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 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The increased reporting of tuberculosis of the pancreas is related to a worldwide increase in tuberculosis and an increase in emigration from countries where tuberculosis is endemic into countries where more sophisticated healthcare and radiological imaging are available. Three recent cases of pancreatic tuberculosis in Auckland, New Zealand, emphasize that tuberculosis should now be included in the differential diagnosis of a pancreatic mass. Diagnostic indicators include emigration from, or recent travel to, a country where tuberculosis is endemic, the association of a pancreatic mass with fever, the presence of abdominal pain and a cystic pancreatic mass in a younger male. Radiological appearances might be similar to a mucinous cystic neoplasm or could show a pancreatic mass with involvement of peripancreatic lymph nodes or a mass centred in a peripancreatic lymph node. When the diagnosis is suspected an human immunodeficiency virus test and a comprehensive screening for tuberculosis at other sites should be performed. If tuberculosis is unable to be diagnosed then pancreatic biopsy and culture is indicated. Endoscopic ultrasound with fine needle aspiration for cytology is likely to become the preferred technique. Most patients have an excellent clinical response to standard antituberculosis regimens.
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PMID:Diagnosis and management of isolated pancreatic tuberculosis: recent experience and literature review. 1514 59

Ever since its first description in 1918, Dientamoeba fragilis has struggled to gain recognition as a significant pathogen. There is little justification for this neglect, however, since there exists a growing body of case reports from numerous countries around the world that have linked this protozoal parasite to clinical manifestations such as diarrhea, abdominal pain, flatulence, and anorexia. A number of studies have even incriminated D. fragilis as a cause of irritable bowel syndrome, allergic colitis, and diarrhea in human immunodeficiency virus patients. Although D. fragilis is most commonly identified using permanently stained fecal smears, recent advances in culturing techniques are simplifying as well as improving the ability of investigators to detect this organism. However, there are limitations in the use of cultures since they cannot be performed on fecal samples that have been fixed. Significant progress has been made in the biological classification of this organism, which originally was described as an ameba. Analyses of small-subunit rRNA gene sequences have clearly demonstrated its close relationship to Histomonas, and it is now known to be a trichomonad. How the organism is transmitted remains a mystery, although there is some evidence that D. fragilis might be transmitted via the ova of the pinworm, Enterobius vermicularis. Also, it remains to be answered whether the two distinct genotypes of D. fragilis recently identified represent organisms with differing virulence.
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PMID:Emerging from obscurity: biological, clinical, and diagnostic aspects of Dientamoeba fragilis. 1525 93

Unlike mucocutaneous infections, disseminated herpes simplex virus infections are rare and often fatal owing to acute liver failure (ALF). Typically, the course of the disease is rapid and the lack of specific symptoms may result in delay in diagnosis. This study reports a case of genital herpes caused by herpes simplex-type 2 that resulted in ALF. The patient was a 24-y-old woman with a 1 y history of Crohn's disease, treated with oral prednisolone. She was hospitalized with fatigue, anorexia and abdominal pain. Blood tests showed pancytopenia, renal failure and coagulopathy. Pelvic examination revealed signs of severe colpitis and prompt therapy with parenteral acyclovir was initiated. Despite the early institution of antiviral therapy, progressive hepatic coma, gastrointestinal bleeding, oliguria and severe intracranial hypertension characterized the clinical course. The patient received intensive supportive care and recovered without liver grafting. A subsequent screening for immunodeficiency diseases revealed an immeasurable blood mannose-binding lectin (MBL) concentration. 10 weeks after admission, she was discharged for further rehabilitation. This case stresses the importance of suspecting disseminated herpes virus infection in patients with ALF without known aetiology as it may secure prompt initiation of antiviral therapy and reduce the risk that transplantation is needed for survival.
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PMID:A case of acute liver failure caused by herpes simplex type 2. 1530 95

Lactic acidosis is an uncommon but potentially life-threatening adverse effect of didanosine. When given concomitantly with tenofovir disoproxil fumarate (DF), the area under the concentration-time curve of didanosine is increased by 48-60%. A 63-year-old man with human immunodeficiency virus (HIV) infection tolerated several didanosine-containing antiretroviral regimens. He developed generalized weakness, loss of appetite, weight loss, nausea, and vomiting 1.5 years after tenofovir DF was added to his didanosine-containing regimen. He was diagnosed with lactic acidosis and died after a 13-day hospital stay, when his lactate level increased to 189.7 mg/dl and his arterial blood gas pH value fell to 6.75. Health care providers should maintain a high index of suspicion for lactic acidosis in patients with HIV infection who receive didanosine and tenofovir DF concurrently. For patients receiving antiretroviral regimens containing this drug combination, it would be prudent to monitor lactate levels periodically. This is especially important when patients experience symptoms suggestive of lactic acidosis, such as weakness, abdominal pain, weight loss, nausea and vomiting, and shortness of breath.
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PMID:Fatal lactic acidosis associated with coadministration of didanosine and tenofovir disoproxil fumarate. 1533 57

