Title : Hydrochlorothiazide induced acute on chronic pancreatitis.
Abstract:
A 75-year-old male with hypertension and GERD, who was a lifelong non-smoker, and consumes very little alcohol presented to our service with acute epigastric pain. He complained of intermittent mild nausea for the past 6 months. CT scan of the abdomen & pelvis showed acute pancreatitis with pancreatic parenchymal atrophy and few calcifications without necrosis (Figure 1). All these findings were new to the patient. His gallbladder was laparoscopically removed 19 years ago. He was started on lisinopril/hydrochlorothiazide by his cardiologist about a year ago and the dosage was increased 10 days prior arriving to our hospital. He did not disclose his chronic nausea to his cardiologist during follow-up appointments. His initial lipase was 69, LFTs and alkaline phosphatase were normal, and triglyceride was 127. His blood ethanol level was <10. MRCP showed normal pancreatic duct and Common Bile Duct (CBD). Ultrasound of the abdomen showed a 7 mm CBD with no sonographic Murphy's sign, stones, or evidence of biliary ductal involvement. His ranson criteria on admission was 2(Age >55 & WBC > 16K) and 48hours later it was 3 (Age, WBC >16K, Fluids needed >6L in 48h). He had persistent leukocytosis that was treated with Zosyn. The Lisinopril/HCTZ was discontinued, and his condition slowly improved in the next 48 hours. His Lipase did not worsen, and his amylase & LFT levels stayed within the normal range during the entire course of the admission. His blood pressure was maintained well on Carvedilol, and he was discharged three days later after aggressive fluid hydration and tolerating a low-fat diet.
Pancreatitis is a morbid condition with a mortality rate up to 55%. Common causes are gallstone, elevated triglycerides or alcohol induced. This patient had mild, nonspecific symptoms for over 6 months which we suspect was from ongoing pancreatitis. By the time he came to our institution, he had developed an acute exacerbation of his chronic pancreatitis. His labs did not show significantly elevated Lipase. An important thing to note that drug induced pancreatitis can manifest in many forms which can include overt image/lab findings and/or subtle image/lab findings. In our case the imaging studies showed clear inflammation of the pancreas whereas the lab work showed only mild inflammation with an elevated lipase of 70, the lab cutoff at our institution was 60. HCTZ has known to cause pancreatitis which has been documented as early as 1959. There are no published reports of Lisinopril causing pancreatitis. There are multiple theories explaining this including pancreatic duct constriction, drug induced hypercalcemia/hypertriglyceridemia and many other unknown forms of cytotoxic and metabolic effects which are not clearly understood. Since HCTZ is a common anti-hypertensive drug, clinicians must have a strong suspicion for uncommon side effects when patients are presenting with nonspecific GI symptoms while being on the drug.
