Pancreatitis In HIV-infected Patients Research Articles

Predicting gallstone pancreatitis in HIV infected patients

Predicting gallstone pancreatitis in HIV infected patients

Nelfinavir/ritonavir reduces acinar injury but not inflammation during mouse caerulein pancreatitis.

There is no clinical treatment that reduces acinar injury during pancreatitis. Human immunodeficiency virus (HIV) protease inhibitors (PI), including nelfinavir (NFV) and ritonavir (RTV), may reduce the rate of pancreatitis in HIV-infected patients. Since permeability transition pore (PTPC)-mediated mitochondrial dysfunction occurs during pancreatitis, and we have shown that PI prevents PTPC opening, we studied its effects in a model of pancreatitis. The effect of NFV plus RTV (NFV/RTV) or vehicle on caerulein-induced pancreatitis in mice was compared by measuring changes in mitochondrial membrane potential in vitro and cytochrome c leakage in vivo. Histological and inflammatory makers were also compared. NFV/RTV improved DiOC6 retention in acini exposed to caerulein in vitro. In vivo NFV prevented cytosolic leakage of cytochrome c and reduced pancreatic acinar injury, active caspase-3 staining, TUNEL-positive acinar cells, and serum amylase (P < 0.05). Conversely, trypsin activity, serum cytokine levels, and pancreatic and lung inflammation were unaffected. NFV/RTV reduces pancreatic injury and acinar cell death in experimental mouse caerulein-induced pancreatitis but does not impact inflammation.

Incidence of pancreatitis in HIV-infected patients, and the association with antiretroviral therapy

Incidence of pancreatitis in HIV-infected patients, and the association with antiretroviral therapy

A Ten-Year Analysis of the Incidence and Risk Factors for Acute Pancreatitis Requiring Hospitalization in an Urban HIV Clinical Cohort

To assess the incidence of and risk factors for acute pancreatitis in HIV-infected patients in the contemporary highly active antiretroviral therapy (HAART) era, we evaluated all cases of acute pancreatitis requiring hospitalization between 1996 and 2006 in patients followed at Johns Hopkins Hospital's HIV clinic. A nested, case-control analysis was employed for initial episodes of acute pancreatitis, and conditional logistic regression was used to assess risk factors. Of 5970 patients followed for 23,460 person-years (PYs), there were 85 episodes of acute pancreatitis (incidence: 3.6 events/1000 PYs). The incidence of pancreatitis from 1996 to 2000 was 2.6 events/1000 PYs; the incidence from 2001 to 2006 was 5.1 events/1000 PYs (p = 0.0014, comparing rates in two time periods). In multivariate regression, factors associated with pancreatitis included female gender (adjusted odds ratio [AOR] 2.96 [1.69, 5.19]; p < 0.001); stavudine use (AOR 2.19 [1.16, 4.15]; p = 0.016); aerosolized pentamidine use (OR 6.27; [1.42, 27.63]; p = 0.015); and CD4 count less than 50 cells/mm(3) (AOR 10.47 [3.33, 32.90]; p < 0.001). Race/ethnicity, HIV risk factor, HIV-1 RNA, and newer non-nucleoside reverse transcriptase inhibitors (NNRTI)- and protease inhibitor (PI)-based HAART regimens were not associated with an increased risk of pancreatitis after adjustment for the above factors. Pancreatitis remains a significant cause of morbidity in the HIV population in the HAART era. Acute pancreatitis is associated with female gender, severe immunosuppression, and stavudine and aerosolized pentamidine usage. Of note, newer antiretrovirals, particularly atazanavir, lopinivir/ritonavir, tenofovir, abacavir, and efavirenz, were not associated with an increased risk of pancreatitis.

Incidence of pancreatitis in HIV-infected patients: comment on findings in EuroSIDA cohort

Incidence of pancreatitis in HIV-infected patients: comment on findings in EuroSIDA cohort

P374 Acute pancreatitis in HIV infected patients. experience in post-HAART era

P374 Acute pancreatitis in HIV infected patients. experience in post-HAART era

Acute pancreatitis in HIV-infected patients: are etiologies changing since the introduction of protease inhibitor therapy?

