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Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because pancreatitis has been reported frequently in adults with human immunodeficiency virus infection, we sought to determine the incidence of pancreatitis in children with acquired immunodeficiency syndrome by reviewing all records of children with AIDS, their serum amylase and lipase levels, and the factors associated with pancreatitis through a case-control analysis. During a 6-year period pancreatitis developed in 9 (17%) of 53 pediatric patients with AIDS. Six children had vertical transmission of infection and three patients had acquired HIV infection through contaminated blood products. Pancreatitis developed at a median age of 5.2 years (range 1.2 to 20 years). All patients had vomiting and abdominal pain. When the patients were first seen, lipase values were elevated more than amylase values (p = 0.028). Amylase and lipase levels declined at comparable rates. In the case-control analysis, pentamidine isethionate was significantly associated with pancreatitis (p = 0.02); the risk was greater in patients who received pentamidine isethionate and had absolute CD4 T-lymphocyte counts less than 100 cells/mm3 (p = 0.001). Infections associated with the onset of pancreatitis included cytomegalovirus (4), Cryptosporidium (1), Pneumocystis carinii pneumonia (3), and Mycobacterium avium intracellulare (1). Coinfection with cytomegalovirus was associated with a protracted course in four children. Ultrasonographic examination demonstrated biliary ductal dilatation 6 months after the onset of pancreatitis in one child. Seven children have died at a mean of 8 months after the initial onset of pancreatitis; the one living child has survived 5 months from the onset of pancreatitis. We conclude that pancreatitis is common in pediatric patients with AIDS and may be related to pentamidine isethionate exposure, especially when absolute CD4 T-lymphocyte counts are less than 100 cells/mm3. Serum amylase levels do not always accurately predict the onset of pancreatitis; serum lipase levels should be measured in children with symptoms. The onset of pancreatitis in an HIV-infected child is a poor prognostic indicator.
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PMID:Pancreatitis in pediatric human immunodeficiency virus infection. 137 Sep 62

Didanosine is a dideoxynucleoside analogue which undergoes intracellular conversion to the putative active triphosphate metabolite. The active metabolite appears to inhibit viral reverse transcriptase and terminate the proviral DNA, and produces virustatic inhibition of actively replicating human immunodeficiency virus (HIV) at clinically relevant concentrations. In phase I studies didanosine had beneficial effects on various surrogate markers of clinical efficacy and also improved clinical manifestations of HIV infection, with a 21-month survival rate of 80% in patients with acquired immune deficiency syndrome (AIDS) and 93% in patients with AIDS-related complex (ARC) in 1 study. Didanosine also improved CD4+ cell counts in a phase II/III trial in patients previously treated with zidovudine, whereas cell counts declined in patients continuing zidovudine therapy. However, the effects of didanosine on clinical end-points (disease progression, survival, HIV encephalopathy) remain to be established. Peripheral neuropathy and pancreatitis are the predominant dose-limiting adverse events and didanosine therapy should be withdrawn in patients developing signs or symptoms of pancreatitis and during acute treatment of Pneumocystis carinii pneumonia. However, at currently recommended clinical dosages didanosine is generally well tolerated with minimal haematological toxicity. Thus, in a therapeutic area with few treatment options, didanosine offers a welcome alternative for patients intolerant of, or resistant to, zidovudine. There are a number of clinical trials in progress evaluating didanosine alone or in combination with other antiviral agents, and these results are awaited with considerable interest.
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PMID:Didanosine. A review of its antiviral activity, pharmacokinetic properties and therapeutic potential in human immunodeficiency virus infection. 137 14

