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THE SOUTH AFRICAN GASTROENTEROLOGY REVIEW 2022 | VOLUME 20 | ISSUE 2 | 9 in the present study had the same duration of CP. The incidence of diabetes mellitus would therefore be expected to be the same in the two groups. A hypothesis may be that HIV initially affects acinar cells. With progression of CP disease islet cells may be affected later in the disease course and thus DM may develop later. Additionally, an increase in the number of pancreatic islets has been shown in HIV infected patients. 14 Further research is required to clarify this finding. Pancreatic insufficiency is underdiagnosed in patients on HIV therapy as many patients in whom a pathogenic infection has been excluded are thought to be suffering from anti-retroviral treatment side effects or have HIV induced small bowel mucosal abnormalities. 19 HIV infection is associated with a malabsorption syndrome that includes steatorrhea, 20 postulated to occur as a result of multiple factors including intestinal mucosal damage and exocrine pancreatic dysfunction. 4 Studies have shown that HIV with steatorrhea-like symptoms have decreased fecal elastase, however the levels do not determine fat malabsorption as high fecal fat excretion in this study occurred independent of fecal elastase levels. 3 Following the introduction of HAART the incidence of steatorrhea as a result of intestinal mucosal damage decreased significantly, resulting in pancreatic insufficiency becoming the dominant cause of steatorrhea. 21 Limitations of this study We do not routinely determine fecal elastase. The patients in this study had severe exocrine insufficiency and not early onset CP. Our diagnosis of CP was based on radiological imaging demonstrating pathognomic pancreatic calcification of chronic calcific pancreatitis. In an HIV positive patient pancreatic calcifications rarely may represent extra-pulmonary infection by pneumocystis jiroveci. However, calcifications in these cases are fine and are often associated with lymph node calcification22 unlike the coarse calcifications seen in CP. Conclusion We have described a group of HIV-infected patients with CP. In comparison with a group of HIV-uninfected patients with CP they had the same risk factors but were significantly younger. HIV infection may be a risk factor for the earlier onset of CP in the presence of known risk factors. Chronic pancreatitis should be considered in the differential diagnosis of persistent non-infective diarrhea, or steatorrhea. Significantly fewer HIV-infected patients with CP had diabetes mellitus, despite having the same duration of CP. There may be a pathological disjunction of islet cell pathology between HIV-infected and –uninfected patients. References 1. Yadav D, Timmons L, Benson JT, Dierkhising RA, Chari ST. Incidence, prevalence, and survival of chronic pancreatitis: a population-based study. Am J Gastroenterol 2011; 106(12): 2192-2199. 2. Jeppe CY, Smith MD. Transversal descriptive study of xe- nobiotic exposures in patients with chronic pancreatitis and pancreatic cancer. JOP 2008; 9(2): 235-239. 3. Carroccio A, Di Prima L, Di Grigoli C, Soresi M, Farinella E, Di Martino D, et al. Exocrine pancreatic function and fat malab- sorption in human immunodeficiency virus-infected patients. Scand J Gastroenterol 1999; 34(7): 729-734. 4. Carroccio A, Guarino A, Zuin G, Verghi F, Berni Canani R, Fontana M, et al. Efficacy of oral pancreatic enzyme therapy for the treatment of fat malabsorption in HIV-infected patients. Aliment Pharmacol Ther 2001; 15(10): 1619-1625. 5. Schwartz MS, Brandt LJ. The spectrum of pancreatic disorders in patients with the acquired immune deficiency syndrome. Am J Gastroenterol 1989; 84(5): 459-462. 