To Study the Clinical, Biochemical and Radiological Features of Acute Pancreatitis in HIV and AIDS

Abstract

BackgroundPancreatitis complicating HIV infection, even in the Highly Active Antiretroviral Therapy (HAART) era, remains a management challenge. We felt there is a need to discern patterns in the biochemical markers, radiological studies, co-infections, length of stay (LOS) in patients with HIV or AIDS AND pancreatitis.MethodsThis is a retrospective study conducted from June, 2008 to August, 2010 on patients admitted with acute pancreatitis to our hospital. We extracted and compared the following parameters: biochemical markers, HBV markers (surface antigen, core antibody and surface antibody), HCV antibody, radiological studies, and length of stay (LOS). The Balthazar Grade score was used to assess radiological severity of disease. We stratified the cohort into comparison subsets according to CD4 count.ResultsNinety-four admissions met the criteria for HIV or AIDS AND pancreatitis; 67 unique patients comprised the cohort. Median age was 48 years (range, 23 to 60 years). Thirty seven (55%) were male, 30 (45%), female. Two third (n = 51) (76%) were African American. Known risk factors included a history of pancreatitis, 17 (25%); cholecystitis, 13 (19%); alcohol abuse, 25 (37%); Intravenous drug abuse, 18 (27%). Only 36 (38%) admissions were on HAART regimen. Biochemical features on admission were: WBC, 6,100/mm3 (900 - 25,700); amylase, 152 U/L (30 - 1,344); lipase, 702.5 U/L (30 - 5,766), triglyceride, 65 mg/dL (57 - 400); glucose, 94 mg/dL (60 - 1,670); lactate, 2.3 mmol/L (1.09 - 5.49); AST, 61.5 U/L (9 - 1,950); LDH, 762 U/L (394 - 5,500); bicarbonate 19.5 mEq/L (3.3 - 82.7). Interestingly, 62% patients had normal pancreas on CT scan on admission. Of 67 individuals, hepatitis profile was available in 43, 21 (49%) were positive for HCV, 11 (26%) had markers for HBV. Four of 11 patients (36) with CD4 < 50 had evidence of persistent HBV (+core, -surface ab). Patients with CD4 < 200 have a median time for hospital course of 8 days (range 4 - 61 days) compare to 3 days in patients with CD4 > 200. P = 0.03 via t-test comparison. One patient with CD4 < 50 died due to acute pancreatitis.ConclusionPancreatitis remains a major cause of morbidity in HIV-infected individuals. This study has provided detailed features in the HAART therapy era about the clinical, biochemical and radiological features of pancreatitis. Half of our patients were positive for HCV; additionally, 36% with CD4 < 50 had persistent HBV. As opposed to earlier studies, we did not find a female predominance. Patients with CD4 < 200 had a 2.67-fold increase length of stay. Future studies are needed for a closer look on viral cofactors which might precipitate episodes of acute pancreatitis.

Acute Pancreatitis in Patients Living with HIV

“…Cases of AP have been reported with zidovudine, corticosteroids, cyclins, acetaminophen, opioids. Furthermore, cotrimoxazole can to a lesser extent than pentamidine, cause pancreatitis [4,17]. In our series, seven cases of AP were associated with taking ARVs (stavudine and didanosine) and only nine patients received cotrimoxazole, suggesting that other risk factors contribute to the AP occurred in patients with a low rate CD4.…”

“…Riedel et al concluded that there is an association between female gender and acute pancreatitis [15]. However, other studies [3], did not adopt this hypothesis and it is the male sex which was considered as a risk factor [4]. In contrast with this, Euro SIDA group found there is no there is no sex difference in [16].…”

“…During HIV infection, the distribution of causes of the AP is different from that of the general population. The drug causes are the most common followed by the OI and specific tumors with a lower incidence of bile causes [4]. The AP is a well-described complication of HIV as antiretroviral drugs.…”

“…Moore et al had reported a risk increase in patients receiving nucleoside reverse transcriptase inhibitors (NRTIs), especially didanosine [23]. Prolonged exposure to these molecules is associated with inhibition of DNA polymerase, the enzyme responsible for mitochondrial DNA replication, causing mitochondrial toxicity [4,18,24]. Under protease inhibitors especially in Lopinavir and Ritonavir, the AP is explained rather by the secondary hypertriglyceridemia, which is due to the decrease in peripheral clearance of triglycérides [25,26].…”

“…It represents a management problem because of its diverse modes of expression, multiplicity of causes and the high mortality rate. [4] Historically, this has been predominantly associated with the usage of nucleoside reverse transcriptase inhibitors (NRTIs) such as didanosine and stavudine [5,6], release of opportunistic agents (cytomegalovirus, cryptosporidiosis, Mycobacterium tuberculosis) or Kaposi disease. The advent of protease inhibitors in the late 1990s enabled a clear regression of incidence of these diseases [7].…”