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)

We report the case history of a 28-year-old homosexual man of Caucasian origin whose diagnosis of acquired immunodeficiency syndrome was established one year before admission on the basis of a positive human immunodeficiency virus serology and cutaneous Kaposi's sarcoma. Severe postprandial vomiting pointed to bowel obstruction in an emaciated, poor risk patient. Endoscopy revealed multifocal, violaceous tumours throughout the upper gastrointestinal tract which, eventually, obstructed the duodenum. Histology confirmed the putative diagnosis of gastrointestinal Kaposi's sarcoma, which responded well to monochemotherapy with vincristine. Significant clinical improvement and repeat endoscopy indicated tumour regression and resolution of bowel obstruction.
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PMID:Successful monochemotherapy of extensive gastrointestinal Kaposi's sarcoma with bowel obstruction in acquired immunodeficiency syndrome. 787 60

Infections of the esophagus are unusual in the general population and strongly imply immunodeficiency, although immunocompetent individuals are not exempt. HIV infection is predominant among risk factors for infectious esophagitis. For all immunocompromised patients, the most frequently identified esophageal pathogens are Candida, CMV, and HSV. Peculiar to HIV-infected patients are idiopathic esophageal ulcers as well as unusual bacteria and parasites. Patterns of presentation differ with each infecting organism, and clinical features should be used as a guide in achieving a correct diagnosis. For example, a patient with AIDS presenting with esophageal symptoms and thrush, along with abdominal pain, nausea, vomiting, and fever, is unlikely to resolve all symptoms with empiric antifungal therapy alone. Parsimony of diagnosis does not hold among immunodeficient patients in whom concurrent infections are common. Accurate and timely diagnoses are essential as effective treatments are available for particular etiologies. Finally, among immunocompromised patients, all esophageal symptoms are not necessarily due to an infection, and possible diagnoses of pill esophagitis, acid-peptic injury, or structural and functional abnormalities should not be overlooked.
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PMID:Esophageal infections: risk factors, presentation, diagnosis, and treatment. 752 21

There are increasing challenges for the practising gastroenterologist in treating AIDS-related gastrointestinal diseases. The differential diagnoses of dysphagia and odynophagia include cytomegalovirus (CMV) and herpes simplex virus (HSV) infection, non-specific aphthous ulceration and non-AIDS oesophageal diseases, especially reflux oesophagitis. Chronic subacute abdominal pain with nausea, vomiting, early satiety and weight loss is suggestive of an obstructive lesion caused by lymphoma or Kaposi's sarcoma. Severe acute abdominal pain can indicate pancreatitis or intestinal perforation due to cytomegalovirus. Right upper quadrant pain (with or without fever, vomiting or abnormal liver function tests with a cholestatic profile) is suggestive of hepatobiliary pathology including cholecystitis, cholangitis, acalculous cholecystitis and AIDS cholangiopathy. Diarrhoea is the most common gastrointestinal symptom of AIDS, affecting 50-90% of patients. Causes of AIDS diarrhoea include protozoa (Cryptosporidium parvum, Isospora belli, Enterocytozoon bieneusi, Septata intestinalis, Cyclospora spp, Entamoeba histolytica and Giardia lamblia), bacteria (Mycobacterium avium-intracellulare, Clostridium difficile, Salmonella, Shigella and Campylobacter jejuni), and viruses (CMV, HSV and possibly HIV). Chronic diarrhoea, malnutrition and weight loss can shorten the life-span of patients with AIDS. Elemental diets, isotonic formulas, medium chain triglycerides and total parenteral nutrition have been tried with little success in AIDS patients with severe diarrhoea and wasting.
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PMID:AIDS and the gut. 805 32

Occurrence of vomiting and diarrhea in patients with acquired immunodeficiency syndrome was most frequently attributed to enteropathogens organism that invade the gastrointestinal tract because of the immunologic unbalance of the host... Among several causes the cryptosporidium has been detected quite often and its predominant localization was the gastrointestinal tract, although other extraintestinal sites has also been reported. In both cases, erosive congestive gastritis was found, while histological examination showed cryptosporidium in gastric biopsy specimens.
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PMID:[Erosive gastritis associated with cryptosporidium in 2 patients with AIDS]. 805 89

