|Year : 2014 | Volume
| Issue : 1 | Page : 56-57
Unusual presentation of acute pancreatitis in falciparum malaria
Saikat Ghosh1, Somak Kumar Das1, Anand Sharma2
1 Department of Medicine, College of Medicine and JNM Hospital, Kalyani, Nadia, West Bengal, India
2 Department of Medicine, College of Medicine and Sagore Dutta Hospital, Kamarhati, West Bengal, India
|Date of Acceptance||17-Dec-2013|
|Date of Web Publication||20-Mar-2014|
Somak Kumar Das
A/14, 2nd Floor, Katjunagar, Jadavpur, Kolkata 700 032, West Bengal
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Malaria is known for its protean manifestations and multi systemic complications. Acute pancreatitis as a consequence of falciparum malaria is rare in the literature. We report a case of falciparum malaria complicated by acute pancreatitis.
Keywords: Acute pancreatitis, falciparum malaria, pain abdomen
|How to cite this article:|
Ghosh S, Das SK, Sharma A. Unusual presentation of acute pancreatitis in falciparum malaria. Trop Parasitol 2014;4:56-7
| Introduction|| |
Plasmodium falciparum malaria is a very commonly encountered disease in eastern India. It presents most commonly as pyrexia and altered sensorium, but has been seen to affect organs such as kidney and the liver commonly. Falciparum malaria affecting the pancreas is a rare occurrence and we report such a case in view of its rarity.
| Case Report|| |
The present case report is about a 40-year-old male patient who presented with high-grade fever associated with chills, jaundice vomiting and abdominal pain for 4 days. There was no history of cough, burning micturition, diarrhea or altered sensorium. On physical examination, he was alert, but febrile (103° Fahrenheit) with mild jaundice. He gradually became drowsy 3 days after admission. Systemic examinations were within the normal limit except epigastric tenderness and abdominal distension with normal bowel sounds. Laboratory investigations revealed hemoglobin - 10.2 g/dl, total leucocyte count - 15,100 (with Neutrophil - 87%) and platelets - 2.75 lacs/cu.mm. Peripheral blood smear revealed ring forms of P. falciparum. Immunochromatographic test for P. falciparum histidine-rich protein 2-based assay was strongly positive. Liver function testing showed serum Total Bilirubin - 4.4 mg/dl (Direct Bilirubin - 2 mg/dl) and serum aminotransferases and alkaline phosphatase were within normal limits. Serum amylase was 525 IU/L and serum lipase was 250 IU/L. Renal function and electrolytes were normal (Serum urea - 32 mg/dl, serum creatinine - 1.2 mg/dl, serum sodium - 140 meq/L and serum potassium - 4.1 meq/L). Urine and blood cultures came out to be sterile. Serum calcium was 9.2 mg/dl and fasting lipid profile was within the normal limits (cholesterol - 170 mg/dl, triglycerides - 103 mg/dl, high density lipoprotein - 36 mg/dl, low density lipoprotein - 114 mg/dl and very low density lipoprotein-20 mg/dl). Chest X-ray was normal and abdominal X-ray showed "Ileus" without air-fluid levels. Ultra sonography abdomen demonstrated an edematous, enlarged pancreas with minimal fluid in the peritoneal cavity. Computed tomography (CT) scan of the abdomen revealed edematous, enlarged pancreas with multiple fluid collections around pancreas and in the peritoneal cavity [Figure 1]. A diagnosis of severe falciparum malaria with acute pancreatitis (Grade E, CT severity index-4) was made and treatment was initiated with intravenous artesunate. There was marked improvement in his clinical symptoms in next 48 h. Acute pancreatitis was managed with analgesics, hydration and supportive therapy. Ryle's tube was initially instituted for bowel rest. After 3 days, his spikes of fever came down. From day 5, he started tolerating oral feeds. His pain abdomen and jaundice subsided after 8 days. He was discharged after a hospital stay of 12 days. On his follow-up visit, 2 months later, he was symptom free and doing well.
|Figure 1: Computed tomography scan (upper abdomen) revealed edematous, enlarged pancreas with multiple fluid collections around pancreas and in peritoneal cavity|
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| Discussion|| |
Abdominal pain is not an uncommon occurrence in Falciparum malaria. In their series of 348 malaria patients, Mahmood et al. found abdominal pain in 23 (21.29%) patients.  It can be attributed to varied causes, acalculous cholecystitis,  splenic rupture,  splenic infarction,  splenic torsion  being the more common ones. Falciparum malaria is a rare cause of acute pancreatitis in literature. A single case of pancreatitis was found to be caused due to falciparum malaria in a series of 105 patients published in 1907.  From India, there have been few isolated case reports of falciparum malaria causing acute pancreatitis. In an article in 2007, Sheshadri et al. have reported a case of acute pancreatitis with subdural hematoma in a patient with Falciparum malaria.
The mechanism proposed for the occurrence of this complication is ischemia of the pancreas caused by microvascular occlusion.  Acute hemolysis may also be a contributing factor. Autopsy studies have demonstrated occlusion of blood vessels of pancreas with parasitized red blood cells (RBC) and rosettes. 
Our patient had developed acute pancreatitis as evidenced by the high amylase and lipase levels as well as the typical appearance on imaging. As there were no evidence of any alcohol intake, gallstones, deranged lipid profile, hypercalcemia or toxin injury which are common causes of acute pancreatitis it can be inferred that the cause was falciparum malaria. His jaundice was probably due to hemolysis and ischemia of the liver due to microvascular occlusion by the parasitized RBCs. The improvement in both the jaundice and pancreatitis with the resolution of malaria bears further evidence of the association.
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