Great strides have been made in the therapy of human immunodeficiency virus (HIV) infection. Currently approved drugs include zidovudine and didanosine. A third drug, dideoxycytidine (zalcitibine), has recently been filed for approval with the Food and Drug Administration. All these drugs work through inhibition of the reverse transcriptase enzyme. Zidovudine is the only drug that has shown clinical efficacy against HIV. Treatment of patients with advanced HIV disease (i.e., acquired immune deficiency syndrome [AIDS] or symptomatic infection with < 200 CD4+ lymphocytes per mm3), results in a prolongation and improved quality of life. Zidovudine is the only antiretroviral agent approved for the treatment of asymptomatic patients. Early intervention with zidovudine has been shown to delay progression to AIDS when patients' CD4+ lymphocyte counts decline to less than 500/mm3, irrespective of clinical signs or symptoms of HIV infection. Didanosine is currently indicated for the treatment of patients with advanced HIV disease who are intolerant to or failing zidovudine therapy. The major toxicity of zidovudine is bone marrow suppression with anemia and granulocytopenia (which occurs in from 1% to 45% of patients, depending on the clinical stage of disease and the dose of the drug). Didanosine and zalcitibine have both been associated with a severe peripheral neuropathy, which is generally reversible on cessation of the drug. In addition, didanosine has been implicated as a cause of pancreatitis that has been fatal in a small percentage of cases. The toxicities of didanosine and zalcitibine range from 1% to 10%, depending on dose, duration of therapy, and the presence of underlying HIV-related peripheral neuropathy or a previous history of pancreatitis. The clinical hallmark of HIV infection is the development of opportunistic infections and malignancies, which are a consequence of the profound immunodeficiency. The risk of an opportunistic infection increases significantly as the T-helper lymphocyte count declines to less than 20%, or 200 to 250/mm3. The spectrum of opportunistic infections ranges from viruses to protozoa. Patients with advanced HIV disease are also at increased risk of infection with nonopportunistic, community-acquired pathogens. Primary and secondary prophylaxis against the most common AIDS-defining opportunistic infection, Pneumocystis carinii pneumonia, is now recommended. Studies are currently underway to determine the efficacy of prophylaxis against other opportunistic pathogens. Treatment of opportunistic infections associated with AIDS has improved significantly over the past 5 years as new drugs and combination regimens of antimicrobials have been developed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:AIDS: Part II. 139 36

Pneumocystis carinii pneumonia (PCP) is a major opportunistic infection in acquired immunodeficiency syndrome (AIDS) and is treated with co-trimoxazole, pentamidine and others. The severe adverse reactions, including bone marrow suppression, by these therapeutic agents often preclude their continued use. A 14-year-old male HIV-positive hemophilia A patient, who was complicated by disseminated intravascular coagulation syndrome (DIC) following acute pancreatitis during treatment for PCP, was treated with proteinase inhibitors and anticoagulant agents. He was improved and discharged. As pentamidine may cause pancreatitis and develop DIC, it is important that pancreatic enzymes should be carefully followed when this agent administrated. In this case, granulocyte colony-stimulating factor and erythropoietin were effective for the bone marrow suppression, suggesting that importance of these agents for the prophylaxis of other secondary infections during the treatment.
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PMID:[HIV-1 seropositive hemophilia A complicated by disseminated intravascular coagulation syndrome and acute pancreatitis during treatment of Pneumocystis carinii pneumonia]. 143 51

To evaluate the adverse effects of intravenous pentamidine isethionate, a retrospective study was carried out over a four-year period. Twenty-one acquired immunodeficiency syndrome (AIDS) patients received intravenous pentamidine as treatment of Pneumocystis carinii pneumonia (PCP). This was 13% of the total number of patients with PCP in the department during that period. Four patients died during treatment and were not evaluated for side effects. Thirteen patients (13/17 = 76%) suffered from one or more minor side effects. The most common of these were gastrointestinal discomfort, pancreatitis, nephro- and hepatotoxicity. Five patients (5/17 = 29%) experienced a major adverse effect. These were cardiac arrest (one patient), severe hypoglycaemia (one patient) and severe pancreatitis (three patients). In two patients, discontinuation of treatment was necessary due to adverse reactions. As long as pentamidine isethionate is the second drug of choice in the treatment of acute PCP, careful biochemical and cardial monitoring of patients during treatment is recommended.
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PMID:Adverse effects associated with intravenous pentamidine isethionate as treatment of Pneumocystis carinii pneumonia in AIDS patients. 152 88

