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| LETTER TO EDITOR |
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| Year : 2010 | Volume
: 9
| Issue : 2 | Page : 107-108 |
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Fibrocalculous pancreatic diabetes in a Nigerian patient
LY Abubakar, AG Habib, G Iliasu, AK Bello
Department of Medicine, Aminu Kano Teaching Hospital, Kano, Nigeria
| Date of Web Publication | 28-Jun-2010 |
Correspondence Address:
L Y Abubakar
Department of Medicine, Aminu Kano Teaching Hospital, PMB 3452, Kano
Nigeria
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1596-3519.64744
How to cite this article:
Abubakar L Y, Habib A G, Iliasu G, Bello A K. Fibrocalculous pancreatic diabetes in a Nigerian patient. Ann Afr Med 2010;9:107-8 |
Sir,
Tropical chronic pancreatitis (TCP) is a juvenile form of chronic calcific nonalcoholic pancreatitis seen almost exclusively in the developing countries of the tropical world. The classical triad of TCP is abdominal pains, diabetes mellitus (DM) and steatorrhea. When DM is present, it is called fibrocalculous pancreatic diabetes (FCPD), a late stage of the disease spectrum. Distinctive features of TCP are younger age at onset, a more aggressive course of the disease and presence of large intraductal calculi. Pancreatic calculi are the hallmark for diagnosis of TCP, and in noncalcific cases ductal dilatation seen on imaging helps in identifying the disease. [1] In the past, FCPD had been reported from all over the tropics, [1],[2],[3] but lately most reports are from south Asia, [1],[4] with fewer reports from Sub-Saharan Africa. Here a case is presented highlighting its manifestations and peculiarities in a Nigerian.
A 12-year-old girl presented with a 2-week history of polyuria, polydipsia, lethargy and weight loss despite good appetite. She had a 4-year history of intermittent central abdominal pain that radiated to the back, with no diarrhea, steatorrhea or jaundice. She had no similar illness in the past and was not a known sickle-cell disease or diabetes mellitus patient. As an infant, up to 18 months of age, she had mixed feeding with breast milk and corn pap, following which she was introduced to the family diet consisting of yams, beans, sorghum, rice and occasionally cassava flour meals. She neither took alcohol nor smoked cigarette. She was a primary IV pupil, and her performance in school had been average. She is the fourth of the 5 siblings, and her siblings were healthy. Her paternal grandmother and aunt had DM.
On examination she was acutely ill-looking and had bilateral parotid enlargement [Figure 1] with some dehydration. She weighed 38.0 kg and measured 1.49 m in height, giving a body mass index (BMI) of 17.1 kg/m 2 . Initial investigations showed random blood sugar of 24.0 mmol/L, significant glycosuria, trace of ketonuria but without proteinuria. Serum bicarbonate was 15 mmol/L with an anion gap of 20.6 mm/L. Her stool, liver and renal function tests were normal. Serum amylase was 37 u/L (normal range, 20-112 u/L). She had anemia with a hematocrit of 26%. Plain abdominal radiograph and ultrasound scan showed pancreatic calcifications [Figure 2]. She was admitted for evaluation and treatment. The patient and her parents were appropriately advised on lifestyle modifications, including dietary discretion. Glycemic control was achieved with a total of 60 units of soluble insulin daily, and the patient was discharged home on insulin regimen of a mixture of soluble and intermediate-acting insulin subcutaneous injection twice daily. The patient is now being followed up as an outpatient and is doing well.
Informed consent was obtained from the patient and her parents for this report, and approval was obtained from the hospital ethical committee of the study center.
The case illustrates new-onset DM, most likely secondary to FCPD, in a Nigerian. It suggests that FCPD may present without diarrhea, steatorrhea or ketonuria. It also shows that serum amylase, a marker of pancreatic inflammation, may be normal. The latter suggests chronic fibrotic 'burnt-out' pancreatic disease. Several possible mechanisms of causation have been suggested to explain development of TCP/FCPD; they include initial stasis due to prolonged lack of proteinaceous foods; and blockage of the pancreatic ducts by laminated secretions or inspissated mucus plugs, which enlarge with repeated infection and ultimately calcify [Figure 1],[Figure 2],[Figure 3]. Other mechanisms include cassava toxicity (cyanogens), genetic factors and oxidative stress. [1],[2] However, these mechanisms have not been consistently confirmed. Opinion is divided on whether FCPD is a part of the TCP spectrum or a different disease entity. [1],[4] DM is usually quite severe and insulin-requiring type, though ketosis resistant. Patients require large insulin doses, but macrovascular complications are less common than in type 1 DM. Both endocrine and exocrine functions may be impaired, and pancreatic enzyme supplements are used for relief of abdominal pains and steatorrhea. Surgery may be required; ductotomy, stone clearance and drainage may give good results. [5] Causes of deaths include diabetic nephropathy and pancreatic adenocarcinoma.
 References | |  |
| 1. | Barman KK, Premalatha G, Mohan V. Tropical chronic pancreatitis. Postgrad Med J 2003;79:606-15.  [PUBMED] [FULLTEXT] |
| 2. | Nwokolo C, Oli J. Pathogenesis of juvenile tropical pancreatitis syndrome. Lancet 1980;1:456-9. [PUBMED] [FULLTEXT] |
| 3. | Yakubu AM, Garg SK, Umar BA, Quaitey GE, Osuide J. Juvenile tropical pancreatitis syndrome in northern Nigeria: A case report. Ann Trop Paediatr 1984;4:79-82. |
| 4. | Khan AA, Ali L. Tropical calcific pancreatitis and fibrocalculus pancreatic diabetes in Bangladesh. J Gastroenterol Hepatol 1997;12:S48-52. [PUBMED] |
| 5. | Ramesh H, Augustine P. Surgery in tropical pancreatitis: Analysis of risk factors. Br J Surg 1992;79:544-9. [PUBMED] |
[Figure 1], [Figure 2], [Figure 3]
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