In order to study maternal mortality in Ilala District, Dar es Salaam, Tanzania, all female deaths in the 12-44 year age group were registered from February 1991 to January 1993. After a follow-up, a relative of the deceased was interviewed to classify the death as associated with pregnancy or not. Eight data collectors were employed to collect information. The team visited each of the 72 areas at least once in 2 weeks. The team also visited mortuaries, grave yards, and religious premises to get information on deaths. All hospitals in the district were regularly visited. A detailed history was taken from a relative of the deceased woman according to a structured questionnaire. 645 female deaths were identified and 117 (18%) were maternal deaths. Most of the interviews (73%) were made at home. In 32% of the cases the interviewee was the mother, in 26% the sister, and in 4-9% the husband, aunt, uncle, father or daughter. Only 10% of the deceased women did not seek any medical treatment prior to death. Three out of 4 women had had fever before death. The second most common symptom was shortness of breath (56%) with a median duration of 6 days. About half of the women had lost weight, complained of abdominal pain, or had been pale or vomiting. Medical records were available in only 44% of the cases. According to the physicians, in 22 (3.5%) women the cause of death was not possible to determine. AIDS (27%), tuberculosis (13%), and malaria (12%) were the most common causes of death. God's will and witchcraft were mentioned as the cause of death for 48 (7.6%) cases. AIDS is a major cause of death in women of reproductive age, therefore AIDS preventive measures must be employed along with more aggressive treatment of malaria and tuberculosis.
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PMID:Female mortality in reproductive ages in Dar es Salaam, Tanzania. 806 68

A prospective study was conducted to evaluate azithromycin in combination with pyrimethamine for treatment of acute Toxoplasma encephalitis in patients with AIDS. Of the 14 patients given 75 mg pyrimethamine and 500 mg azithromycin daily for four weeks, eight were evaluable for clinical response. Five responded favorably, one had an intermediate response and two an unfavorable response. Of the nine patients evaluable for radiological response, six responded favorably, and three had an intermediate response. Eleven adverse events occurred in nine patients: rash (n = 5), abnormal liver function (n = 2), vomiting (n = 3) and hypoacousia (n = 1). This pilot study suggests that the combination of pyrimethamine and azithromycin may be further investigated and that the optimal dosage of azithromycin has yet to be determined.
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PMID:Pyrimethamine plus azithromycin for treatment of acute toxoplasmic encephalitis in patients with AIDS. 811 57

Enterocytozoon bieneusi is a newly described microsporidia in humans thought to be responsible for chronic diarrhoea in acquired immunodeficiency syndrome (AIDS) patients. The epidemiology of this parasite is still unknown; it could be a strictly opportunistic agent or a human enteropathogen. E. bieneusi spores were searched for in stool smears of two populations using a modified chromotrope 2R staining. The first population consisted of 60 patients infected by the human immunodeficiency virus (HIV) and the second of 990 children aged from one month to six years consulting two primary care centers in Niamey, Niger. E. bieneusi spores were found in 4 out of the 60 HIV-positive patients (7%). These 4 patients belonged to a subgroup of 35 patients with < 50 CD4 cells/microliters. Out of 990 children, 8 shed E. bieneusi spores in their stools; the presence of spores was not associated with a particular clinical phenotype (diarrhoea, fever, dehydration, vomiting). Although HIV status could not be evaluated, the HIV prevalence rate among women consulting the same care centers was low (0.5%) and it is therefore unlikely that all eight children were HIV-infected. The results show for the first time that E. bieneusi can infest HIV-negative subjects. Microsporidiosis is frequent in AIDS patients with low CD4 cell counts. Further work is needed to define the prevalence and the possible pathogenic effect of E. bieneusi in immunocompetent subjects.
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PMID:[Prevalence of Enterocytozoon bieneusi spores in the stool of AIDS patients and African children not infected by HIV]. 812 4