Extensive acute necrotizing pancreatitis occurred in three patients with the acquired immunodeficiency syndrome who had received both aerosolized pentamidine as prophylaxis and intravenous pentamidine for Pneumocystis carinii pneumonia. The clinical manifestations along with gross and microscopic pathologic findings at autopsy are presented.
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PMID:Pathology of pentamidine-induced pancreatitis. 173 11

A 37-year-old black man with presumed Pneumocystis carinii pneumonia who was treated with systemic IV pentamidine had fatal pancreatitis and massive hepatomegaly. Fatal pancreatitis can occur with no hemorrhagic changes seen at autopsy. Awareness of the relationship between pentamidine and pancreatitis should be emphasized. With current clinical trials testing other routes of administration, fatal complications associated with IV pentamidine therapy will be minimized.
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PMID:Edematous pancreatitis associated with intravenous pentamidine. 205 80

Of 18 AIDS patients with Pneumocystis carinii pneumonia treated with pentamidine mesylate parenterally, four developed serious to severe hypoglycaemia, three hypoglycaemia followed by insulin-requiring diabetes, and two others diabetes alone. Hypoglycaemia (blood glucose 2.1 +/- 0.2 (+/- SE) mmol l-1) occurred 9 (2-22) days after starting treatment, and diabetes (initial blood glucose 30 +/- 6 mmol l-1) after 60 (20-90) days. The other patients remained euglycaemic. The dysglycaemic patients (hypo- and hyper-glycaemic) had a higher pentamidine dosage (p less than 0.01), and higher serum creatinine levels at end of treatment (p less than 0.001), consistent with drug accumulation and dose-dependent toxicity. Plasma C-peptide levels were low in the diabetic patients, in the basal state (0.25-0.28 nmol l-1) and following stimulation by IV glucagon (0.35-0.40 nmol l-1), vs 0.80 +/- 0.06 nmol l-1 (basal) and 1.83 +/- 0.16 nmol l-1 (stimulated) in 23 healthy control subjects (mean +/- SE). Islet cell or insulin antibodies were not detected. Serum amylase levels rose abnormally in the dysglycaemic group, and pancreatitis was proved in one, and suspected in another patient. None of 28 similar AIDS patients whose P. carinii pneumonia was treated with cotrimoxazole showed blood glucose disturbance.
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PMID:Hypoglycaemia and diabetes mellitus following parenteral pentamidine mesylate treatment in AIDS patients. 214 64

Two patients without risk factors or a prior history of pancreatitis developed acute pancreatitis soon after initiating pentamidine isethionate therapy for Pneumocystis carinii pneumonia associated with the acquired immunodeficiency syndrome. In both patients the pancreatitis improved following medication cessation. One patient did not redevelop pancreatitis when he subsequently received inhaled pentamidine. Review of the literature revealed five previously reported cases of this drug reaction. Pentamidine-associated pancreatitis appears to develop within three weeks of initiating therapy and after receiving more than 1 g in cumulative dosage. Glucose abnormalities, renal insufficiency, and non-specific abdominal pain may be early warning signs of pentamidine-associated pancreatitis.
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PMID:Pentamidine-associated pancreatitis. 279 17

Severe hemorrhagic pancreatitis developed in a patient with the acquired immunodeficiency syndrome (AIDS) during pentamidine isethionate treatment for Pneumocystis carinii pneumonia. Despite prompt withdrawal of administration of the drug, the patient died of complications of pancreatitis. Pentamidine is known to be toxic to pancreatic islet cells, causing both hypoglycemia and hyperglycemia in clinical use. However, it rarely causes symptomatic pancreatitis. A review of the literature indicates that this is the second report of fatal pancreatitis associated with pentamidine therapy.
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PMID:Pentamidine-associated fatal acute pancreatitis. 349 May 88


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