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 Table of Contents  
Year : 2022  |  Volume : 12  |  Issue : 1  |  Page : 49-52

Profile of patients with fibrocalculous pancreatopathy seen in Benin City, Nigeria

1 Department of Internal Medicine, University of Benin Teaching Hospital, PMB 1111, Benin City, Edo State, Nigeria
2 Department of Chemical Pathology, University of Benin Teaching Hospital, PMB 1111, Benin City, Edo State, Nigeria
3 Department of Ophthalmology, University of Benin Teaching Hospital, PMB 1111, Benin City, Edo State, Nigeria
4 Department of Medicine, University of Benin Teaching Hospital, PMB 1111, Benin City, Edo State, Nigeria

Date of Submission06-Apr-2022
Date of Decision14-Jul-2022
Date of Acceptance16-Jul-2022
Date of Web Publication02-Sep-2022

Correspondence Address:
Prof. Andrew E Edo
Department of Internal Medicine, University of Benin/University of Benin Teaching Hospital, Benin City, Edo State
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajem.ajem_5_22

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Fibrocalculous pancreatopathy is a rare cause of diabetes mellitus in the young. We report two cases of fibrocalculous pancreatopathy in two young female Nigerians. The first patient was a 21-year-old student who presented with polyuria, weight loss, and itching of the vulva. Random blood sugar was 272 mg/dL. Abdominal X-ray showed pancreatic calcification. The second patient was a 20-year-old student who presented with complaints of polyuria, weight loss, and amenorrhea. Her fasting blood sugar was 336 mg/dL. Urinalysis confirmed the presence of proteinuria++, glucosuria+, ketonuria++; urine βHCG was found to be negative, and HbA1c was 12.7%. Plain abdominal X-ray showed pancreatic calcifications. Their clinical diagnosis was fibrocalculous pancreatopathy. Hyperglycemia was controlled with insulin in both the patients.

Keywords: Diabetes mellitus, fibrocalculous pancreatopathy, pancreatic calcification

How to cite this article:
Edo AE, Idogun SE, Edo GO, Eregie A. Profile of patients with fibrocalculous pancreatopathy seen in Benin City, Nigeria. Afr J Endocrinol Metab 2022;12:49-52

How to cite this URL:
Edo AE, Idogun SE, Edo GO, Eregie A. Profile of patients with fibrocalculous pancreatopathy seen in Benin City, Nigeria. Afr J Endocrinol Metab [serial online] 2022 [cited 2023 Jun 10];12:49-52. Available from: http://www.ajemjournal.org/text.asp?2022/12/1/49/355335

  Introduction Top

Fibrocalculous pancreatopathy (FCPP) is a secondary form of diabetes mellitus. FCPP is now classified under the class “others” in the new classification of diabetes mellitus.[1] Its etiology is not well defined. It is commoner in the poorer developing countries of the world. It was also termed tropical pancreatic disease. It is different from the typical type 1 diabetes mellitus (DM). They may have features of malnutrition because of the involvement of the exocrine function of the pancreas resulting in steatorrhea. It is usually characterized by the presence of malnutrition and pancreatic calcification and DM in a non-alcoholic patient. FCPP has been reported in all age spectra from pediatric age to the elderly.[2],[3] The diagnosis is made before the age of 30 years in most patients. Mohan et al.[4] reported a decrease in the prevalence of FCPP from 1.6% during 1991–1995 to 0.2% during 2006–2010. The decline in FCPP probably reflects improved nutrition. In Ethiopia, no single case of malnutrition-related diabetes mellitus was found.[5] FCPP was reported in a 20-year-old Ugandan female.[6] Olurin and Olurin[7] found pancreatic calcification in 45 patients in the late 1960s. Thirty-seven of them had DM. Steatorrhea was documented in 15 (33%) of them. Nzeh and Erasmus[8] found pancreatic calcification in 4 (5.2%) of the 77 cases of DM reviewed in Ilorin. The rarity of DM in young Nigerians was demonstrated by Akanji,[9] who found only 45 out of 756 DM presented when aged 15–30 years in 1984. Akanji[10] found pancreatic calcification in17% of 30 young patients with DM. FCPP has scarcely been reported in Nigeria after the year 2000. We report two cases of FCPP in two female Nigerians.


Patient (OA) was a 21-year-old student who presented with polyuria, weight loss, and vulvar itching. There was no history of abdominal pain or steatorrhea. There was no family history of DM. On examination, the patient was afebrile, not pale and anicteric. Pulse rate was 90/minute, regular, normal volume. Blood pressure was 120/80 mmHg. Height is 1.65 m, weight 59 kg, waist circumference 81 cm, hip circumference 103 cm, BMI 21.67 kg/m2.

