Vol 43 # 3 September 2011 - Kma.org.kw

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226 Duodenal Diverticulum Mimicking Pancreatic Abscess September 2011 pseudocyst, or pancreatic abscess has been reported [4] . One may be unable to distinguish duodenal diverticula on CT or MR (magnetic resonance) imaging, if their content is purely fluid. In a study of duodenal diverticula mimicking cystic pancreatic neoplasms, even retrospectively analyzing the images, they found that with only a single examination and without the benefit of past or future scans, it was not possible to definitively identify the diverticula in some cases [1] . CONCLUSION A duodenal diverticulum should be considered in the differential diagnosis of any cystic lesion identified between the duodenum and the head of the pancreas on CT or MR imaging. Thus careful review of imaging studies should always be performed. Further evaluation with barium studies and endoscopy are needed for confirmation prior to any surgical intervention. REFERENCES 1. Macari M, Lazarus D, Israel G, Megibow A. Duodenal diverticula mimicking cystic neoplasms of the pancreas: CT and MR imaging findings in seven patients. AJR Am J Roentgenol 2003; 180:195-199. 2. Mazziotti S, Costa C, Ascenti G, Gaeta M, Pandolfo A, Blandino A. MR cholangiopancreatography diagnosis of juxtapapillary duodenal diverticulum simulating a cystic lesion of the pancreas: usefulness of an oral negative contrast agent. AJR AmJ Roentgenol 2005; 185:432-435. 3. To’o KJ, Raman SS, Yu NC, et al. Pancreatic and peripancreatic diseases mimicking primary pancreatic neoplasia. Radiographics 2005; 25:949-965. 4. Hariri A, Siegelman SS, Hruban RH. Duodenal diverticulum mimicking a cystic pancreatic neoplasm. Br J Radiol 2005; 78:562-564. 5. Martínez Cecilia D, Arjona- Sánchez A, Gomez-Álvarez M, et al. Conservative management of perforated duodenal diverticulum: A case report and review of the literature. World J Gastroenterol 2008; 28:1949–1951.
September 2011 KUWAIT MEDICAL JOURNAL 227 Case Report Fenofibrate-Induced Rhabdomyolisis in a Dialysis Patient with Subclinical Hypothyroidism: Case Report Funda Sari, Metin Sarikaya, Ramazan Cetinkaya Division of Nephrology, Antalya Education and Research Hospital, Ministry of Health, Antalya, Turkey Kuwait Medical Journal 2011; 43 (3): 227-229 ABSTRACT Although there have been a few reports regarding fenofibrate-induced rhabdomyolysis in patients with hypothyroidism, there are no data in literature that this could occur in patients with subclinical hypothyroidism. We report a case of subclinical hypothyroidism and end-stage renal failure who presented with rhabdomyolysis while taking fenofibrate for dyslipidemia. Two weeks after beginning fenofibrate, a 54-year-old male patient with end-stage renal failure was admitted to our hospital with complaints of myalgia and muscle weakness. Laboratory tests revealed a creatine kinase of 51,858 U/l, thyroid stimulating hormone of 10.26 μIU/ml, free T3 3.61 pg/ml, free T4 0.74 ng/dl. Fenofibrate was stopped and tiroxin dosage increased. Hemodialysis was performed four times. During follow-up, serum creatine kinase level decreased to 160 U/l at the end of one week. Physicians should be aware of potentially lethal adverse effects including rhabdomyolysis after fenofibrate therapy in patients with subclinical hypothyroidism and end-stage renal failure. They should carefully follow-up hepatic and muscle enzymes. KEY WORDS: dyslipidemia, end-stage renal failure, myalgia INTRODUCTION Rhabdomyolysis is a biochemical and clinical syndrome resulting from skeletal muscle injury and the release of muscle cell components into the extracellular compartments [1] . The presenting clinical features are myalgia, myoglobinuria and an elevated serum creatine kinase [2] . Rhabdomyolysis results from inherited muscle enzyme deficiencies, toxins such as alcohol abuse and cocaine, trauma, drugs such as statins, muscle overexertion, infections, and other disorders [3] . Drug-induced rhabdomyolysis occurs rarely. Fenofibrate is a potent hypolipemic agent, widely used in patients with renal insufficiency in whom dyslipidemia is frequent. Rhabdomyolysis with the use of fenofibrate alone has been reported in a few cases [4-6] . Hypothyroidism is a predisposing factor for fenofibrate-induced rhabdomyolysis [7-9] . In hypothyroidism, mitochondrial activity in muscle cell and some metabolic activities including fatty acid catabolism are inhibited [9,10] . CASE REPORT A 54-year-old male patient was admitted to our hospital with complaints of myalgia and muscle weakness for the last week. His medical history revealed that totally thyroidectomy was performed for treatment of multinodular goiter 15 years ago. He was a case of end-stage renal failure secondary to hypertensive nephropathy treated with continuous ambulatory peritoneal dialysis (CAPD) for about 15 months. He was on aspirin 300 mg, calcium 1000 mg, folic acid 5 mg, amilodipine 10 mg, enapril 20 mg, iron 100 mg, calsitriol 0.5 ug and L-troksin 100 ug per day, and darbepoetin 0.25 ug/kg per week. Micronized fenofibate, 200 mg/day, was added to his medication because of an increasingly poor lipid control in spite of a low lipid diet two weeks ago. Indeed, before the fenofibrate therapy, his total triglyceride was noted to be 782 mg/dl (normal=50-179). The physical examination was completely normal except for muscle weakness. Routine laboratory tests revealed a creatine kinase (CK) of 51,858 U/l (normal range: 24-195), which was approximately 265 times the upper limit of normal. Further laboratory results showed hemoglobin 11.8 g/dl, white blood cell count 8500 /mm 3 , platelet count 317,000 mm 3 . The erytrocyte sedimentation rate was 36 mm/h. His blood urea nitrogen (BUN) was 62 mg/dl (normal range: 7 - 18), creatinine 8.5 mg/dl (normal range: 0.7-1.3), fasting blood glucose 90 mg/dl (normal range: 65 - 100), albumin 4 g/dl (3.5 - 5), potassium 4.8 mmol/l (normal range: 3.5 - 5.1), calcium 9.0 mg/dl (normal range: 8.2- 10.9), phosphorus 6.4 mg/dl (normal range: 2.7 - 4.5), Address correspondence to: Funda Sari, MD, Antalya Education and Research Hospital, Ministry of Health, Division of Nephrology, Antalya, Turkey. Tel: +90 242 2494400 Fax: +90 242 2494462, E-mail: fbahceci@inonu.edu.tr
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