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)

Human adenoviruses are classified into 47 serotypes and six subgenera (A-F) with different tropisms. In recent years adenovirus type 40 (Ad40) and 41 (Ad41) of subgenus F have been shown to be causative agents in enteric infections, which is second in importance only to rotaviruses as a cause of infantile gastroenteritis. Infection with EAds occurs worldwide and has been associated with 4-17% of cases of diarrhoea in children. AD40 and Ad41 primarily affect young children less than 2 years of age and occur throughout the year. The clinical characteristics include watery diarrhoea accompanied by vomiting, low grade fever and mild dehydration. A distinct feature of EAds infection is the protracted diarrhoea (mean 8.6 and 12.2 days for Ad40 and Ad41, respectively). Respiratory symptoms are infrequent. Serotypes Ad40 and Ad41 differ from all other (established) adenoviruses by being unable to replicate in conventional cell cultures. These fastidious viruses only grow in selected cell lines, 293 cells being the most commonly used. In spite of the difficulty of isolating Ad40 and Ad41, they can be directly identified and typed by ELISA and solid-phase immune electron microscopy. The amount of viral DNA in stool specimens is sufficient for identification by DNA restriction and dot-blot assays. The recent development of highly sensitive and specific monoclonal antibody-based ELISAs enable accurate diagnosis of adenovirus gastroenteritis in routine work and make possible the evaluation of the role of the enteric adenoviruses in diarrhoeal disease in the developing countries.
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PMID:Enteric adenoviruses. 196 27

In a prospective one year study, comprising children with acute gastroenteritis admitted to hospital or treated as outpatients, the clinical and laboratory features of rotavirus diarrhoea (168 cases) were compared with those of enteric adenovirus (32 cases), bacterial (42), mixed (16), and non-specific (135) infections. The rotavirus disease was remarkably consistent, with a sudden onset of vomiting, a high frequency of fever and dehydration, and a mean duration of diarrhoea of 5.9 days. Outpatients excreting rotavirus had a similar but milder illness, mainly on account of less pronounced vomiting. The predominant symptom of enteric adenoviruses was long lasting diarrhoea (mean 10.8 days). Abdominal pain, bloody stools, prolonged diarrhoea (mean 14.1 days), leucocytosis, and a raised erythrocyte sedimentation rate strongly suggested a bacterial aetiology. Mixed infections caused longer lasting diarrhoea (mean 8.0 days) than rotavirus alone, but the severity of the illness was not increased. The clinical features of infection with unidentified pathogens most resembled those of bacterial infections. Respiratory symptoms were not significantly associated with any particular pathogen. Hypernatraemia and complications were uncommon. This study showed that the clinical features of gastroenteritis with rotavirus, enteric adenoviruses, and bacteria each exhibited patterns that could guide the experienced clinician to a presumptive diagnosis.
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PMID:Clinical features of acute gastroenteritis associated with rotavirus, enteric adenoviruses, and bacteria. 301 37

Experimental and clinical experience with compounds containing antimony have shown that the trivalent compounds are generally more toxic than the pentavalent ones. APT can cause severe pain and tissue necrosis and is therefore not given by intramuscular or subcutaneous injection. APT has the actions and uses of AST, but it is less soluble and more irritating than the sodium salt which is therefore more suitable for intravenous use. Trivalent antimony compounds are toxic when used topically. Adverse effects are similar for all trivalent compounds, and include nausea, vomiting, weakness and myalgia, abdominal colic, diarrhoea, and skin rashes, including pustular eruptions. Hypersensitivity reactions also occur. Respiratory symptoms include cough, dyspnoea, and chronic lung changes. Cardiotoxicity is the most important and may produce arrhythmias, myocardial depression and damage, Stokes-Adams attacks, heart failure, and cardiac arrest. Hepatic damage and necrosis, as well as blood dyscrasias, may occur. Toxic effects on the kidney may follow chronic use. Continuous treatment with small doses of antimony may give rise to symptoms of subacute poisoning, similar to those of chronic arsenic poisoning, due to accumulation of antimony in the body, especially if trivalent compounds are used, because of their long biological half-lives. Reproductive disorders and chromosome damage have been reported; antimony compounds are, therefore, potentially toxic to reproduction and have mutagenic, and oncogenic potential. Antimony compounds should, therefore, not be used during pregnancy or in the presence of hepatic, renal, or heart disease. Pentavalent antimony preparations especially the organic compounds, together with non-metallic synthetic preparations, such as the diamidines, have now replaced APT for use in leishmaniasis. Because of the toxicity of antimony compounds, investigations have been undertaken to reduce their adverse effects by combining them with chelating agents. These preparations appear to have reduced the toxic effects of antimony without affecting the efficacy of the preparations. Liposome-encapsulated antimony products have, more recently, been shown to be much less toxic because of the reduced dose of the antimony compound required for effective therapy. The historical uses of antimony were based on the belief that the topical and systemic adverse effects, for example, skin eruptions and diarrhoea and vomiting, were signs that the condition being treated was responding by being brought to the surface to relieve congestion at the diseased area. There is no evidence in topical use, but there is evidence that such use can cause severe reactions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Toxicity of antimony and its compounds. 330 36

