Keywords
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| Betamethasone; Case Report; Chemicals and Drugs Category; Pancreatitis; Risk Factors; Roxithromycin |
INTRODUCTION
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| Among macrolides, erythromycin [1, 2, 3] and less frequently clarithromycin [4, 5], have been responsible for drug-induced pancreatitis. To our knowledge, roxithromycin has only been involved in two cases of pancreatic disorders [6, 7]. Regarding glucocorticoids, their pancreatotoxicity still remains controversial despite several reports [8, 9]. |
| In the following, we report the case of a possible roxithromycin- and betamethasoneinduced acute pancreatitis occurring during the treatment of an upper respiratory tract infection. |
CASE REPORT
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| A 58-year-old man was admitted to the hospital in November 2001 presenting severe epigastric pain with dorsal and lumbar irradiation. Two days before admission, he had started taking roxithromycin (300 mg per day) and betamethasone (4 mg per day) for an upper respiratory tract infection. He had no notable past medical history except for having had an operation for a herniated disk in 1982. There was no history of alcohol or tobacco use nor had he had cholecystectomy; he had not undergone any other drug therapy and had never suffered from pancreatic disorders before. |
| Serum amylase and lipase were significantly elevated at 631 UI/L (reference values: 10 to 55 UI/L) and 1,240 U/L (reference values: less than 190 U/L), respectively, and CRP was at 14 mg/L (reference values: less than 2 mg/L). Other causes of pancreatitis such as hyperlipidemia and hypercalcemia, were excluded, and hepatic, renal and thyroid functions were found normal. Viral serodiagnostics for Epstein Barr virus, cytomegalovirus, hepatitis B virus, hepatitis A virus, hepatitis C virus, HIV and coxackie were negative. Bacterial serodiagnostics for Salmonella, Yersinia and Mycoplasma were also negative. Abdominal ultrasonography performed upon admission showed a hypoechogenic swollen pancreatic head (diameter: 35 mm) with a blurred contour but no abnormality of the biliary tracks. The computed tomography scan performed on the following day showed a harmonious moderate hypertrophy of the pancreatic head without any focal damage or collection. No irregularities existed regarding the main biliary track. Mild hepatic steatosis was noted after contrast medium injection. A nuclear magnetic resonance cholangiopancreatography was not performed since the clinical features were sufficient to confirm acute pancreatitis. |
| The patient’s clinical state quickly and spontaneously improved in the 48 hours following cessation of roxithromycin and betamethasone. Serum amylase and lipase returned to normal within a few days. A delayed endoscopic ultrasonography did not show any evidence of chronic pancreatitis, congenital abnormality of the pancreatic duct system or intraductal papillary mucinous tumor of the pancreas. |
DISCUSSION
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| In this case, the short delay between roxithromycin and betamethasone ingestion and the onset of the symptoms suggests an iatrogenic origin of the acute pancreatitis presented here. This is confirmed, first, by spontaneous clinical improvement and second, by the normalization of the biological pancreatic parameters upon cessation of both drugs. Finally, all the investigations performed (biological, ultrasonographic, endoscopic) as well as a rigorous questioning of the patient allowed us to exclude any other origin for this pancreatitis. Moreover, a 16 month follow up with no intake of these two drugs showed no reoccurrence. |
| Erythromycin pancreatic toxicity is described in many reports [1, 2, 3]; however, no specific study has been performed in animals. Roxithromycin has only been reported twice in pancreatic disorders. In the first report, Souweine et al. [6] described a case in which roxithromycin was administered immediately following a 6-day course of erythromycin. In the second report, de La Fuente Aguado et al. [7] observed a slight elevation of serum amylase and lipase three days after the introduction of roxithromycin in an HIV positive patient who had been treated by zidovudine and antitubercular therapy. |
| As for betamethasone and glucocorticoids in general, their pancreatic toxicity remains controversial despite several reports [8, 9]. |
| Our case suggests possible drug-induced acute pancreatitis. It sheds new light on glucocorticoid pancreatotoxicity and confirms the role of macrolides as potential pancreatotoxic drugs. |
References
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- Gumaste VV. Erythromycin-induced pancreatitis. Am J Med 1989; 86:725. [PMID 2729328]
- Hawksworth CR. Acute pancreatitis associated with infusion of erythromycin lactobionate. Br Med J 1989; 298:190. [PMID 2493857]
- Fang CC, Wang HP, Lin JT. Erythromycininduced acute pancreatitis. J Toxicol Clin Toxicol 1996; 34:93-5. [PMID 8632521]
- Liviu L, Yair L, Yehuda S. Pancreatitis induced by clarithromycin. Ann Intern Med 1996; 125:701. [PMID 8849171]
- Rassiat E, Michiels C, Jouve JL, Sgro C, Faivre J, Hillon P. Pancreatite aiguë après la prise de clarithromycine et de beta-methasone. Gastroenterol Clin Biol 2003; 27:123. [PMID 12594377]
- Souweine B, Fialip J, Ruivard M, Aumaitre O, Lavarenne J, Philippe P. Acute pancreatitis associated with roxithromycin therapy. DICP Ann Pharmacother 1991; 25:1137. [PMID 1803808]
- de la Fuente Aguado J, Prieto Lopez MI, Bordon JM, Rivera Gallego A, Sopena Perez-Arguelles B. Hiperamilasemia asociada a roxitromicina. An Med Interna 1993; 10:260. [PMID 7686052]
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- Di Fazano CS, Messica O, Quennesson S, Quennesson ER, Inaoui R, Vergne P, et al. Two new cases of glucocorticoid-induced pancreatitis. Rev Rhum Engl Ed 1999; 66:235. [PMID 10339782]
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