[Diabetic muscle infarct]. / Diabetischer Muskelinfarkt.

HISTORY AND CLINICAL FINDINGS: A 64-year-old diabetic man with secondary failure of treatment with oral hypoglycemic agents was admitted to our clinical department to initiate insulin therapy. The patient was otherwise in good health. Before his dismissal he acutely developed symptoms of pain in his left calf. In addition, the patient was unable to move his left leg and presented palpable pea-sized nodules of his left calf. INVESTIGATIONS: Laboratory investigations revealed elevated serum creatine kinase levels on day two after the onset of clinical symptoms (peak value: 2238 U/I). There was evidence for antinuclear antibodies, c-reactive protein was normal. An ultrasound investigation showed a focal edema or bleeding located to the musculus gastrocnemius. Duplex-sonography excluded thrombosis or embolisation. Magnetic resonance imaging showed a diffuse enhancement of signal intensity within the musculus soleus and in areals of the musculus gastrocnemius, as signs of increased blood supply. All clinical findings were consistent with the diagnosis of diabetic muscle infarction. TREATMENT AND COURSE: Under symptomatic treatment with tramadol, diclofenac ointment, and fragmented heparin serum creatine kinase returned to normal levels (105 U/I) within 14 days. In accordance, symptoms of local pain disappeared completely. After two weeks of treatment the patient was able to move his leg without pain. CONCLUSION: This is the first presentation of a patient with diabetic muscle infarction from the onset of symptoms until full recovery. In addition, this case confirms previous descriptions that this condition can be diagnosed by clinical and sonographic findings in combination with magnetic resonance imaging without invasive histologic techniques.

Activated platelets in subjects at increased risk of IDDM. DENIS Study Group. Deutsche Nikotinamid Interventionsstudie.

Activated platelets respond to activated leukocytes and endothelial cells via adhesion molecules linking inflammation and thrombosis. Platelets of recent-onset insulin-dependent diabetic (IDDM) patients have been shown to be activated independent of metabolic control. This study evaluates the levels of circulating activated platelets exposing adhesion molecules in healthy subjects at increased risk of IDDM (surface markers were: P-selectin (CD62), thrombospondin, lysosomal GP53 (CD63). From the DENIS and the ENDIT screening programmes 19 identified islet cell antibody positive (titre > or = 20 Juvenile Diabetes Foundation units) first degree relatives of IDDM patients (male/female 9/10; age 22 +/- 15 years; body mass index (BMI): 20.0 +/- 4.3 kg/m2) with clearly normal metabolism (HbA1: 6.1 +/- 0.8%; fasting blood glucose: 4.95 +/- 0.67 mmol/l) were available for this investigation. Platelet CD62 as well as thrombospondin and CD63 expression were determined by flow cytometry. We matched 50 normal volunteers for age (29 +/- 6 years), anthropometric measures (male/female 26/24; BMI: 22.3 +/- 2.8 kg/m2) and metabolic parameters (HbA1: 5.8% +/- 0.3; fasting blood glucose: 4.41 +/- 0.53 mmol/1) served as control subjects. The mean number of CD62+ platelets was increased 3.2-times in prediabetic patients: 1.94 x 2.91 (+/- 1) vs 0.60 x 1.83 (+/- 1%), p < 0.0001. Thrombospondin+ and CD63+ platelet levels were concomitantly increased (1.45 x 2.38( +/- 1)/5.97 x 2.89 (+/- 1)% vs 0.52 x 2.01 (+/-1)/1.64 x 2.26 (+/-1)%, p < 0.0001 for both comparisons). Thus, intravasal platelet activation is already present in potentially prediabetic subjects representing an antecedent, potentially pathogenic feature of IDDM.

Exposure of adhesion molecules on activated platelets in patients with newly diagnosed IDDM is not normalized by near-normoglycemia.

It has been suggested that platelet hyperactivity contributes to the early evolution of diabetic vascular disease per se. This study directly evaluates the level of intravascular platelet activation in newly diagnosed IDDM patients before and after tight metabolic control. Platelet activation was determined by the Duesseldorf-III flow cytometry assay in 21 recent-onset hyperglycemic IDDM patients before insulin, after 3 days of treatment with intravenous insulin, and after 14 and 60 days of intensified conventional insulin therapy. The intravasal platelet activation status was quantified by the percentage of platelets exposing the activation-dependent molecules CD62 (P-selectin), thrombospondin (TSP), and CD63 (GP53) as well as the activated fibrinogen receptor (GPIIB/IIIA). Fifty matched normal subjects served as control subjects. Fourteen patients completed the 60-day study design. After initial recompensation, near-normoglycemic control was achieved after 14 days (fasting blood glucose, 117.0 +/- 19.0 mg/dl), and the HbA1 concentration was 7.6 +/- 1.2% after 60 days. CD62+ (4.0 +/- 4.5%), TSP+ (2.0 +/- 1.8%), CD63+ (11.0 +/- 7.0%), and activated-GPIIB/IIIA+ (7.6 +/- 7.7%) platelet levels were initially 5, 3.3, 5.7, and 2.8 times higher than the mean level of normal. There was no correlation with any of the nearly normalized metabolic parameters. Thus, more activated platelets circulate in newly diagnosed IDDM patients, which supports the assumption of a prethrombotic condition even in disease stages without apparent vascular damage.(ABSTRACT TRUNCATED AT 250 WORDS)