Hypertriglyceridemia is a well-established cause of acute pancreatitis in the general population. Protease inhibitor (PI) therapy, introduced in 1996 for HIV infection, is associated with moderate to severe hypertriglyceridemia. To determine whether the prevalence of hyperlipidemic pancreatitis in HIV-infected patients has increased since the introduction of PIs. This was a retrospective study of patients with acute pancreatitis and HIV infection admitted to three local hospitals between 1990 and 2001. Before PIs became available (1990-1995), 30 index cases of acute pancreatitis in the setting of HIV infection were identified, and one of these cases (3.3%) was attributed to hypertriglyceridemia. After the introduction of PIs (1996-2001), 54 cases of acute pancreatitis in HIV-infected patients were identified, and two of these cases were attributed to hypertriglyceridemia (3.7%; p = 0.6). In both time periods, medication-induced pancreatitis was the most common cause of pancreatitis in HIV-infected patients. Despite the well-established association between PIs and hypertriglyceridemia, there was no significant increase in the prevalence of hyperlipidemic pancreatitis in this HIV-infected population after the introduction of PIs. Medication-associated pancreatitis remains the most common cause of acute pancreatitis in the era of potent antiretroviral therapy.

Incidence of pancreatitis in HIV-infected patients receiving nucleoside reverse transcriptase inhibitor drugs.

Pancreatitis is a known adverse effect of the nucleoside reverse transcriptase inhibitors, particularly didanosine. Hydroxyurea has been used to potentiate the antiviral efficacy of didanosine, but recently there has been concern that severe and even fatal pancreatitis may be more likely to occur when hydroxyurea is used in combination with didanosine. We investigated the incidence of pancreatitis in patients using nucleoside analogues with or without hydroxyurea. Data were obtained from patients followed longitudinally on the Johns Hopkins HIV Clinic. Incidence rates of pancreatitis were calculated for each antiretroviral regimen that included zidovudine, stavudine, didanosine (+ hydroxyurea), and didanosine + stavudine (+ hydroxyurea). Poisson regression was used to compare the relative rate of pancreatitis for each regimen adjusting for other covariates. A total of 2613 patients received at least one of the nucleoside reverse transcriptase inhibitor-containing regimens. There were 33 cases of pancreatitis. The crude incidence rate of pancreatitis ranged from 0.18 cases per 100 person-years on therapy for zidovudine to 6.25 cases per 100 person-years for didanosine + hydroxyurea. Compared to didanosine alone, and adjusting for CD4 cell count and other variables, the relative risk (RR) of pancreatitis was 8.56 [95% confidence interval) CI, 1.85-35.59] for didanosine + hydroxyurea, and 2.35 (95% CI, 0.46-11.89) for didanosine + stavudine + hydroxyurea. For any use of hydroxyurea, the RR = 4.01 (95% CI, 1.02-15.89). Other risk factors for pancreatitis included a CD4 cell count < 200 x 106 cells/l, female sex, and a history of pancreatitis. Our data show that the risk of pancreatitis is four-fold higher when hydroxyurea is used. The use of hydroxyurea with didanosine should probably be discouraged if other treatment options are available.

Fatal pancreatitis as a complication of therapy for HIV infection

Acute pancreatitis in HIV-infected patients with or without AIDS has been reported with increasing frequency over the past several years. Drugs used to treat HIV-infected patients are often the cause. We report a case of a 46-year-old HIV-infected man who presented to the emergency department with abdominal pain and was diagnosed with acute pancreatitis. The patient had recently begun taking 2′,3′-dideoxyinosine (ddI). He died shortly after admission to the hospital; CT scan and autopsy confirmed the cause of death as hemorrhagic pancreatitis. We briefly review the literature on the incidence and severity of pancreatitis in association with ddI and pentamidine therapy.