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LETTER TO EDITOR |
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| Year : 2012 | Volume
: 33
| Issue : 2 | Page : 144-145 |
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Tropical calcific pancreatitis in HIV patient
Sunil Kumar, Sanjay K Diwan, Vikram Kokate
Department of Medicine, Jawahar Lal Nehru Medical College, DMIMS, Sawangi, Wardha, Maharastra, India
| Date of Web Publication | 9-Oct-2012 |
Correspondence Address:
Sunil Kumar
Department of Medicine, DMIMS, Sawangi, Wardha, Maharashtra
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0253-7184.102134
How to cite this article:
Kumar S, Diwan SK, Kokate V. Tropical calcific pancreatitis in HIV patient. Indian J Sex Transm Dis 2012;33:144-5 |
How to cite this URL:
Kumar S, Diwan SK, Kokate V. Tropical calcific pancreatitis in HIV patient. Indian J Sex Transm Dis [serial online] 2012 [cited 2023 Nov 28];33:144-5. Available from: https://ijstd.org/text.asp?2012/33/2/144/102134 |
Sir,
A 36-year-old female from rural central Maharashtra with known case of human immunodeficiency virus infection (CD4 cell count, 249 per cubic millimeter) for six months on regular anti retroviral drugs presented with epigastric pain, nausea, and few episodes of vomiting for 3 days. She was taking a combination of lamivudine and zidovudine (from local civil hospital where anti retroviral drugs are provided free of cost). There were similar episodes of such type of abdominal pain. Abdominal pain was mid epigastric, dull aching in nature, increased after taking meal and some times radiating to back. She was also diagnosed recently as insulin diabetes mellitus and taking regular insulin. She was a nonsmoker and nonalcoholic. We had no reports regarding investigations performed during previous episodes and had not identified other causes of pancreatitis. On examination, vitals were stable and tenderness was present in the epigastric region. There was no palpable abdominal mass or other specific findings noted on physical appearance. At the time of admission, hemoglobin was 7.9 g/dl, total leukocyte count was 4800 and platelet count was 431,000. Her fasting and post meal blood sugar were 180 and 220 mg per dl on regular insulin. Her serum lipase was 193 U per liter (normal range up to 180 U/litre). Serum amylase and lipase levels are widely used as screening tests for acute pancreatitis in patients with acute abdominal pain or back pain. Values greater than three times the upper limit of normal virtually clinch the diagnosis if gut perforation or infarction is excluded. [1] In this case, value of serum lipase was marginally raised which may suggest pancreatitis. Her serum triglyceride, amylase and calcium levels were within normal limits. Liver function tests were within normal range. Ultrasonography of the upper abdomen [Figure 1] and computed tomographic images of the abdomen [Figure 2] revealed coarse, well-defined, and dense calcifications within the body of the pancreas (arrows). The pattern is typical of the large intraductal calculi of tropical calcific pancreatitis, which has been increasingly recognized as a cause of nonalcoholic, chronic pancreatic disease in tropical developing nations. Tropical pancreatitis is chronic calcific, non-alcoholic pancreatitis, prevalent in developing countries like India which is seen in malnourished patients and in diets rich in tapioca (cassava, Manihot esculenta), a staple diet of poor people in Kerala. [2] Hypertriglyceridemia, hypercalcemia, obstruction of the main pancreatic duct by stenosis, stones, cancer, genetic mutations are some of the less common causes. [3],[4] The cause of this condition remains unknown, although a study from Bangladesh showed association between the serine protease inhibitor Kazal type 1 (SPINK1 N34S) mutation and increased risk of several forms of pancreatic disease, including fibrocalculous pancreatic diabetes, tropical calcific pancreatitis, and non-insulin-dependent diabetes mellitus, [5] No reports are available regarding tropical calcific pancreatitis caused by HIV infection or due to antiretroviral therapy. However, further studies are required to prove this hypothesis and come to any conclusion.
 References | |  |
| 1. | Greenberger NJ, Conwell DL, Banks PA. Approach to the patient with pancreatic disease. In: Longo DL,Fauci AS, Kasper DL, Hauser SL, Jameson JL ed. Harrison's principles of internal medicine,18 th edn. New York: McGraw-Hill Inc, 2012;2631. 
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| 2. | Mahurkar S, Reddy DN, Rao GV, Chandak GR. Genetic mechanisms underlying the pathogenesis of tropical calcific pancreatitis. World J Gastroenterol 2009;15:264-9.
[PUBMED] |
| 3. | Kakaraparthi S, Prabhu R. Chronic Calcific Pancreatitis with Concurrent Autoimmune Hemolytic Anemia: A Case Report. Webmed Central Pancreas 2011;2:WMC001905.
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| 4. | Banks PA. Epidemiology, natural history, and predictors of disease outcome in acute and chronic pancreatitis. Gastrointest Endosc 2002;56:S226-30.
[PUBMED] |
| 5. | Schneider A, Suman A, Rossi L, Barmada MM, Beglinger C, Parvin S, et al. SPINK1/PSTI mutations are associated with tropical pancreatitis and type II diabetes mellitus in Bangladesh. Gastroenterology 2002;123:1026-30.
[PUBMED] |
[Figure 1], [Figure 2]
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