Seventy nine cases of sporadic, community acquired legionnaires' disease have been reviewed. Annual and seasonal variation in incidence was noted. The mean age of the patients was 53 years and 50 (63%) were male. Pre-existing chronic diseases were present in only 23 (29%), including two patients receiving immunosuppressive treatment. Common symptoms included unproductive cough, dyspnoea, chest pain, headache, confusion, nausea, vomiting, and diarrhoea. Respiratory symptoms were absent, however, in 17 (22%). Localising chest signs were present in 74 (95%) cases. Frequent laboratory findings included lymphopenia, high erythrocyte sedimentation rate, hyponatraemia, raised urea and creatinine concentrations, abnormal liver function, hypophosphataemia, hypoalbuminaemia, proteinuria, and haematuria. Thirteen patients died (16%), including nine of 20 who received assisted ventilation. The mortality rate in patients treated with erythromycin (11%) was lower than in those who received other antibiotics (23%), but this difference was not statistically significant. Of the features noted on admission, only a high plasma urea concentration was significantly associated with death. Sporadic community acquired legionnaires' disease is a not uncommon disorder, which with appropriate treatment has a prognosis similar to that of other forms of community acquired pneumonia.
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PMID:Legionnaires' disease: a review of 79 community acquired cases in Nottingham. 378 45

Fastidious enteric adenovirus have recently been recognized as an important cause of acute gastroenteritis in young children. Their inability to grow in vitro has hampered classification by conventional methods. With modern immunological and chemical techniques the enteric adenoviruses have been shown to be distinct from the 39 established human adenovirus serotypes. In a prospective study of the viral, bacterial and parasitic aetiology of acute gastroenteritis 410 children and 205 age-matched controls were studied. An enteropathogenic agent was detected in 67% of the diarrhoeic patients and 57% were of viral origin. Rotavirus was the major agent found in 43% of the patients whereas adenovirus was found in 13%. Of the 50 adenovirus specimens, so far fully characterized by electron microscopy, ELISA-assays, DNA-restriction analysis and isolation studies 70% were identified as enteric adenoviruses. Two serotypes, adeno 40 and 41, were detected representing the new subgroups F and G. Twelve of 17 paired serum specimens, from children with enteric adenovirus showed a significant rise in hemagglutination inhibition titers. Infection with enteric adenoviruses showed 2 small seasonal peaks in summer and late winter. Infection occurred early in life, 85% of the children aged less than 3 years. Diarrhoea was the main symptom with an average duration of 9 days. Adenovirus type 41 seemed to cause diarrhoea of longer duration. Fever and vomiting was mild with a mean of 2 days. Respiratory symptoms occurred in 20% of the cases. The incubation period could be estimated as 7 days. Virus was excreted for 10-14 days.
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PMID:Two new serotypes of enteric adenovirus causing infantile diarrhoea. 630 84

