Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011991 (diarrhea)
 57,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The first patient of Turkish descent with hyperdibasicaminoaciduria is described. Recurrent diarrhea was observed only during the first three months of life. The infant exhibited low plasma levels of ornithine and arginine. Intestinal absorption of lysine was decreased. Hyperammonemia was noticed only after an i.v. alanine load. It was prevented by addition of arginine.
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PMID:Hyperdibasicaminoaciduria in a Turkish infant without evident protein intolerance. 43 55

Congenital hyperdibasicaminoaciduria without cystinuria was detected in a mentally but not physically retarded boy. Plasma lysine and arginine were normal, whereas plasma ornithine was decreased. Although oral or intravenous loading tests could not be performed, the history without vomiting or diarrhea, and the normal physical development indicated an unimpaired intestinal transport of basic aminoacids. Our case could be a further mutant of this transport defect which concerns the renal tubuli only.
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PMID:[Congenital hyperlysin-arginin-ornithinuria in a mentally retarded child (author's transl)]. 91 28

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

369 E. coli strains that are agglutinated in A or B anti E. coli enteroinvasive (EIEC) polyvalent sera and inducing no keratoconjunctivitis in the guinea pig's eye have been selected. The biochemical reactions of E. coli strains that can be agglutinated in A or B EIEC polyvalent sera occupy an intermediary position between those of Shigella genus and the classical features of Escherichia, i.e.; 87% are motile bacteria, 88%--ferment lactose, 81% form acid from sodium mucate and lysine is not decarboxylated by 87% of the strains. As for the antigenic behaviour with 15 out of the 16 sera employed, the strains under consideration have agglutinated by slide test in one or several sera, with varying intensities. None of the strains agglutinated on slide in the O164 antiserum. Subsequently, agglutinations have been performed in tubes only with the strains that agglutinated on the slide with a +3 or +4 intensity. Out of the 369 strains under consideration only 25 have agglutinated in the tube, all the false positive reactions representing 6.7%. The data presented lead to the conclusion that such strains that have been isolated from ill or healthy patients cannot be considered as pathogenic diarrhoea agents, the differentiation from the invasive strains (in the absence of the guinea pig for the pathogenicity test) cannot be made on the basis of the biochemical reactions, but only by means of a set of monovalent sera and by performing the tube agglutination tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Study of strains agglutinable with enteroinvasive anti E. coli polyvalent sera isolated from ill and healthy subjects for optimizing the laboratory diagnosis of diarrhoea. 129 66

To elucidate the biosynthetic processing of the precursor for vasoactive intestinal peptide (prepro-VIP) in tumours producing VIP we have used newly developed radioimmunoassays directed against the five functional domains of the VIP precursor molecule: preproVIP 22-79, peptide histidine methionine (PHM), preproVIP 111-122, VIP and preproVIP 156-170 in combination with HPLC to identify and quantify the peptides in tumour specimen and plasma from patients with the watery diarrhoea syndrome. Elevated quantities of all the five peptides were found in the 13 tumours (nine neurogenic tumours, one pheochromocytoma, three pancreatic carcinomas) examined. The preproVIP derived peptides were expressed in non-equimolar amounts and the relative proportion of the various peptides differed markedly from tumour to tumour. The pheochromocytoma was the only tumour type which contained large amounts of preproVIP 156-170 in comparison with the other peptides. A proportion of the VIP precursor which varied from 7% to 73% followed a pathway in which the dibasic conversion site after PHM was uncleaved as evidenced by the presence of PHV, a C-terminally extended form of PHM. It was also found that unlike normal tissue a fraction of the C-terminal VIP precursor peptide, preproVIP 156-170, was having its C-terminal lysine residue removed during processing. The findings indicate that various post-translational processing pathways of preproVIP exist. All the peptide sequences produced in the tumour tissue were secreted as evidenced by their presence in plasma in elevated concentrations. The plasma levels of preproVIP 22-79, preproVIP 111-122 and PHV exceeded those of the remaining preproVIP-derived peptides suggesting that determination of these peptides in patients with VIP-secreting tumours may be better markers than VIP.
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PMID:PreproVIP-derived peptides in tissue and plasma from patients with VIP-producing tumours. 164 52

