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Clinical Specialist Department of Gynecology-Obstetrics Polyclinique Saint-André Reims, France
Clinical Specialist Department of Gastroenterology Clinique Saint-Vincent Epernay, France
Clinical Pharmacist Pharmacovigilance Regional Center Centre Hospitalier Universitaire (CHU) Reims
Director Pharmacovigilance Regional Center CHU 45 Rue Cognacq-Jay 51092 Reims, France fax 33 3 26 78 84 56 pharmacovigilance{at}chu-reims.fr
Published Online, October 4, 2005. www.theannals.com, DOI 10.1345/aph.1G292
Case Report. A 57-year-old woman, with no preexisting or primary hypertriglyceridemia (triglycerides 0.36 g/L, reference range 0.40-1.65), developed acute pancreatitis during treatment with sequential combined estradiol 2 mg/gestodene 0.05 mg oral therapy and hormone replacement therapy (HRT) in the management of menopausal symptoms and osteoporosis prevention. She had received treatment for 5 days when she was hospitalized for epigastric pain, nausea, and vomiting.
Laboratory tests revealed increased serum amylase and lipase levels at 1349 IU/L (reference range <53) and 3680 IU/L (<60), respectively; transaminase levels were normal. Also reported were elevated C-reactive protein level (228 mg/L; <10), hyperglycemia (glucose 181 mg/dL), and leukocytosis (white blood cell count 11.2 x 103/mm3). Abdominal ultrasound examination was normal.
HRT was discontinued, and the patient received a symptomatic treatment (analgesic). The following day, serum amylase and lipase levels decreased to 892 and 1643 IU/L, respectively; these levels normalized within a few days. She was discharged from the hospital 7 days later. The Naranjo probability scale indicated a probable association between HRT and acute pancreatitis in this case.2
Discussion. Acute pancreatitis is a common disease, with the incidence of relatively high morbidity and mortality rarely reported.3 Drug-induced acute pancreatitis presents with the same clinical profile as pancreatitis derived from other etiologic origins. Diagnosis is based on abdominal pain confirmed by blood tests denoting raised amylase levels, leukocytosis, and hyperglycemia and modified diagnostic imaging; however, none of these markers is pathognomonic.
Estrogens are an uncommon but known risk factor for pancreatitis in women with preexisting hyperlipidemia.4 Exogenous estrogens increase production of triglycerides and reduce levels of lipoprotein lipase and hepatic lipase, thus diminishing triglyceride clearance. Reduction in triglyceride clearance may lead to severe hypertriglyceridemia with pancreatitis.5 In an observational survey, Goldenberg et al.3 demonstrated the relationship between estrogen therapy and pancreatitis when triglyceride levels are significantly elevated.
To our knowledge, as of this writing, there has been only one case of acute pancreatitis reported with estrogen therapy and normal plasma lipid levels.6 Our case suggests that mechanisms other than hypertriglyceridemia may be responsible for the onset of pancreatitis during estrogen treatment. Yet, we recommend that plasma triglyceride levels be measured before exogenous estrogen administration to identify possible risk factors for pancreatitis.
References
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