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 dysentery outbreak in the Central African Republic village of Zemio was diagnosed as "Shigella flexneri" by the Pasteur Institute in Bangui (IPB) in February 1996; 2 months later there was an outbreak of hemorrhagic colitis. 108 patients presented with bloody diarrhea; cramping abdominal pain, fever, nausea, and vomiting were uncommon. The illness lasted between 5 days and 3 weeks (average, 8 days). Antibiotics were ineffective. Four patients died and several developed hemolytic-uremic syndrome. Stool cultures done at IPB tested negative. PCR was used to detect enterohemorrhagic Shiga-like toxin (SLT) 1 and 2, the invasivity gene ipaH, and the attaching and effacing gene eaeA. DNA fragments of 130 and 494 nucleotides corresponding to amplified SLT1 and eaeA were found in 80% of the specimens tested. No amplification was obtained for SLT2 or for ipaH in specimens collected during the second epidemic. These results suggest the presence of enterohemorrhagic Escherichia coli and the absence of Shigella. The number of reported cases of acute bloody diarrhea in infants and adults in Bangui has increased since 1996. E. coli O157:H7 was isolated from two fatal adult cases. Smoked zebu meat was suspected in several hospital cases (bloody diarrhea, hemolytic anemia, and renal insufficiency) in which non-fermenting sorbitol E. coli O157:H7 was not isolated. In two cases of acute diarrhea, other serotypes of E. coli were indicated by retrospective PCR on stools which were positive for SLT1 and for eaeA and negative for invasivity. A study was conducted in Bangui on 290 cases (33 with bloody diarrhea) and 140 controls. Patients were not paired because of civil unrest in the city. The questionnaire included demographic and socioeconomic characteristics, environmental factors, and habitual food consumption. The major contributing factor was consumption of locally made meat pies (kanda), which were made with smoked zebu meat. Kanda is stored at ambient temperature, often for days, before it is sold in markets or along roads. Before 1996, E. coli was not reported as a cause of bloody diarrhea in the Central African Republic.
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PMID:Enterohaemorrhagic Escherichia coli in Central African Republic. 918 91

The purpose of this study was to determine the effectiveness of an amino acid-based infant formula in infants with continued symptoms suggestive of formula protein intolerance while they were receiving casein hydrolysate formula (CHF). Twenty-eight infants, 22 to 173 days of age, were enrolled; each had received CHF for an average of 40 days (10 to 173 days) and continued to have bloody stools, vomiting, diarrhea, irritability, or failure to gain weight, or a combination of these symptoms. Sigmoidoscopy with rectal biopsy was performed in all infants. The infants then received an amino acid-based infant formula, Neocate, for 2 weeks. After 2 weeks of treatment, 25 of the infants demonstrated resolution of their symptoms and underwent challenge with CHF. Of the 25 who were challenged, eight tolerated the CHF and the remainder had recurrence of their symptoms. The histologic features in these infants varied from eosinophilic infiltration to normal. We conclude that not all infants with apparent formula protein-induced colitis respond to CHF and that these infants may have resolution of their symptoms when fed an amino acid-based infant formula.
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PMID:Intolerance to protein hydrolysate infant formulas: an underrecognized cause of gastrointestinal symptoms in infants. 940 41

This review illustrates the changing paradigms in the understanding of the pathogenesis of pneumatosis intestinalis. Although many theories have been evoked, pragmatically there appear to be four major clinical and diagnostic imaging considerations. The most common and most emergent life-threatening cause of intramural bowel gas is the result of bowel necrosis due to bowel ischemia, infarction, necrotizing enterocolitis, neutropenic colitis, volvulus, and sepsis. In the stomach, intramural gas can be caused by emphysematous gastritis or ingestion of caustic agents. These situations represent surgical emergencies. Pneumatosis is found secondary to mucosal disruption presumably due to over-distention from peptic ulcer, pyloric stenosis, annular pancreas, and even to more distal obstruction. Disruption can also be caused by ulceration, erosions, or trauma, including the trauma of child abuse. Disruption can also be iatrogenic from intracatheter jejunal feeding tubes, stent perforation, sclerotherapy, or surgical or endoscopic trauma. In these cases, the gas may be focal or linear. Treatment depends on the extent of the disruption and the underlying cause. A more subtle form of mucosal disruption may occur due to mucosal erosions and also to defects in intestinal crypts secondary to acute and subclinical enteritides that allow intraluminal bacterial gas under pressure to percolate into the bowel wall layers, particularly the submucosa (29). Pneumatosis, often linear or cystic in appearance, is seen with increased frequency in patients who are immunocompromised because of steroids, chemotherapy, radiation therapy, or AIDS. In these cases, the pneumatosis may result from intraluminal bacterial gas entering the bowel wall due to increased mucosal permeability caused by defects in bowel wall lymphoid tissue. Clinical and imaging findings are important in the differentiation of this transient pneumatosis from fulminant life-threatening causes in this subset of patients. A pulmonary cause must still be considered in cases of chronic obstructive pulmonary disease, asthma, and cystic fibrosis. It can occur with barotrauma and after chest tube placement. It may relate to increased intrathoracic pressure associated with retching and vomiting. The possibility remains that occasionally the origin of pneumatosis intestinalis will remain cryptogenic--caused but unexplained.
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PMID:Pneumatosis intestinalis: a review. 953 Feb 94

