Drug-induced Acute Pancreatitis in a Bodybuilder

A Case Report

Seyed Ali Safizadeh Shabestari; Samuel B. Ho; Priyadarshini Chaudhary; Rahul A. Nathwani

Disclosures

J Med Case Reports. 2022;16(114) 

In This Article

Case Presentation

A 31-year-old Arab male bodybuilder presented to the emergency department with an acute onset of severe epigastric pain radiating to the back with associated nausea. He did not report any constitutional symptoms of weight loss, fever, chills, fatigue, or cardiovascular, respiratory, neurological, musculoskeletal, hematological, or endocrinological diseases. There was no significant medical or surgical history. There was no known malignancy, infection, trauma, or exposure to scorpions. Family history was insignificant, including for pancreatitis. The patient denied any history of smoking or alcohol consumption. His diet is protein-rich, with high meat consumption. He admitted to starting the following cocktail of drugs a month before: Halotestin (fluoxymesterone), Proviron (mesterolone), Masteron four times per week (drostanolone propionate), Winstrol four times per week (stanozolol), Nolvadex (tamoxifen), "test-E" two times per week (testosterone enanthate), "prop" four times per week (testosterone propionate), "tren" four times per week (trenbolone acetate), "clen" three times per week (clenbuterol), and multiple vitamin supplements. He was also injecting growth hormone five times per week from an inexpensive supplier at double the recommended dose.

On admission, he was hemodynamically stable. His physical examination revealed significant epigastric tenderness without rebound. Laboratory studies revealed slightly low hemoglobin: 12.9 (13.5–17.5) g/dL; normal white blood cell count (WBC): 9.2 × 109 (4.5 to 11.0) × 109/L; elevated C-reactive protein (CRP): 12.9 (13.5–17.5) g/dL; normal troponin, and creatinine: 0.713 (0.2–1.2) mg/dL; elevated creatine protein kinase (CPK): 221 (30–190) U/L; sodium (Na+): 137 130–145) mmol/L; potassium (K+): 4.57 (3.5–5.4) mmol/L; slightly elevated aspartate aminotransferase (AST): 47 (6–34) U/L; and total bilirubin: 22.70 (3.4–20.50) U/L, with normal remaining liver tests: alanine aminotransferase (ALT): 45 (0–55) U/L; alkaline phosphatase (AP): 33 (1–60) U/L; and elevated amylase and lipase: 525 (30–11) U/L and 503 (23–300) U/L, respectively. An abdominal CT scan with both oral and intravenous contrast revealed hepatomegaly and diffuse thickening and edema of the body and tail of the pancreas with peripancreatic fat stranding but no evidence of fluid collection or pancreatic necrosis (Figure 1). Based on clinical presentation and CT findings, the patient was diagnosed with acute pancreatitis with Bedside Index of Severity in Acute Pancreatitis (BISAP) score of 0 (< 1% risk of mortality), which is characterized by the absence of organ failure and local or systemic complications.

Figure 1.

Abdominal computed tomography in the axial plane showing diffuse thickening and edema of the body and tail of the pancreas with peripancreatic fat stranding and no evidence of pancreatic necrosis

To identify the cause of his acute pancreatitis, extensive history and workup with additional labs were done, including IgG4 levels, serum triglyceride levels, and serum calcium levels, all of which were normal. A hereditary pancreatitis gene panel revealed no evidence of CFTR, PRSS1, or SPINK gene mutations. He improved clinically with aggressive intravenous hydration and pain management and was discharged after 3 days. An abdominal ultrasound was performed a week later, showing slight hepatomegaly with no evidence of cholelithiasis, and a normal pancreas.

The most likely etiology for his pancreatitis was the mixture of drugs he had started using a month before his presentation, given the exclusion of all other possible causes and the temporal relation between the intake of the substances and the onset of symptoms. Subsequently, he was advised against using any further steroids, growth hormones, or other supplements. He has been symptom-free during a follow-up period of 1 year, with no further evidence of pancreatitis, which is another reason to suspect it was DIAP. Table 1 summarizes our case's timeline.

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