Published online Dec 15, 1997. doi: 10.3748/wjg.v3.i4.248
Revised: June 3, 1997
Accepted: June 28, 1997
Published online: December 15, 1997
- Citation: Wang HG, Yang GZ, Li HY. Pancreatitis associated with herpes zoster: A case report. World J Gastroenterol 1997; 3(4): 248-248
- URL: https://www.wjgnet.com/1007-9327/full/v3/i4/248.htm
- DOI: https://dx.doi.org/10.3748/wjg.v3.i4.248
The etiology of acute pancreatitis has been well studied and is known to be diverse, but pancreatitis caused by herpes zoster (HZV) has rarely been reported. We encountered a case of pancreatitis associated with HZV in our hospital and report it below.
A 28-year-old woman was admitted to our hospital with complaints of anorexia, nausea and epigastric pain that had lasted for 6 d. The patient denied recent alcohol ingestion, previous food intolerance, jaundice or abdominal pain, and she had no history of peptic ulcer disease, hyperlipidemia, abdominal trauma or recent use of medication. Physical examination revealed umbilicated vesicles on an erythematous base at the right hypogastric region and extending dorsally along the right ribs. There was marked tenderness in the epigastric region, and auscultation revealed diminished bowel sounds. No abnormal mass or enlargement of the liver or spleen was detected by palpation. Both the Grey-Turner’s sign and Cullen’s signs were absent. Pelvic examination revealed no tenderness of the cervix or cul-de-sac. Initial laboratory tests included a white blood cell count of 7.7 × 109/L, hemoglobin level of 123 g/L, serum amylase of 603 U/L (normal, < 180 U/L), urine amylase of 3864 U/L (normal, < 1200 U/L), serum lipase of 2780 U/L (normal, < 100 U/L) and positive serum HZV (by PCR).
Abdominal ultrasound showed a normal liver, gallbladder, and pancreas. Bile ducts were not dilated. There was a small amount of fluid detected in the peritoneal cavity. The serum potassium level was 2.3 mmol/L, but the serum levels of calcium, cholesterol and triglycerides were normal. The diagnostic impression was acute pancreatitis and HZV. Treatment included intravenous fluids, electrolyte replacement, interferon and nasogastric suction. A week later, the patient’s abdominal pain disappeared gradually and she resumed eating. Repeated abdominal B-ultrasonography showed no fluid in the peritoneal cavity. The vesicles presence resolved.
Acute pancreatitis is a process of autodigestion of the pancreas caused by premature activation of zymogens, leading them to become active proteolytic enzymes. The etiology of acute pancreatitis is diverse and reported causes include the mumps virus, rubella virus, Coxsackie B virus, Epstein Barr virus and hepatitis A virus; however, the association between HZV and pancreatitis has rarely been reported.
The pathogenic mechanism underlying HZV-related pancreatitis remains unknown. One plausible mechanism for virus-associated acute pancreatitis is inflammation and destruction of pancreatic acinar cells directly induced by the virus. In the case described herein, HZV was detected in the serum by PCR and other coincidental etiologies, such as alcohol abuse, gallstone disease, drug-induced pancreatitis, trauma, hyperlipidemia, and ulcer diseases, were excluded by clinical examination and history taking.
Original title: China National Journal of New Gastroenterology (1995-1997) renamed World Journal of Gastroenterology (1998-).
L- Editor: Filipodia E- Editor: Liu WX