The basic proteinase inhibitor from bovine organs, aprotinin, was first identified in 1930 and its effect on enzyme and other biological systems has since been extensively studied. Aprotinin can only be administered intravenously and has a half-life of about 2 hours. Its administration at the start of cardiopulmonary bypass surgery appears to reduce blood loss and to protect against global myocardial ischaemia. Similarly, a smaller infarct size seems to result from early administration of aprotinin within the first hour after myocardial infarction, though further studies are needed to confirm this effect. A combination of aprotinin with tranexamic acid may be effective in preventing or delaying rebleeding after rupture of an intracerebral aneurysm; the addition of aprotinin seems to decrease the incidence of delayed cerebral vasospasm and ischaemic complications which are sometimes noted when tranexamic acid alone is used. Aprotinin is also effective as adjuvant treatment in traumatic haemorrhagic shock. The recommended loading dose is 15,000 to 20,000 KIU/kg bodyweight administered as a short intravenous infusion, followed by 50,000 KIU/hour by continuous infusion. Side effects of aprotinin are very rare. Epsilon-Aminocaproic acid (EACA), p-aminomethylbenzoic acid (PAMBA) and tranexamic acid are synthetic antifibrinolytic amino acids. Saturation of the lysine binding sites of plasminogen with these inhibitors displaces plasminogen from the fibrin surface. On a molar basis tranexamic acid is at least 7 times more potent that epsilon-aminocaproic acid and twice as potent as p-aminomethylbenzoic acid. All 3 compounds are readily absorbed from the gastrointestinal tract and excreted in active form in the urine. The plasma half-life of tranexamic acid is about 80 minutes. The main indications for tranexamic acid are the prevention of excessive bleeding after tonsillectomy, prostatic surgery, and cervical conisation, and primary and IUD-induced menorrhagia. It is possible that gastric and intestinal bleeding can also be reduced as well as recurrent epistaxis. Tranexamic acid could also be useful after ocular trauma. The value of fibrinolysis inhibitors in the prevention of bleeding after tooth extraction in patients with haemophilia is well documented, as is the treatment of hereditary angioneurotic oedema. The usual dose of tranexamic acid is 0.5 to 1g (10 to 15 mg/kg bodyweight) given intravenously 2 to 3 times daily, or 1 to 1.5 g orally 3 to 4 times daily. This dose needs to be reduced in patients with renal insufficiency. The main side effects of tranexamic acid are nausea or diarrhoea.
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PMID:Clinical application of inhibitors of fibrinolysis. 258 Jun 84

To elucidate the pathophysiological changes leading to postantibiotic diarrhoea caused by Clostridium difficile and its cytotoxin, oral ampicillin was given to rabbits, and jejunal, ileal, and caecal segments of those that developed diarrhoea were investigated in vitro. The rabbits that, in response to treatment, harboured Clostridium difficile in their colonic lumen were studied, and the results expressed according to the presence or absence of Clostridium difficile and/or its cytotoxin. Thus, we refer to either CD+ or CD- segments. The influx of glucose, phenylalanine, glycylphenylalanine, and lysine across the brush border of jejunum and ileum of CD+ segments was severely impaired, while only slightly blunted in CD-. No significant change was detected in the influx of glutamic acid in the jejunum of all treated animals and in the CD- ilea. Morphologic damage in ileum and caecum of CD+ was also more evident than in CD-. Transepithelial ion transport across short circuited ileal mucosa (CD+ and CD-) revealed secretory changes in Cl net transport that were more marked in CD-. We conclude that: (1) Clostridium difficile may also colonise the upper intestinal tract, where it induces morphological and functional damage, severely impairing nutrient absorption; and (2) the ileum contributes to the diarrhoea caused by CD even when the micro-organism is confined to the more distal gut by showing moderate impairment of nutrient absorption and marked electrolyte secretion.
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PMID:Pathogenesis of postantibiotic diarrhoea caused by Clostridium difficile: an in vitro study in the rabbit intestine. 339 47

