. Although all patients had fever and chills, classic malarial fever was seen in only seven patients; nausea, vomiting and diarrhea were common. Hepatomegaly and splenomegaly occurred in about half the patients. Blood smears stained in routine fashion by Wright's stain were positive in 23 of 24 patients. A normal leukocyte count was present in 19 of the 24 patients and thrombocytopenia in 16 of 23. The most frequent complications were those of central nervous system involvement. Therapy consisted mainly of chloroquine phosphate but other drugs, including quinine, pyrimethamine, sulfonamides and primaquine, were used in special situations. Suggestions for prophylaxis, diagnosis and therapy were made.
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PMID:Malaria - the mime. Recent lessons from a group of civilian travellers. 78 38

Five children with tuberculosis were treated with isoniazid (20 mg./Kg./day) and rifampin (15 mg./Kg./day). After five to twenty seven days of treatment they presented anorexia, vomiting and jaundice. Hepatomegaly was found in two of them. High indirect bilirubin, S.G.O.T. and S.G.P.T. and low prothrombin levels were present in all of them. Eight to thirty one days after withdrawal of rifampin, all patients were well and their laboratory data was normal.
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PMID:[Toxic hepatitis caused by rifampin and isoniazid in treatment of tuberculosis (author's transl)]. 86 41

Ninety-four children with typhoid fever presented with the primary complaints of fever, diarrhea, and vomiting. Fifty-two percent had hepatomegaly and derangements of SGOT and LDH. None developed hepatic decompensation and all had rapid clinical recovery. The abnormal liver function test served no prognostic purpose.
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PMID:Gastrointestinal phenomena in childhood typhoid fever. 94 10

An unexplained increase in the frequency of pyogenic liver abscesses of unknown etiology has, fourtunately, been paralleled by significant advances in diagnostic and therapeutic methods. This report reviews experience with 14 patients operated upon at NYU Medical Center since 1971. Eight cases (57%) were cryptogenic. Other abscesses were associated with biliary disease (3); abdominal sepsis (2); and trauma (1). Abscesses were present on hospitalization in 12 patients. Clinical findings included fever (101-108 F); 100%; leucocytosis, 71%; anorexia and vomiting, 50%; localized tenderness and hepatomegaly, 50%; hypoalbuminemia, 86%; hypocholesterolemia, 78%; elevated SGOT, 71%; and elevated aikaline phosphatase, 43%. Technetium hepatic scintiscans showed focal defects in 10 of 12 patients (83%), but did not detect multiple abscesses in 2 of these. Hepatic arteriography performed in 10 patients was highly accurate, outlining single abscesses in 6 and multiple abscesses in 4. Furthermore, in one patient a false positive scintiscan was demonstrated by negative arteriography, confirmed by autopsy. In 4 patients, arteriography indicated an abscess in the posterior-superior area of the right hepatic lobe. With precise anatomical localization, a trans-thoracic approach permitted uncomplicated drainage in each case. This approach provides excellent exposure and direct drainage for abscesses in this area. An additional therapeutic adjunct in two patients, with 4 and 11 abscesses each, was postoperative intraportal infusion of antibiotics through the umbilical vein. Thirteen patients (83%) recovered, one dying from pulmonary embolism. Primary hepatic abscesses occur with increasing frequency. Primary hepatic abscesses occur with increasing frequency. Primary hepatic abscesses occur with increasing frequency. The methods described allow more precise preoperative diagnosis and direct surgical drainage.
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PMID:New diagnostic and therapeutic techniques in the management of pyogenic liver abscesses. 113 Aug 69

Lysinuric protein intolerance (LPI), an autosomal recessive defect of diamino acid transport, is characterized chemically by renal hyperdiaminoaciduria, especially lysinuria, and by impaired formation of urea with hyperammonemia after protein ingestion. Our 20 patients thrived during breast-feeding, but ingestion of cow's milk caused diarrhea and vomiting. When able to select their diet, they rejected all protein-rich foods. They were short staturated and had weak atrophic muscles, osteoporosis, hepatomegaly and often splenomegaly. Four patients were mentally retarded. Fifteen patients had leukocyte counts below 4,000/mm3, and 17 patients had platelet counts below 150,000/mm3. Serum lactate dehydrogenase activity was constantly increased, and transaminase and aldolase activities were often increased. In the infants' livers, changes were only revealed by electron microscopy: increased and vesicular smooth endoplasmic reticulum, and abundance of glycogen particles in the hepatocytes. In the older patients, light microscopy demonstrated clearly limited areas where hepatocytes had large pale cytoplasm and small pyknotic nuclei. The diamino acids lysine, arginine and ornithine had plasma concentrations only one-third to one-half the normal mean; the renal clearances were clearly increased. Oral diamino acid loading tests suggested impaired intestinal absorption. Urea is built in the liver through transformation of ornithine to arginine, and cleavage of arginine to ornithine and urea. The addition of ornithine to an intravenous I-alanine loading prevented the hyperammonemia and normalized the urea production. Therefore, the diet has been supplemented with arginine, and more protein has been added. This therapy has lead to a remarkable catch-up growth in some patients. The pathophysiology of LPI is explained. Because of defective intestinal absorption and incrased renal loss, the diamino acids have a low plasma concentration. Their transport from plasma to hepatocytes is also impaired, and the liver becomes deficient in ornithine. This retards the urea cycle, and leads to postprandial hyperammonemia and protein aversion. The presence of the transport defect in the hepatocytes distinguishes LPI from other hyperdibasicaminoacidurias.
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PMID:Lysinuric protein intolerance. 115 80

Carbenicillin disodium was temporally associated with eight episodes of a mild reversible anicteric hepatitis characterized by nausea, vomiting, and a tender, somewhat enlarged liver. Serum glutamic and oxaloacetic transaminase as well as alkaline phosphatase levels rose, but serum bilirubin values remained normal. There usually were no signs of concomitant allergy to penicillin, and other penicillins could be given subsequently without ill effects. Biopsy specimens of the liver showed spotty liver cell necrosis with no cholestasis.
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PMID:Anicteric carbenicillin hepatitis. Eight episodes in four patients. 117 85


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