We report two cases of fulminant hepatic failure in HIV-1-infected patients treated with didanosine (ddI). Clinical manifestations including vomiting, diarrhoea and dyspnoea were identical in both cases. Biological data mainly revealed hepatic failure and lactic acidosis. Histological examination of liver biopsies showed diffuse microvesicular steatosis. The outcome was fatal in both patients. The only comparable case previously reported (Lai et al., 1991) showed close similarities in the clinical, biological and histological manifestations with microvesicular steatosis. This prompted us to suspect that ddI might be responsible for fulminant hepatitis in all three AIDS patients. This toxic effect may be added to the list of potential adverse events occurring during ddI therapy.
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PMID:Fulminant hepatitis with severe lactate acidosis in HIV-infected patients on didanosine therapy. 815 Dec 70

This was an open, single centre study, to evaluate the safety and efficacy of ondansetron in the treatment of co-trimoxazole associated nausea and vomiting in AIDS patients. Sixteen patients presenting with their first episode of HIV-associated Pneumocystis carinii pneumonia (PCP) on high dose co-trimoxazole were given ondansetron 8 mg orally, every 8 h. Measurements were made from data recorded by each patient on diary cards. In this study 11 out of 16 (69%) patients on ondansetron experienced good control of emesis (2 or less emetic episodes) on their 'worst day' of therapy and 8 out of 16 (50%) of patients demonstrated good control of emesis throughout their treatment with co-trimoxazole. Good control of nausea (mild or none) was achieved in 7 out of 16 (47%) patients. A total of 7 patients were able to complete the full course of co-trimoxazole whilst on ondansetron. One serious adverse event (Stevens-Johnson syndrome) was reported and felt to be unrelated to ondansetron. If conventional anti-emetics fail to achieve control of symptoms or have unacceptable side effects, ondansetron may represent a possible alternative.
Int J STD AIDS
PMID:Ondansetron usage in HIV positive patients: a pilot study on the control of nausea and vomiting in patients on high dose co-trimoxazole for Pneumocystis carinii pneumonia. 821 17

The range of oral antifungal therapy has been expanded recently by the introduction of itraconazole, and terbinafine. These agents have a broader spectrum of activity than griseofulvin and flucytosine, and induce less liver toxicity than ketoconazole. Treatment with these agents may be optimised by application of pharmacokinetic principles. Griseofulvin, ketoconazole and itraconazole should be administered with food to ensure adequate absorption. Maximal absorption of griseofulvin is achieved by administration of the drug as a solid solution in polyethylene glycol. Absorption of azole antifungal agents is impaired by high gastric pH, which is observed in some patients with acquired immunodeficiency syndrome. It is also impaired by frequent vomiting, which commonly occurs in patients with neutropenia. Furthermore, antacids, H2-antagonists and sucralfate interfere with absorption of ketoconazole. The newer oral antifungals are more slowly eliminated and associated with less pronounced drug interactions than ketoconazole. As with ketoconazole, itraconazole and fluconazole influence cyclosporin metabolism. These effects are of clinical relevance and necessitate cyclosporin dosage reduction. However, the cyclosporin dosage reduction required during coadministration of itraconazole and fluconazole (50 to 55%) is less than that required when ketoconazole is concomitantly administered (85%). Monitoring of cyclosporin concentrations during coadministration with these agents is necessary to avoid nephrotoxicity. Drug monitoring is also advisable when phenytoin, carbamazepine or rifampicin (rifampin) are administered concomitantly with azoles, due to a mutual influence on drug metabolism. The antifungal activity of itraconazole is not related exclusively to free drug concentrations. Therefore, the low protein binding of fluconazole does not place this agent at an advantage over itraconazole in the treatment of fungal meningitis. However, terbinafine may be superior to itraconazole for the treatment of tinea unguium, another recalcitrant fungal disease, because terbinafine more rapidly penetrates the nail plate. During repeated use, itraconazole concentrations increase slowly in the nail plate. Steady-state concentrations are reached in the stratum corneum only after several weeks' administration. Following cessation of treatment, terbinafine, itraconazole and ketoconazole concentrations in keratinised tissues decline slowly. This allows a short duration of drug treatment. Some clinical trials suggest that low concentrations of flucytosine, griseofulvin and itraconazole are associated with treatment failure. Flucytosine-induced myelotoxicity also appears to be concentration dependent. This adverse reaction may be caused by fluorouracil (which is produced by metabolism of flucytosine by enterobacillary flora in the gut) rather than by the parent compound.
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PMID:Pharmacokinetic optimisation of oral antifungal therapy. 826 15


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