Q J Med 2003; 96: 868-869
© 2003 Association of Physicians
Correspondence |
Acute pancreatitis and exacerbation of hepatitis B following reduced dose of prednisolone
Sir,Hepatitis virus type B (HBV) infects the pancreas1,2 and may cause acute pancreatitis.1–5 Immunosuppressive therapy results in enhanced replication of HBV and depressed host immunity. The discontinuation of therapy causes a rebound of the immune system, resulting in development of hepatitis. Here, we report a patient with underlying HBV infection, who had acute/non-fluminant hepatitis with acute pancreatitis after a decrease in dose of an immunosuppressive agent.
A 48-year-old Japanese male HBV carrier (HB surface antigen-positive) was diagnosed with Graves’ disease, and was treated with propylthiouracil 300 mg/day. After 8 days treatment, he developed a high fever. Examination revealed glomerular nephritis associated with positive perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA). The serum titre of p-ANCA was 179 IU/ml. Renal biopsy showed a crescentic glomerulonephritis. Propylthiouracil has been reported to be associated with ANCA-positive pauci-immune glomerulonephritis, and was therefore discontinued. He was then treated with corticosteroids and cyclophosphamide. Pulse therapy with 1000 mg of methylprednisolone for 3 days was followed by oral prednisolone (PSL) 60 mg/day and cyclophosphamide (CPA) 100 mg/day. Around the 4th week of PSL and CPA treatment, the patient suffered from chest pains. He was diagnosed as having ischaemic heart disease; isosorbide dinitrate and aspirin were started.
After 8 weeks CPA treatment, CPA was discontinued. Serum p-ANCA titres became negative after the 9th week of PSL treatment. At that time, serum total bilirubin (TB), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and amylase levels were within the normal ranges [0.4 mg (normal < 1.2), 13 IU/l (10–34), 18 IU/l (7–42), 59 IU/l (40–123), respectively]. CT scans showed no abnormal findings in liver or pancreas. The PSL dose was reduced by 5 mg every week after the 12th week of PSL treatment.
In the 18th week, when the PSL dose was 30 mg/day, the patient developed fever (38.5 °C) and slight epigastric pain. There was mild abdominal tenderness, but no rebound tenderness, back pain, nausea, or vomiting. Laboratory investigations indicated hepatitis and acute pancreatitis, with elevated leukocytes (from 10.5 x 104/ml 3 days before to 14.5 x 104/ml), C-reactive protein 19.5 mg/dl (normal < 1.0), AST 51 IU/l, ALT 123 IU/l, amylase 157 IU/l, urine amylase 750 IU/l (normal < 500), serum phospholipase A2 493 ng/dl (130–400) and serum trypsin 820 ng/ml (110–460). Serum blood urea nitrogen and creatinine levels were normal (16 mg/dl and 0.8 mg/dl, respectively). Ultrasonography of the abdomen revealed slight swelling in the pancreas. Serology demonstrated activated HBV with an increase of the HBV-DNA concentration (3726) in serum. Blood cultures were negative. The patient’s abdominal symptoms resolved after 3 days, although serum amylase levels increased up to 167 IU/ml but then normalized after 7 days. Hepatitis also improved with occasional therapy (glycylone and famotidine). Serum TB, AST, and ALT increased to 32.0 mg/dl, 686 IU/l, and 1315 IU/l, respectively, and normalized 8 weeks after the symptoms appeared (26th week of PSL treatment). CT findings at that time were consistent with acute pancreatitis; diffuse swelling and multiple large cysts of the pancreas were visible (Figure 1). The patient was discharged on 10 mg PSL daily, and no relapse of hepatitis and pancreatitis has been seen during 6 months follow-up.
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Fulminant hepatitis is sometimes accompanied by acute pancreatitis as a complication, partly as a component of multiple organ failure. However, the occurrence of acute pancreatitis in non-fluminant hepatitis is rare; only several cases have been reported (reviewed in reference 4). No changes in drug administration except the PSL decrease coincided with the occurrence of hepatitis and pancreatitis. Although corticosteroids have themselves been associated with acute pancreatitis, in those patients the disorder developed within several days of administration, and improved after discontinuation.5,6 These drugs were therefore not the direct cause of the pancreatitis in our case. Other likely causes (alcohol ingestion, cholelithiasis) were also excluded.
The findings presented here therefore suggest that (i) HBV may cause acute pancreatitis and (ii) immune responses to HBV may play a role in the development of acute pancreatitis as well as hepatitis in HBV carriers. Unfortunately, details of the infection status (HBeAg/anti-HBeAb or HBV-DNA concentrations) before hepatitis are not available for this patient. We believe, however, that this is the first reported case of the development of acute pancreatitis and exacerbation of hepatitis B following the reduction in dose of an immunosuppressive agent.
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Second Department of Internal Medicine University of the Ryukyus Okinawa Japan. e-mail: ooshiro{at}aol.com
References
1. Cavallari A, Vivarelli M, et al. Fatal necrotizing pancreatitis caused by hepatitis B virus infection in a liver transplant recipient. J Hepatol 1995; 22:685–90.[CrossRef][Web of Science][Medline]
2. Shimoda T, Shikata T, et al. Light microscopic localization of hepatitis B virus antigens in the human pancreas. Possibility of multiplication of hepatitis B virus in the human pancreas. Gastroenterology 1981; 81:998–1005.[Web of Science][Medline]
3. de Oliveira LC, Rezende PB, et al. Concurrent acute hepatitis and pancreatitis associated with hepatitis B virus: case report. Pancreas 1998; 16:559–61.[Web of Science][Medline]
4. Mishra A, Saigal S, et al. Acute pancreatitis associated with viral hepatitis: a report of six cases with review of literature. Am J Gastroenterol 1999; 94:2292–5.[CrossRef][Web of Science][Medline]
5. Felig DM, Topazian M. Corticosteroid-induced pancreatitis. Ann Intern Med 1996; 124:1016.
6. Yoshizawa Y, Ogasa S, et al. Corticosteroid-induced pancreatitis in patients with autoimmune bullous disease: case report and prospective study. Dermatology 1999; 198:304–6.[CrossRef][Web of Science][Medline]
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