In 1983, the vernacular name Enteric Group 77 was coined for a group of strains that had been referred to our laboratory as "possible Vibrio cholerae except for gas production." By DNA-DNA hybridization (hydroxyapatite, 32P), 8 of 10 strains of Enteric Group 77 were very highly related to the labeled strain 1169-83 (74 to 100% at 60 degrees C and 75 to 100% at 75 degrees C; percent divergence, 0.0 to 2.5). Type strains of six other Aeromonas species were 45 to 66% related (60 degrees C) to strain 1169-83, but type strains of 27 Vibrio species were only 2 to 6% related. The name Aeromonas veronii is proposed for the highly related group of nine strains formerly known as Enteric Group 77. The type strain is designated as ATCC 35604 (CDC 1169-83). Strains of A. veronii grew well at 36 degrees C and had positive reactions at this temperature for indole, methyl red, Voges-Proskauer, citrate, lysine and ornithine decarboxylases, DNase, lipase, and motility; the strains had negative reactions for arginine decarboxylase, H2S, urea, and malonate. The following sugars were fermented: D-glucose (acid and gas), cellobiose (seven of nine strains), D-galactose, maltose, D-mannitol, D-mannose, alpha-methyl-D-glucoside (eight of nine strains), salicin, sucrose, and trehalose. The following sugars were not fermented: adonitol, L-arabinose, D-arabitol, dulcitol, erythritol, myo-inositol, lactose, raffinose, L-rhamnose, D-sorbitol, and D-xylose. The positive ornithine decarboxylase reaction differentiates A. veronii from other Aeromonas species. The antibiogram of A. veronii is typical of other Aeromonas strains (resistance to ampicillin and carbenicillin and susceptibility to most other agents). A. veronii strains were isolated from three clinical sources: respiratory secretions of four victims of drowning or near drowning in fresh water (probably not clinically significant); infected wounds of two patients previously exposed to fresh water (unknown clinical significance); and stools from three patients with diarrhea (probably clinically significant).
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PMID:Aeromonas veronii, a new ornithine decarboxylase-positive species that may cause diarrhea. 358 25

Production of cytotoxin and enterotoxin by Aeromonas strains obtained from stools of 50 children in Mexico and Texas and from blood of 9 children with sepsis was determined. Results were correlated with clinical features of infected children as well as with biochemical traits of Aeromonas strains. Cytotoxin was produced by 40 of 42 Aeromonas strains (95%) isolated from stools of children with diarrhea, by all 8 isolates from stools of well children, and by all 9 isolates from children with sepsis. There was no difference in the quantities (amount of cytotoxin per milligram of protein required to kill 50% of the cells) of cytotoxin produced and in clinical manifestations among the groups. None of the isolates produced a toxin that could be neutralized by antiserum raised against Shiga toxin produced by Shigella dysenteriae 1 60R. Heat-labile-like enterotoxin (LT) was produced by 26 of 42 stool isolates (62%), while only 1 of the 42 isolates (2%) produced enterotoxinlike activity in suckling mice; 65% of the cytotoxin-producing strains also produced an LT-like material. All strains from blood produced LT-like material, and 2 of 6 (33%) produced activity in suckling mice. All strains produced hemolysin; 37 of 57 (65%) were Voges-Proskauer positive; 27 of 57 (47%) were lysine decarboxylase positive by API 20E strips, none were positive for lysine decarboxylose production by lysin-iron agar slants at 24 h, but 17 of 54 (31%) were positive at 48 h. There was no correlation between biochemical reactions and enterotoxin or cytotoxin production. There appears to be no correlation between toxin production by Aeromonas spp. and gastroenteritis.
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PMID:Clinical and biochemical significance of toxin production by Aeromonas hydrophila. 358 26

The ability of polyriboinosionic acid [poly(rI)].polyribocytidylic acid [poly(rC)], mismatched analog poly (rI).poly[r(C12Uracil)n], and poly(rI).poly(rC) complexed with poly L-lysine and carboxymethylcellulose [poly(ICLc)] to induce interferon and the comparative toxicity of each in cats were evaluated. Each induced high levels of circulating interferon, although poly(ICLC) injected intravenously at 1 to 4 mg/kg induced up to 10 times more interferon than the other compounds. Each compound was pyrogenic and caused a transient decrease in leukocyte numbers. Poly(rI).poly(rC) and the mismatched analog caused severe diarrhea and nausea at the highest drug concentrations (1 to 4 mg/kg), but poly (ICLC) did not. Each compound also caused depression and lethargy and impaired coordination.
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PMID:Interferon induction by and toxicity of polyriboinosinic acid [poly(rI)].polyribocytidylic acid [poly (rC)], mismatched analog poly (rI).poly[r(C12Uracil)n], and poly(rI).poly(rC) L-lysine complexed with carboxymethylcellulose. 615 63


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