Scientific Papers

Clopidogrel-induced non-diabetic hypoglycemia reported from Tikur Anbessa Specialized Hospital, Addis Ababa, Ethiopia: a case report | Journal of Medical Case Reports

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A 33-year-old Ethiopian male patient with a history of hypertension and hypertensive heart disease for the past 6 years but on treatment for 3 years on enalapril (5 mg po daily), bisoprolol (5 mg po daily), and aspirin (81 mg po daily).

He currently presents with a squeezing type of retrosternal chest pain, diaphoresis, and vomiting of ingested matter of 3 days duration, for which he was admitted to Gondar Hospital for 3 weeks and treated for possible acute coronary syndrome with dual antiplatelet therapy (aspirin and clopidogrel), and atorvastatin 80 mg po daily. However, there was no evidence of myocardial injury or ischemia on troponin, electrocardiogram, or echocardiography. After admission to the intensive care unit, he started to develop recurrent symptomatic hypoglycemia, with the lowest record being 21 mg/dl, which improves with eating. He was taking meals every 3 hour due to the symptoms. The measurements were confirmed in the hospital laboratory in addition to a glucometer-based investigation.

He has no personal or family history of diabetes mellitus, dyslipidemia, smoking, substance abuse, a history of change in mentation, or a family history of cardiac illness. All his family members are healthy, and they are not taking any drugs. The patient’s hypoglycemia was approached systematically based on guidelines recommendations [5]. There were no clinical or laboratory suggestions of hormonal deficiencies, critical illnesses, non-islet cell tumors, or others as causes of hypoglycemia. Among the drugs he was taking, bisoprolol was discontinued and shifted to diltiazem. However, his blood sugar was persistently low. On subsequent follow-up, clopidogrel was discontinued, and his blood glucose normalized since the next day of clopidogrel withdrawal. He has repeated measurements of blood sugar levels above 70 mg/dl.

There were no pertinent physical findings, including cardiac and chest evaluations. Basic laboratory tests, including complete blood count, renal function test, and serum electrolytes, were all normal. He also has normal HbA1C (4.8%), normal serum cortisol (18.9 mcg/dl), non-revealing urine analysis, normal thyroid function tests (Free T4 1.56 ng/dl, TSH 2.4 mIU/L), a normal coagulation profile (INR = 0.89, PT = 12.8 seconds, aPTT = 28.5 seconds), and normal 24-hour urine catecholamines (epinephrine 4.68 mcg, norepinephrine 28.56 mcg, dopamine 225.4 mcg, normetanephrine 380 mcg, metanephrines 80.46 mcg).

He has a normal resting sinus rhythm, but stress electrocardiography showed intermediate risk; he had exercise-limiting anginal pain before he achieved his estimated heart rate, and the exercise test was discontinued. Echocardiography showed normal 2D and Doppler imaging and no evidence of resting ischemia. The angiography finding was normal epicardial coronary arteries.

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