To estimate the frequency of adverse effects associated with the use of the transdermal nicotine patch, we abstracted and analysed data from 47 reports of 35 clinical trials. The meta-analysis presented here represents a synthesis of data from 41 groups of nicotine patch recipients totalling 5501 patients, and 33 groups of placebo recipients totalling 3752 patients. Smoking abstinence was the primary outcome in 32 of the trials, and relief of colitis symptoms was the primary outcome in 2 of the trials; 1 study of contact sensitisation was included in the skin irritation analysis. The patch was clearly effective as an aid to smoking abstinence. Despite the large number of patients in the analysis, few adverse cardiovascular outcomes (myocardial infarction, stroke, tachycardia, arrhythmia, angina) were reported, and no excess of these outcomes was detected among patients assigned to nicotine-patch use. The incidences of several minor adverse effects were clearly elevated among the nicotine-patch groups, especially sleep disturbances, nausea or vomiting, localised skin irritation and respiratory symptoms, but the background rates and risk ratios varied considerably across studies. The incidence of nausea or vomiting appeared to be lowest when the patch dose was tapered. The results of this meta-analysis indicate that very large studies would be needed to assess the effect of the patch, if any, on serious, rare outcomes. These results also suggest that the rate of minor adverse effects might be lowered by modifying patch-use protocols.
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PMID:A meta-analysis to assess the incidence of adverse effects associated with the transdermal nicotine patch. 956 40

A case report of a young patient (born in 1980) with a 2-year history of chronic ulcerative proctocolitis was described. Checking colonoscopy 6 months from the beginning of disease showed multiple and even confluent polypoid lesions in transverse gut starting from hepatic flexure in addition to diffuse inflammatory rectosigmoideal changes. Biopsy found only colic mucosa without any tumorous structures. Five months later the patient's state got worse accompanied instantly by vomiting, weight loss and malabsorption symptoms. A duodenocolic fistula was supposed according to gastroduodenoscopy and biopsy. Because of progressive suffering of the patient colectomy with ileoduodenoanastomosis and ileosigmoidoanastomosis was performed. Polypous lesions were observed from the blind gut up to descendent colon and a transversoduodenal fistula was proved. The removed part of gut was completely changed into a dense network of elongated polypous lesions. In microscopy, bigger polyps showed an inner stromal part often with bands of smooth muscle cells covered by nearly normal gut mucosa. Smaller polyps were formed by hypertrophic gut mucosa only. At the base of polyps, a stagnation of gut contents was found as well as ulcerous defects of various depth. Macroscopy and microscopy of polypoid lesions formed by non-neoplastic gut mucosa were those of so called bizzare ("giant") inflammatory polyposis of the gut. Up to now the patient's clinical picture and local finding in the stump of resected gut have been typical for chronic ulcerous colitis and polypous lesions were not revealed by checking investigations.
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PMID:[A bizarre inflammatory polyposis of the colon in chronic ulcerative proctocolitis]. 962 28

Predictive factors for the development of hemolytic uremic syndrome (HUS) were evaluated in 88 inpatients who suffered from enterohemorrhagic E. coli infections in the outbreak in Sakai, 1996. All in- and outpatients received oral or intravenous fosfomycin within acute phase of hemorrhagic colitis, and HUS complicated 1.4% of them. Persistence of bloody stools and diarrhea were longer in HUS patients than in non-HUS patients, but persistence of abdominal pain was not different in either group. Leukocytosis with leukocyte counts over 15,000/microliters and/or elevated CRP level over 2.0 mg/dl at admission, and fever and/or vomiting in the course of hemorrhagic colitis were more frequent in HUS patients than in non-HUS patients. Early intensive treatments including gammaglobulin, urinastatin, aspirin, and dipyridamole were employed in 34 high risk patients for prevention of HUS. These patients were estimated to be at risk of developing HUS because of incomplete HUS, nephropathy, elevated LDH level, thrombocytopenia, or age younger than two years old. These treatments were clinically effective.
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PMID:[Predictive factors for development of hemolytic uremic syndrome (HUS) and early intensive treatments for prevention of HUS enterohemorrhagic Escherichia coli infection]. 965 3