Atazanavir is the first once-daily protease inhibitor for the treatment of human immunodeficiency virus type 1 infection and should be used only in combination therapy, as part of a highly active antiretroviral therapy (HAART) regimen. In addition to being the most potent protease inhibitor in vitro, atazanavir has a distinct cross-resistance profile that does not confer resistance to other protease inhibitors. However, resistance to other protease inhibitors often confers clinically relevant resistance to atazanavir. Currently, atazanavir is not a preferred protease inhibitor for initial HAART regimens. In treatment-naive patients, atazanavir can be given as 400 mg/day. However, atazanavir should be pharmacologically boosted with ritonavir in treatment-experienced patients or when coadministered with either tenofovir or efavirenz. Patients who receive atazanavir experience similar rates of adverse events compared with patients receiving comparator regimens. An exception is an increased risk of asymptomatic hyperbilirubinemia, which is due to competitive inhibition of uridine diphosphate-glucuronosyltransferase 1A1. Although hyperbilirubinemia is a common adverse drug reaction of atazanavir therapy (22-47%), fewer than 2% of patients discontinue atazanavir therapy because of this adverse effect. Common adverse effects reported with atazanavir include infection, nausea, vomiting, diarrhea, abdominal pain, headache, peripheral neuropathy, and rash. Of significance, fewer abnormalities have been observed in plasma lipid profiles in patients treated with atazanavir compared with other protease inhibitor-containing regimens. As with other protease inhibitors, atazanavir is also a substrate and moderate inhibitor of the cytochrome P450 (CYP) system, in particular CYP3A4 and CYP2C9. Clinically significant drug interactions include (but are not limited to) antacids, proton pump inhibitors, histamine type 2 receptor antagonists, tenofovir, diltiazem, irinotecan, simvastatin, lovastatin, St. John's wort, and warfarin. We conclude that atazanavir is a distinctively characteristic protease inhibitor owing to its in vitro potency, once-daily dosing, distinct initial resistance pattern, and infrequent association with metabolic abnormalities.
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PMID:Atazanavir for the treatment of human immunodeficiency virus infection. 1558 41

This study focuses on the identification of aetiological agents of vaginitis in Nigerian women. Study subjects are drawn from patients presenting with lower abdominal pain, vaginal discharge and itching at the gynaecology clinic of Lagos University Teaching Hospital and at the Clinical Centre of the Nigerian Institute of Medical Research, Yaba, Lagos, between January 2001 and July 2002. A total of 250 patients gave informed consent to participate in the study. The patients also had pre- and post-test human immunodeficiency virus (HIV) counselling. Each patient completed a questionnaire in order to provide biographical data, past clinical history and socio-economic background information. A cervical swab (CS) and a high-vaginal swab (HVS) were obtained from each patient. Swab samples were examined for pH and under light microscopy by Gram's stain and as wet preparations in 10% potassium hydroxide. Subsequently, samples were cultured on appropriate media at optimal conditions and a drug sensitivity profile for all isolates was determined by standard methods. Blood samples were screened and confirmed for HIV antibodies. Bacterial, fungal and parasitic pathogens were identified or isolated in samples from 241 (96.4%) of the women. Bacterial agents (Neisseria, Streptococcus and Staphylococcus species) were predominant in 128 (51.2%) patients, followed by fungi in 108 (43.2%) and parasites (Trichomonas vaginalis) in five (2.0%). Sensitivity to ciprofloxacin was seen in 40% of Staphylococcus species and in 90% of Neisseria species. Positive HIV serology was seen in 25 (10%) of the 250 women studied, 20 (80%) of which had concurrent microbial infections. Overall, a broad spectrum of microbial agents were shown to be responsible for vaginitis in the group of patients studied.
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PMID:Aetiological agents of vaginitis in Nigerian women. 1564 8

