BES2020 BES 2020 Diabetic muscle infarction (1 abstracts)
1Department of Endocrinology and Nutrition, Cliniques universitaires Saint-Luc, UCL, Brussels, Belgium; 2Department of Medical Imaging, Cliniques universitaires Saint-Luc, UCL, Brussels, Belgium; 3Department of Anatomic Pathology, Cliniques universitaires Saint-Luc, UCL, Brussels, Belgium
Case: A 77-year-old woman, with a 50-year history of type 2 diabetes mellitus and multiple micro- and macrovascular complications, was hospitalized for a foot ulcer on a chronic Charcot foot. On admission, systematic anamnesis revealed back pain around L1-L2 for a week. There was no history of trauma or fever. Examination was normal except a symetrical loss of sensitivity on the feet related to his diabetic polyneuropathy. On admission, blood test showed an inflammatory syndrome with elevated C-reactive protein (CRP) at 191.3 mg/l (N<5 mg/l), leukocytosis at 13.770 10³/l and rhabdomyolyses with creatinine kinase (CK) at 8027 U/l (N: 20180 U/l). The glycosylated hemoglobin was in the target at 6.1%. Coronarography revealed a short minor stenosis on the anterior intraventricular artery. Magnetic resonance imaging (MRI) of the spine revealed an herniated disc and, incidentally, an increased signal intensity on T2 of the right gluteal muscle. To exclude myositis associated with connective tissue disease and infectious myopathies, we had searched antinuclear antibodies, antineutrophil cytoplasmic antibodies and done blood cultures who were negative. A muscle biopsy showed a necrotic and inflamed muscle. Finally, a PET-CT looking for other muscle lesions highlighted an onset of necrosis in the left gluteal muscle. The diagnosis of bilateral and asymptomatic diabetic muscle infarction was made. The treatment consisted of analgesia, aspirin and bed rest. The control after three months was favorable with a normalization of the blood test and a regression of the T2 hypersignal and the peripheral enhancement of the gluteal muscles. She underwent surgery for the hernia.
Discussion: Diabetic muscle infarction also referred as spontaneous diabetic myonecrosis is a rare but well-recognized complication of longstanding and poorly controlled diabetes mellitus with microvascular complications. First reported in 1965, less than 200 cases reports were published in the literature. Diabetic muscle infarction is more common in women and occurs in both type 1 and 2 diabetes mellitus. The mean age of onset is 44.6 years. The pathogenesis of this muscle lesion remains unclear but seems related to atherosclerosis, diabetic microangiopathy, vasculitis with thrombosis and ischemia-reperfusion injury. The typical clinical presentation includes acute pain in the affected muscle and local swelling. Diabetic muscle infarction occurs most often in the thigh muscles but other locations were reported. Bilateral affection occurs in less than 33% of cases. Biological findings are nonspecific such as elevated CK, CRP and leukocytes. MRI with intravenous contrast enhancement is the most useful diagnostic technique that shows an increased signal of the affected muscle in T2-weighted. Muscle biopsy can provide a definitive diagnosis by showing muscle necrosis and oedema as well as occlusion of arterioles and capillaries by fibrin but it is generally not recommended because it delays the recovery and is associated with recurrences. The treatment is conservative and includes rest, low-dose acetylsalicylic acid, analgesia and optimal glycemic control. The mean duration of symptoms is about 4 weeks. Recurrence rates exceeds 40% and usually involves different muscles.
Conclusion: We report a case of bilateral and asymptomatic diabetic muscle infarction as an unusual cause of elevated CK in a patient with long-stading diabetes mellitus.
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