We report the case of a 21-year-old man who had been developing acute renal failure with Methicillin-resistant Staphylococcus aureus (MRSA) colitis and sepsis. He was admitted for consciousness disturbance, nausea, vomiting, and diarrhea. Oliguria was also observed and his serum creatinine level was elevated to 10 mg/dl. Urinary protein was positive and an abundance of hyaline cast were seen in urinary sedimentation. Diarrhea and pyrexia were prolonged and serum C-reactive proteins were elevated, but lymphocyte and leukocyte counts temporarily decreased from the 3rd to the 6th hospital day and remained low until normalizing after the 14th day. His clinical symptoms improved with hemodialysis (HD) and effective antibiotic therapies. An MRSA strain producing toxic shock syndrome toxin-1 (TSST-1), a super antigen which specifically stimulates human V beta 2-positive T cells, was separated from his feces and blood. To ascertain the cause of his renal dysfunction, a renal biopsy was performed on the 8th day. His renal histology revealed acute interstitial nephritis with severe inflammatory cell infiltration around the medullary areas without glomerular changes. Most of the infiltrated cells were small monocytes, and lymphoid cells were rich in the interstitium. With immunohistochemical staining, over 70% of T-cells were V beta 2-positive. TSST-1-producing MRSA was detected in his blood specimen. Furthermore, V beta 2-positive T cells were accumulated in the renal intersititium, and transient lymphocytopenia was observed. These data suggested the following possible pathogenesis for interstitial nephritis: TSST-1 acts as a super antigen in the renal interstitium where major histocompatibility complex (MHC) is class-2-positive, thereby resulting in interstitial nephritis with T cell migration.
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PMID:[A case of interstitial nephritis induced by a super antigen produced by methicillin-resistant Staphylococcus aureus (MRSA) presenting as acute renal failure]. 1036 25

A 31/2-year-old girl presented with persistent abdominal pain, fever, vomiting, and diarrhea accompanied by rash, oral ulceration, anemia, and an elevated sedimentation rate. Initial evaluation revealed no pathogens and was extended to include abdominal ultrasound and computed tomography showing marked ileocecal edema and mesenteric adenopathy. Colonoscopy revealed focal ulceration from rectum to cecum with histology of severe active colitis with mild chronic changes. Enteroclysis demonstrated a nodular, edematous terminal ileum. Because of the patient's clinical deterioration despite antibiotics, these features were construed consistent with Crohn's disease, and glucocorticoid therapy was begun. By the ninth hospital day, admission cultures grew Yersinia enterocolitica, and trimethoprim/sulfamethoxazole was begun followed by prompt clinical improvement. The delay in diagnosis afforded an unusually comprehensive clinical description of the presentation and diagnosis of Yersinia enterocolitis in childhood.
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PMID:Yersinia enterocolitis mimicking Crohn's disease in a toddler. 1046 19

Digestive disorders in Legionella pneumophila pneumonia such as nausea, vomiting, diarrhoea, are common; they are clinical arguments to suspect this bacteria to be responsible for this pneumonia. In this case-report, a patient with pneumonia due to Legionella pneumophila serogroup I presented in the follow-up with signs of enteritis with ascites. We looked ahead in literature who made us discover the multiple organ involvement that may happen in Legionnaires' disease. Diagnostic procedures consist in simple tests as ultrasonography, abdominal computerised tomography, that show inflammatory disease signs and sometimes ascites. Exceptionally, Legionella pneumophila has been demonstrated with direct immunofluorescent microscopic study, in inflammatory colitis pieces with haemorrhagic necrosis in different stage processes. Pathogenesis could be explained by the systemic spread of the organism and formation at distance of necrotising enteritis focus. It is initiated by necrotising factors of bacterial origin and hypersensitivity reactions (type I and III).
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PMID:[Digestive disorders and Legionnaires' lung disease. Accompanying signs or visceral location?]. 1085 68

We report a case of a nine-year old boy with vomiting, abdominal pain and fever, who underwent surgery with a diagnosis of appendicitis in Mendoza and from whom a Shiga toxin-producing Escherichia coli (STEC) O127:H21 strain was recovered. Forty-eight hours after surgery he presented bilious vomiting and two episodes of intestinal bleeding. Laboratory findings included: hematocrit, 35%; blood urea nitrogen, 0.22 g/L. The urinary output was normal. The following day physical examination showed an alert mildly hydrated child, without fever but with distended and painful abdomen. The patient was again submitted to surgery with a diagnosis of intestinal occlusion. Bleeding and multiple adhesions in jejunum and ileum were found. The patient still had tense and painful abdomen and presented two bowel movements with blood; hematocrit fell to 29% and blood urea nitrogen rose to 0.32 g/L. STEC O127:H21 eae(-)/Stx2/Stx2vh-b(+)/E-Hly(+) was isolated from a stool sample. He was discharged after 10 days of hospitalization and no long-term complications such as HUS or TTP were observed. This is the first report, to our knowledge, on the isolation of E. coli O127:H21, carrying the virulence factors that characterize STEC strains, associated to an enterohemorrhagic colitis case. This serotype was previously characterized as a non-classic enteropathogenic E. coli (EPEC). STEC infections can mimic infectious or noninfectious pathologies. Therefore an important aspect of clinical management is making the diagnosis using different criteria thereby avoiding misdiagnoses which have occasionally led to invasive diagnostic and therapeutic procedures or the inappropriate use of antibiotics.
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PMID:Intestinal bleeding and occlusion associated with Shiga toxin-producing Escherichia coli O127:H21. 1096 19


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