Results of investigations: Urinalysis: glucosuria (+), RBC 4–5, trace proteinuria, and no ketones. Random blood sugar was 272 mg/dL. Lipid profile: total cholesterol 173 mg/dL, triglyceride 93 mg/dL, high-density lipoprotein (HDL) cholesterol 65 mg/dL, low-density lipoprotein (LDL) cholesterol 87 mg/dL. Plain abdominal X-ray showed pancreatic calcification [Figure 1].
Figure 1: Arrow pointing to pancreatic calcifications

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Treatment given: Premeal subcutaneous soluble insulin was administered to control hyperglycemia. She was discharged home on Mixtard 30: 24 U am, 12 U pm. At follow-up 2 weeks later, fasting blood glucose was 105 mg/dL, and BP was 110/80 mmHg. The insulin dose was reduced to 20 U am and 10 U pm. She has not been regular with her clinic attendance.


ES was a 20-year-old student who presented with complaints of polyuria, weight loss, and amenorrhea. There was no abdominal pain or a change in bowel habit. There was no steatorrhea. She had some hyperpigmented patches on the neck and on the right hand. There was no family history of DM in any first-degree relatives. On examination, the patient was underweight, afebrile, not pale, and anicteric. Fasting blood sugar was 336 mg/dL. Result of electrolytes: sodium 141 mmol/L, potassium 4.6 mmol/L, chloride 100 mmol/L, bicarbonate 22 mmol/L, urea 31 mg/dL, serum creatinine 0.5 mg/dL. Urinalysis: specific gravity 1.030, pH 6, and proteinuria ++, glucosuria +, blood +++, ketones ++, anion gap 23.6, serum osmolality 315 mOsm/kg; urine β-human chorionic gonadotropin-negative; lipid profile: total cholesterol 130 mg/dL, HDL 55 mg/dL, triglyceride 223 mg/dL, LDL 31 mg/dL; liver function test: aspartate transaminase 14 IU/L, alanine transaminase 8 IU/L, alkaline phosphatase 223 IU/L, total protein 6.5 g/dL, albumin 4.0 g/dL, total bilirubin 0.5 mg/dL, conjugated bilirubin 0.2 mg/dL; serum calcium 6.6 mg/dL (decreased) and HbA1c 12.7% (increased). Retroviral screening was negative for HIV 1 and HIV 2. Chest X-ray was normal. Plain abdominal X-ray showed pancreatic calcifications [Figure 2].
Figure 2: Erect plain abdominal X-ray showing nodular calcifications overlying the body of L1 and L2, consistent with pancreatic calcifications. There is also a huge rounded ring calcific density within the pelvis consistent with urinary bladder wall calcification

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There was a huge rounded ring calcific density within the pelvis consistent with urinary bladder wall calcification. No ovum of schistosomiasis haematobium was found in the urine.

She was managed as a case of diabetic ketoacidosis with intravenous 0.9% normal saline infusion and soluble insulin. She was discharged home on subcutaneous insulin. Patient was not regular with her follow-up clinic appointments. She presented 4 years later in the Emergency Room with a referral from a peripheral hospital stating that she had renal impairment and needed dialysis. She died the same day from presumed renal impairment.

  Discussion Top

FCPP commonly has features of malnutrition, abdominal pain, and steatorrhea.[1] The exact pathogenetic mechanism(s) responsible for the development of FCPP is not known; malnutrition, dietary toxins (e.g., cyanide present in cassava), genetic and immunological factors, and lack of micronutrient antioxidants have all been proposed.[11],[12] The serine protease inhibitor Kazal type 1 (SPINK1) is an important gene for FCPP susceptibility, although other known or unknown genetic or environmental factors are necessary to precipitate pancreatic disease.[13] SPINK1 N34S mutations have been reported in 33–55% of the patients with FCPP in the Indian subcontinent.[14] A female preponderance was reported among 83 children and adolescents with FCPP admitted in a Pediatric Unit in Bangladesh over a 7-year period. Ninety percent of them were females.[15] Abubakar et al.[16] reported a case of FCPP in a Nigerian girl. Kibirige et al.[6] also reported a case of FCPP in an adolescent in Uganda. The reasons for this observed female preponderance are not known.

Our patients did not have abdominal pain or steatorrhea. This is similar to the case reported by Abubakar et al. The absence of steatorrhea was also noted in the report by Kibirige et al.[6] Steatorrhea is rare in patients with FCPP in areas with low dietary fat intake.[17] Ketosis is rare among patients with FCPP. This is because of the residual pancreatic beta-cell reserve and a low glucagon reserve and decreased adipose tissue mass.[18] ES had ketosis which was also documented in the report by Abubakar et al. ES was underweight and indigent. She was unable to procure regular supply of insulin to control hyperglycemia. OA has also been irregular with clinic attendance, sometimes defaulting clinic for several months. These cases are being reported to highlight the fact that a high index of suspicion is needed to make the diagnosis of FCPP, especially in the absence of steatorrhea and abdominal pain in newly diagnosed young diabetic patients.

There were challenges in managing these patients. There were serious financial constraints in managing ES. The required investigations could not be done as requested. The Endocrine Unit had to donate insulin to ES on several occasions. Blood glucose monitoring was poor. Patients were not regular with their clinic appointments. ES had calcification of the bladder but no ovum of schistosomiasis haematobium was found in her urine. There were no renal stones seen. Her serum calcium levels were low. Schistosomiasis (Schistosoma haematobium) was associated with pancreatic calcification in three patients reported by Akanji.[10] In one of them, both the pancreas and the urinary bladder were calcified and there were schistosoma ova in the urine. There is no reported causal relationship between schistosomiasis and pancreatic calcification.