6. Johnson CD, Hosking S. National statistics for diet, alcohol consumption, and chronic pancreatitis in England and Wales, 1960-88. Gut 1991; 32(11): 1401–1405. 7. Jaakkola M, Nordback I. Pancreatitis in Finland between 1970 and 1989. Gut 1993; 34(9): 1255-1260. 8. Hirota M, Shimosegawa T, Masamune A, Kikuta K, Kume K, Hamada S, et al. The sixth nationwide epidemiological survey of chronic pancreatitis in Japan. Pancreatology 2012; 12(2): 79-84. 9. Masamune A, Kikuta K, Nabeshima T, Nakano E, Hirota M, Kanno A, et al. Nationwide epidemiological survey of early chronic pancreatitis in Japan. J Gastroenterol 2017; 52(8): 992-1000. 10. Valicenti P, Tomassi L, Acevedo L. Calcified chronic pan- creatitis in an HIV positive patient. Medicina (B Aires) 2005; 65(3): 255. 11. Bilgin M, Balci NC, Erdogan A, Momtahen AJ, Alkaade S, Rau WS. Hepatobiliary and pancreatic MRI and MRCP findings in patients with HIV infection. AJR Am J Roentgenol 2008; 191(1): 228-232. 12. Brivet FG, Naveau SH, Lemaigre GF, Dormont J. Pancreatic lesions in HIV-infected patients. Baillieres Clin Endocrinol Metab 1994; 8(4): 859-877. 13. Chehter EZ, Longo MA, Laudanna AA, Duarte MI. Involvement of the pancreas in AIDS: a prospective study of 109 post-mor- tems. AIDS 2000; 14(13): 1879-1886. 14. Barbosa AG, Chehter EZ, Bacci MR, Mader AA, Fonseca F. AIDS and the pancreas in the HAART era: a cross sectional study. Int Arch Med 2013; 6(1):28. 15. STATS SA. Mid-year population estimates 2018. [Internet] Statistical release P0302. Statistics South Africa. [cited 2019 March 13]. Available from: https://www.statssa. gov.za/publi- cations/P0302/P03022018.pdf 16. Chehter EZ. HIV and Pancreas: What do we know till now? J Pancreas 2018; 19(2): 107-108. 17. Abebe SM, Getachew A, Fasika S, Bayisa M, Demisse AG, Mesfin N. Diabetes mellitus among HIV-infected individuals in follow-up care at University of Gondar Hospital, Northwest Ethiopia. BMJ Open 2016; 6:e011175. 18. Kavishe B, Biraro S, Baisley K, Vanobberghen F, Kapiga S, Munderi P, et al. High prevalence of hypertension and of risk factors for non-communicable diseases (NCDs): a population based cross-sectional survey of NCDS and HIV infection in Northwestern Tanzania and Southern Uganda. BMC Med 2015; 13: 126. 19. Price DA, Schmid ML, Ong EL, Adjukeiwicz KM, Peaston B, Snow MH. Pancreatic exocrine insufficiency in HIV-positive patients. HIV Med 2005; 6(1): 33-36. 20. Poles MA, Fuerst M, McGowan I, Elliott J, Rezaei A, Mark D, et al. HIV-related diarrhea is multifactorial and fat malabsorption is commonly present, independent of HAART. Am J Gastroen- terol 2001; 96(6): 1831-1837. 21. Canani RB, Spagnuolo MI, Cirillo P, Guarino A. Ritonavir com- bination therapy restores intestinal function in children with advanced HIV disease. J Acquir Immune Defic Syndr 1999; 21(4): 307-312. 22. Miller FH, Gore RM, Nemcek AA Jr, Fitzgerald SW. Pancreati- cobiliary manifestations of AIDS. AJR Am J Roentgenol 1996; 166(6): 1269-1274. REVIEW GPA’s Non-PPI (Antacids, H2 blockers) PPI Habits Smoker Alcohol use Indication Headache Musculoskelet Gastrointestin Other Pattern of use General advic Take with mea Frequency Daily Twice daily Three times d Four times dai >Four times daily NSAID non-steroidal the counter; GPA’s ga pump inhibitors; H2 h Discus ion The South African Ess ibuprofen as an altern first line management for ibuprofen, and co common in South Afri tertiary hospitals in th where patterns of OT UGIT bleeds have not During the study p who were admitted w 85% (n=183) of who pr scription. 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