Nucleoside reverse-transcriptase inhibitors (NRTIs) have been associated with functional and structural mitochondrial abnormalities, leading to several adverse events, such as increased serum lactic acid levels and lactic acidosis. Mild-to-moderate, asymptomatic hyperlactataemia has been frequently reported in human immunodeficiency virus (HIV)-infected patients treated with NRTIs, with an estimated prevalence between 15% and 35%. On the contrary, symptomatic, severe hyperlactataemia and lactic acidosis are less common, with an incidence ranging from 1.7 to 25.2 cases per 1000 person-years of antiretroviral treatment, and are associated with a remarkable mortality rate, which varies from 30% to 60% in different studies. The clinical presentation of lactic acid syndrome is non-specific and includes asthenia, malaise, nausea, vomiting, abdominal pain, weight loss, tachypnoea, dyspnoea, liver steatosis and increased transaminase levels, and risk factors include previous or concurrent therapy with stavudine or didanosine. Management of symptomatic lactic acid alterations involves NRTI-therapy interruption and supportive care, while natural history of hyperlactataemia is still unknown, and it is uncertain whether asymptomatic patients with increased lactate concentrations are at increased risk of developing lactic acidosis.
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PMID:Hyperlactataemia and lactic acidosis in HIV-infected patients receiving antiretroviral therapy. 1568 Oct 97

Immunosuppression for therapeutic reasons (e.g. post transplantation, post chemotherapy), as well as pathologic immunodeficiency due to certain pathologic conditions (e.g. AIDS, leukemia), is increasingly encountered in daily medical practice. As a result, the concomitant risk for opportunistic infections is higher and immunocompromised patients may present with uncommon clinical and radiologic conditions. We report on a case of a 33-year-old immunocompromised woman with a history of recurrent T-cell lymphoblastic lymphoma, which presented with abdominal pain. Computed tomography (CT) images demonstrated significant small bowel dilatation, wall thickening, and high-density intestinal content, with a focal point of transition in the pelvis. Extensive fungal enteritis due to Candida Albicans with partial small bowel obstruction was found on autopsy.
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PMID:Small bowel obstruction secondary to disseminated candidiasis in an immunocompromised patient: radiologic-pathologic correlation. 1579 64

Patients with immunodeficiency or treatment-related immunosuppression are at an increased risk of developing severe herpes simplex virus (HSV) infection. We present a fatal case of a generalized HSV-1 infection in a 22-year-old female afflicted by acute lymphoblastic leukemia who was treated with polychemotherapy. The terminal clinical course was characterized by abdominal pain, progressive hepatic failure, and disseminated intravascular coagulation. Autopsy revealed non-perioral herpetic skin lesions and mucosal ulceration of the esophagus and colon. Punctuated areas of yellow-tan necrosis with hyperemic rims were detected in the liver, spleen, and lung. Numerous petechiae were observed on the mucosal surface of the esophagus, jejunum, ileum, and colon. Microscopically, lesions demonstrated the cellular changes characteristic of herpetic infection. Immunohistochemistry for identification of the virus using monoclonal antibodies against HSV-1 and HSV-2 showed positive staining for HSV-1. Polymerase chain reaction and sequencing confirmed HSV-1 positivity. Emphasis must be placed on clinical awareness of a generalized HSV infection in immunocompromised patients. Absence of orofacial or genital lesions does not rule out the possibility of active HSV infection.
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PMID:Generalized herpes simplex virus infection in an immunocompromised patient--report of a case and review of the literature. 1590 Nov 33

An increased incidence of thrombotic thrombocytopenic purpura has been reported among human immunodeficiency virus-infected patients or those with acquired immunodeficiency syndrome (AIDS). Despite this association, hitherto only a single case of thrombotic thrombocytopenic purpura has been reported in an HIV-infected patient during pregnancy. We describe a young multiparous patient with long-standing AIDS who presented with lower abdominal pain. Following findings of thrombocytopenia, microangiopathic hemolytic anemia, renal failure, low-grade fever, and mental status changes, thrombotic thrombocytopenic purpura was diagnosed after initially considering the diagnosis of severe preeclampsia, and the patient was delivered by cesarean section. The patient required multiple plasma exchanges during a protracted postpartum course, and was discharged in good health. This first report of thrombotic thrombocytopenic purpura and AIDS in pregnancy demonstrates that when encountering preeclampsia in patients with AIDS, thrombotic microangiopathy should be strongly considered. In addition, these patients may exhibit an attenuated response to plasma exchange therapy and despite previous reports in nonobstetric patients, a favorable outcome is attainable in these critically ill patients.
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PMID:Thrombotic thrombocytopenic purpura in a patient with acquired immunodeficiency syndrome at 28 weeks gestation. 1590 17


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