Diabetic sensorimotor neuropathy: electrophysiological, Histopathological and Immunohistochemical study

To determine the role of IgM and IgG deposition in the neuronal tissue in the pathogenesis of diabetic sensorimotor neuropathy. This study was carried out on 30 diabetic patients. They were divided into three groups, group I comprised 10 insulin dependent diabetic patients with peripheral neuropathy, group II 10 non-insulin dependent diabetic patients with peripheral neuropathy and group III 10 diabetic patients without peripheral neuropathy as a control group. All patients were subjected to clinical examination, laboratory investigations [urine analysis for proteinuria, fasting and postprandial blood glucose levels], neurophysiological studies including EMG and motor nerve conduction studies of median and common peroneal nerves and sensory conduction studies of median and sural nerves. Sural nerve biopsies were taken and subjected to histopathological examination under transmission electron microscope and immunohistochemical examination for detection of IgG and IgM deposition. Motor and sensory nerve conduction velocities were diminished in all patients of, group I and II. There were significant correlations between motor nerve conduction velocities with age, duration of diabetes and neuropathy. As regards histopathological examination, there were endoneurial capillary closure, segmental demyelination and axonal degeneration in addition to vascular changes in the form of thickening of the basement membrane, medial thickening and endothelial proliferation. There were immunoglobulin M and G deposition in the sural nerve biopsies at two identical sites perineurial and endoneurial. In, group III, electrophysiological studies were abnormal in only one patient and histopathological studies revealed no important detectable abnormalities, also immunohistochemical examinations showed no significant immunoglobulins [Igs] deposition. The deposition of immunoglobulins in the peripheral nerves of diabetic patients with peripheral neuropathy might be related to primary and specific activation of immune system effectors against unknown neuronal antigens or may be secondary to destruction of the blood nerve barrier, possibly by hyperglycemia. Neural deposition of Igs should be considered as an additional evidence for a role for the humeral immune mechanisms in the pathogenesis of diabetic sensorimotor neuropathy

Cardiac involvement in primary sjogren's syndrome patients detected with echocardiography

To determine a pattern of cardiac involvement in primary Sjogren's syndrome patients and to evaluate these cardiac abnormalities in asymptomatic patients. The study was carried out on 20 primary Sjogren's syndrome patients [PSS] as well as 10 healthy controls matched in age and sex. None of the patients had evidence of cardiac symptoms. All subjects had complete history, clinical examination, laboratory tests [Rh F, ANA and anti Ro and anti La], chest X-ray, ECG and echocardiography. Cardiac abnormalities were detected in 7 [35%] primary Sjogren's syndrome patients out of 20 [PSS] patients examined with echocardiography. Seven [35%] presented with left ventricle diastolic dysfunction and 6 [30%] presented with pulmonary hypertension but only [15%] showed left ventricle hypertrophy, there were 2 patients with mitral regurge and only 1 patient with mitral stenosis and prolapse and also, 1 [5%] presented with aortic regurge and 1 [5%] patient by tricuspid regurge. There was significant difference between PSS patients and control subjects as regards to diastolic functions [E peak, A peak, E/A and DFT] and there was no correlation between the occurrence of these silent cardiac abnormalities and the clinical and laboratory findings. Cardiac involvement is common in PSS but clinically with silent manifestations. Thus, echocardiography should be done for all patients with PSS to detect any cardiac abnormalities