A 20 year old female patient was referred from a rural hospital to the endocrine unit with a three year history of generalised body weakness associated with progressive weight loss and recurrent generalised abdominal pain. She also had a five month history of polydipsia, polyuria and a day’s history of high grade fever with dysuria. She had no history of steatorrhoea.
Prior to her referral, she was being treated as a patient with type 1 DM for 4 months in a rural hospital. She also received analgesics and multi vitamins as treatment for the generalised abdominal pain and body weakness respectively. However, due to inadequate resources at that rural hospital, no specific clinical investigation was done to determine the cause of her recurrent abdominal pain. Her HIV serology was negative.
She was the 5th child of seven and all her siblings were healthy. There was no familial history of diabetes. She had no history of alcohol ingestion. Her diet since childhood was predominantly rich in carbohydrates.
Physical examination revealed a young lady with a low body mass index of 15.8kg/m2. She had sparse silky hair with bilateral cataracts, mild pallor of the mucous membranes, atrophic glossitis, leuconychia and bilateral pedal oedema. No skin changes or any bleeding tendencies were noted.
On the neurological examination, she was fully conscious but appeared apathetic. She had a slow thought process and poor short-term memory. Deep tendon reflexes, joint position and vibration senses were not assessesed because the patient was very unco-operative. Musculoskeletal examination revealed generalised muscle atrophy with tenderness of the bones and over the spine vertebrae.
At presentation to the endocrine unit, the haematological investigations done included a raised random blood sugar level of 26.7 mmol/l (normal: 3.5-7.7). The complete blood count showed a leucocytosis of 21,900/mm3 (normal: 4,000-10,000), mild normocytic normochromic anemia of 10.8 g/dl (normal: 12–16) and a thrombocytopenia of 60,000/mm3 (normal: 150,000-400,000). She had severe hypoalbuminemia of 18.9g/dl (normal: 35–50) and a corrected hypocalcaemia of 7.2 mg/dl (normal: 9–10.5 mg/dl). The serum vitamin B12 levels were reduced (128.9 pg/ml [normal range: 204–900]). The lipid profile, renal and liver function tests were normal. The urinalysis showed glycosuria, numerous pus cells, mild proteinuria but no ketonuria. The stool analysis revealed no fat globules, ova and cysts. However, this was done without prior fat loading.
Assessment of the glycated haemoglobin (HbA1c) and fasting C-peptide levels were not done because of the high costs involved and were unavailable at the hospital at the time of the patient’s admission.
The abdominal X-ray showed multiple pancreatic calcifications (Figure 1). An abdominal ultrasound scan showed diffuse calcifications in the head, body, and tail of the pancreas.
A diagnosis of FPD with severe oedematous malnutrition and micronutrient deficiency complicated by a urological sepsis was made.
The patient achieved good glycemic control on pre-mixed insulin (Mixtard) in small doses of 10IU pre breakfast and 5IU pre supper. She also received pancreatic enzyme granules given with meals and the co-existing micro nutrient deficiencies were corrected with vitamin A, D, B12 and calcium replacement. The urinary tract infection was treated with oral ciprofloxacin.
She was adequately counselled on the features of both hypoglycemia and hyperglycemia since she could not afford a glucometer to do regular self blood glucose monitoring. She also received dietary counselling with emphasis on a high protein diet. She was discharged when she had greatly improved. All serial fasting blood glucose levels done prior to discharge were within the normal ranges. Unfortunately, she has been lost to follow-up because she could not afford the transport costs needed for the clinic reviews.