Long-term survival of patients with fibrocalculous pancreatic diabetes appears to have improved possibly because of earlier diagnosis, better management of diabetes, and improved nutrition. Diabetic nephropathy was the main cause of death in patients with FCPP. Pancreatic cancer, malnutrition, and infections were also important contributors to mortality.[19] ES died of presumed renal impairment.

Despite the scarce reports of FCPP in our locale, a high index of suspicion is needed so we do not miss such cases in our daily practice as these patients may not present with the classic symptoms of abdominal pains steatorrhea and malnutrition.

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  References Top

American Diabetes Association: World Health Organization. Definition, Diagnosis and Classification of Diabetes Mellitus and its Complication. Report of a WHO Consultation. Geneva: WHO; 1999.  Back to cited text no. 1
Papita R, Nazir A, Anbalagan VP, Anjana RM, Pitchumoni C, Chari S, et al. Secular trends of fibrocalculous pancreatic diabetes and diabetes secondary to alcoholic chronic pancreatitis at a tertiary care diabetes centre in South India. JOP 2012;13:205-9.  Back to cited text no. 2
Bashir MI, Misgar RA, Wani AI, Gupta V, Masoodi SR, Chandak GR, et al. Juvenile fibrocalculous pancreatopathy—A patient report. J Pediatr Endocrinol Metab 2006;19:947-50.  Back to cited text no. 3
Mohan V, Suresh S, Suresh I, Ramachandran A, Ramakrishnan S, Snehalatha C, et al. Fibrocalculous pancreatic diabetes in the elderly. J Assoc Physicians India 1989;37:342-4.  Back to cited text no. 4
Lester FT A search for malnutrition-related diabetes mellitus among Ethiopian patients. Diabetes Care 1993;16:187-92.  Back to cited text no. 5
Kibirige D, Kibudde S, Mutebi E Fibrocalculous pancreatic diabetes in a young Ugandan patient, a rare form of secondary diabetes. BMC Res Notes 2012;5:622.  Back to cited text no. 6
Olurin EO, Olurin O Pancreatic calcification: A report of 45 cases. Br Med J 1969;4:534-9.  Back to cited text no. 7
Nzeh DA, Erasmus RT Pancreatic calcification in diabetes mellitus at Ilorin, Nigeria. Trop Doct 1990;20:121-3.  Back to cited text no. 8
Akanji AO Malnutrition-related diabetes mellitus in young adult diabetic patients attending a Nigerian diabetic clinic. J Trop Med Hyg 1990; 93:35-8.  Back to cited text no. 9
Akanji AO Clinical experience with adolescent diabetes in a Nigerian teaching hospital. J Natl Med Assoc 1996;88:101-5.  Back to cited text no. 10
Bhatia E, Choudhuri G, Sikora SS, Landt O, Kage A, Becker M, et al. Tropical calcific pancreatitis: Strong association with SPINK 1 trypsin inhibitor mutations. Gastroenterology 2002;123:1020-5.  Back to cited text no. 11
Whitcomb DC, Gorry MC, Preston RA, Furey W, Sossenheimer MJ, Ulrich CD, et al. Hereditary pancreatitis is caused by a mutation in the cationic trypsinogen gene. Nat Genet 1996;14:141-5.  Back to cited text no. 12
Hassan Z, Mohan V, Ali L, Allotey R, Barakat K, Faruque MO, et al. SPINK1 is a susceptibility gene for fibrocalculous pancreatic diabetes in subjects from the Indian subcontinent. Am J Hum Genet 2002;71: 964-8.  Back to cited text no. 13
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.  Back to cited text no. 14
Zabeen B, Khaled Z, Nahar J, Nabi N, Mohsin F, Akhter S, et al. Cataract in children and adolescents with fibrocalculous pancreatic diabetes. Mymensingh Med J 2013;22:331-5.  Back to cited text no. 15
Abubakar LY, Habib AG, Iliasu G, Bello AK Fibrocalculous pancreatic diabetes in a Nigerian patient. Ann Afr Med 2010;9:107-8.  Back to cited text no. 16
Mohan V Fibrocalculous pancreatic diabetes (FCPD) in India. Int J Diabetes Dev Ctries 1993;13:14-21.  Back to cited text no. 17
Mohan V, Nagalotimath SJ, Yajnik CS, Tripathy BB Fibrocalculous pancreatic diabetes. Diabetes Metab Rev 1998;14:153-70.  Back to cited text no. 18
Mohan V, Premalatha G, Padma A, Chari ST, Pitchumoni CS Fibrocalculous pancreatic diabetes. Long-term survival analysis. Diabetes Care 1996;19:1274-8.  Back to cited text no. 19


  [Figure 1], [Figure 2]


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