Differentiation between abacavir hypersensitivity and viral respiratory infections is problematic. Fifteen cases of abacavir hypersensitivity were matched to 30 controls with culture proven influenza A with no abacavir exposure. Rash was associated with hypersensitivity (odds ratio [OR] = 13.1, P = 0.02) as was the presence of nausea (OR = 30, P < 0.001), vomiting (OR = 17.1, P = 0.001) or diarrhoea (OR = 22, P < 0.001). The number of gastrointestinal symptoms was also predictive of hypersensitivity reaction (P < 0.001). Respiratory symptoms (cough, sore throat, or dyspnoea) were not associated with abacavir hypersensitivity (OR = 0.08, P = 0.001). Multivariate analysis confirmed the following associations for abacavir hypersensitivity: the number of gastrointestinal symptoms (OR = 8.6, P = 0.0032), cough (OR = 0.039, P = 0.02) and rash (OR = 16.9, P = 0.07). Abacavir hypersensitivity is strongly associated with gastrointestinal (GI) symptoms. Cough without GI symptoms is associated with influenza.
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PMID:Comparison of symptoms of influenza A with abacavir-associated hypersensitivity reaction. 1286 29

INFVA is an important cause of pulmonary infections in patients receiving BMT, and is associated with considerable morbidity and mortality for a readily preventable and treatable infection. Few studies have addressed the impact of the new neuraminidase inhibitors in the prognosis of influenza after BMT. The aim of this study is to assess the impact of oseltamivir on the control of INFVA infection in BMT recipients. INFVA was screened in NPA and/or bronchoalveolar lavage using IF in all BMT recipients having respiratory symptoms. Three URTI and one associated upper and LRTI were diagnosed in three BMT recipients out of six patients admitted to the BMT unit, during eight-wk period (March and April 2008). All patients having INFVA respiratory infection were treated by oral oseltamivir 60 mg/day, begun more than 48 h after symptom onset. Respiratory symptoms disappeared within a mean of 60 h (48-96 h) of treatment. However, viral tests had remained positive for 8-39 days. Outside the initial associated URTI and LRTI, no further viral pneumonia occurred. No patient died of INFVA. Oseltamivir was well tolerated outside vomiting during the first three days of treatment in one patient. Oseltamivir appears to play an important role in the outcome of INFVA infection as well in URTI as in severe LRTI in patients receiving BMT.
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PMID:Successful treatment of influenza A virus by oseltamivir in bone marrow transplant recipients. 1917 Sep 30

In the past two decades, peanut allergy prevalence has increased in the West but has been perceived as having remained low in Asia. To review the clinical presentation of Asian children with peanut hypersensitivity and measure their IgE responses to major peanut allergens. We enrolled 31 children presenting with various allergies and a positive skin prick test to peanut from the Children's hospital outpatient allergy clinic in Singapore. A detailed questionnaire was completed by parents. The children's serum IgE specific to native Ara h 1, native Ara h 2, and recombinant Ara h 3 were detected using ELISA. Of the 31 patients, 19 had previously documented reactions to peanuts, while 12 had no previous clinical reaction. Most, 89.5% (17/19) of first reactions featured skin changes (urticaria, erythema, angioedema), but only 36.8% (7/19) involved skin symptoms alone. Respiratory symptoms and GI symptoms occurred in 42.1% and 26.3% of patients respectively and did not occur as the sole manifestation of reaction. The most common GI manifestation was emesis, present in 26.3% (5/19) of subjects. Two children experienced impaired consciousness with systemic, anaphylactic events. Although most sought treatment for their first peanut reaction only one patient received epinephrine. Half of our patients reported a subsequent accidental ingestion after the diagnosis of peanut allergy, with a median time from diagnosis to first accidental ingestion of 4 months and a reported increased severity of reaction in approximately half of the repeat exposures. Eighty-seven percent of children had specific IgE directed against at least one of the major peanut allergens. Among all patients, 87.1% had IgE specific to both Ara h 1 and Ara h 2 and 54.8% to rAra h 3. Asian children with peanut sensitization have clinically similar presentations and respond to the same major allergenic proteins as their Western counterparts. The perceived differences between the populations in this context do not stem from divergent clinical or immunological responses.
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PMID:Serological and clinical characteristics of children with peanut sensitization in an Asian community. 1970 75