Cases reported "Diabetic Neuropathies"

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1/6. Perivascular siderophages in skeletal muscle from a patient with diabetic neuropathy.

    hemosiderin deposition in skeletal muscle histiocytes is uncommon but has been occasionally noted in hemochromatosis, hemosiderosis and Waldenstrom's macroglobulinemia. The purpose of this report is to describe the light microscopic and ultrastructural characterization of this abnormality in a patient with diabetes mellitus. A 56-year-old diabetic male presented with paresthesias and intermittent diffuse lower extremity myalgias. neurologic examination was remarkable only for diminished vibratory sense in the toes, diminished deep tendon reflexes, and ankle-level stocking distribution hypalgesia. There was no clinical evidence of hemochromatosis and laboratory studies ruled out Waldenstrom's macroglobulinemia. Muscle biopsy showed modest variability in myofiber diameter with a few scattered angular atrophic type II fibers. There were numerous collections of granular pigment-containing histiocytes in endomysial and perimysial perivascular areas and marked thickening of blood vessels walls. The histiocytic pigment was bright blue with the Prussian blue stain. No pigment was seen in the myofibers. Ultrastructural examination revealed numerous perivascular histiocytes filled with hemosiderin containing granules of variable size and density and marked thickening of capillary walls with striking reduplication of basement membranes. A modest number of subsarcolemmal paracrystalline mitochondrial inclusions were present. X-ray dispersion analysis of the histiocytic pigment material confirmed the presence of iron in the lysosomal granules.
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2/6. Normocytic normochromic anemia due to automatic neuropathy in type 2 diabetic patients without severe nephropathy: a possible role of microangiopathy.

    We describe here four male patients with long-term and poorly controlled type 2 diabetes mellitus. They shared many common characteristic complications, such as severe autonomic neuropathy, proliferative retinopathy and normocytic normochromic anemia without progressive renal failure and macroangiopathy. They also showed normal levels of erythropoietin and reticulocyte, which was considered relatively low. The coefficient of variation of R-R, a useful method to estimate autonomic failure, showed markedly advanced autonomic neuropathy in all four patients. coronary angiography did not reveal stenosis, anomaly or collateral vessels, but left ventriclography showed diffuse or partial hypokinesis. Massive proteinuria, high urinary levels of N-acetyl-beta-D-glucosamidase (NAG) and beta2-microglobulin (beta2M) were detected, though creatinine clearance (Ccr) was not so deteriorated. Treatment with recombinant erythropoietin increased their hemoglobin and hematocrit levels. These common points have a possibility to be brought about by tubulointerstitial damage and microangiopathy may be involved in it.
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3/6. The use of adjuvant hyperbaric oxygen in treatment of the diabetic foot.

    Hypoxia in the relatively ischemic diabetic foot impairs leukocyte bacterial killing and fibroblast-collagen support for capillary angiogenesis. infection in even the relatively young, "warm-foot" diabetic with microangiopathy, neuropathy, and infection leads to hypoxia due to local high oxygen consumption. The 1100 to 1300 mm Hg arterial PO2 achievable with hyperbaric oxygen results in elevation of wound PO2. Periodic correction of wound hypoxia improves leukocyte bacterial killing and support for capillary angiogenesis. Hyperbaric oxygen is usually futile in the elderly diabetic with significant and generalized large-vessel occlusion.
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4/6. Acute ischemic atrophy of papilla disc and diabetes.

    Acute ischemic neuropathy is the acute ischemic necrosis of the optic nerve fibers occurred by the occlusion of small vessels which distribute widely to lamina cribrosa and anterior et posterior area of lamina cribrosa. Pale coloured edema and light swelling are seen generally on the optic disc, and after a few months falls in simplex nerve atrophy. I have explained my 3 cases of ischemic neuropathies. They have some things in common, and causes are considered arteriosclerosis or temporal arteritis in old people, and often takes place based on diabetes mellitus, lupus erythematosis or another many diseases etiologically.
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5/6. Successful treatment of neuropathies in patients with diabetes mellitus.

    OBJECTIVES: To report and characterize two forms of disabling progressive peripheral neuropathy in patients with diabetes mellitus, which respond to anti-inflammatory and/or anti-immune treatment. DESIGN: review of clinical, electrophysiologic, and pathologic findings and results of treatment. SETTING: University medical center. patients: Twenty-one patients with diabetes mellitus to whom we gave anti-inflammatory and/or anti-immune treatment for progressive peripheral neuropathy during the past 6 years. MAIN OUTCOME MEASURES: patients were interviewed and examined at intervals before and after beginning treatment with intravenous immunoglobulin (n = 15), prednisone (n = 13), cyclophosphamide (n = 5), plasma exchange (n = 3), and azathioprine (n = 1) (alone or in combination). RESULTS: Fifteen patients had evidence of axonal neuropathy by electrophysiologic studies (group A). All 15 patients had non-insulin-dependent diabetes mellitus, 10 patients had weight loss, and 13 patients had prominent involvement of thighs and/or thoracic bands consistent with diabetic amyotrophy or mononeuropathy multiplex. Small vessel disease was seen in all 10 patients who underwent biopsy, with perivascular or vascular inflammation seen in seven patients. Six patients had demyelinating neuropathy by electrophysiologic criteria (group B). All these patients had insulin-dependent diabetes mellitus, and no one had weight loss. The process was asymmetric in three patients and involved thoracic or abdominal regions in two patients. Onion bulbs were seen in all four patients who underwent biopsy, but no vascular inflammation or occlusion was seen. In all patients in both groups, worsening of their conditions stopped and improvement started after beginning treatment. CONCLUSION: Neuropathies responsive to anti-inflammatory and/or anti-immune therapy in patients with diabetes mellitus include (1) multifocal axonal neuropathy caused by inflammatory vasculopathy, predominantly in patients with non-insulin-dependent diabetes mellitus, indistinguishable from diabetic proximal neuropathy or mononeuropathy multiplex, and (2) demyelinating neuropathy indistinguishable from chronic inflammatory demyelinating polyneuropathy, predominantly in patients with insulin-dependent diabetes mellitus.
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6/6. Arterio-venous shunting and proliferating new vessels in acute painful neuropathy of rapid glycaemic control (insulin neuritis).

    insulin neuritis, or painful neuropathy following rapid improvement in glycaemic control, is well recognised but its aetiology is unclear. An understanding of the processes involved in the genesis of acute painful neuropathy of rapid glycaemic control may give an insight into the early pathogenetic factors leading to diabetic nerve damage in general. We have identified five subjects with insulin neuritis including one who developed severe autonomic neuropathy following treatment with insulin. Subjects underwent: 1) assessment of neuropathic symptom and deficit scores; 2) quantitative sensory and electrophysiological studies and 3) sural nerve epineurial vessel photography and fluorescein angiography in vivo. The sural nerve photographs were independently graded by an ophthalmologist. All subjects with insulin neuritis presented with severe sensory symptoms but clinical examination and electrophysiological tests were normal except in the subject with the severe autonomic neuropathy in whom all the tests were abnormal. On nerve photography, there was an abundance of epineurial nutrient vessels although these showed severe abnormalities including arteriolar attenuation, tortuosity and arterio-venous shunting in all subjects. Proliferating neural 'new vessels' which bear striking similarities to those found in the retina and that were more leaky to fluorescein than normal vessels, were observed in three subjects. Venous distension and/or tortuosity was also observed in three subjects and this was most marked in the subject with severe autonomic neuropathy. This study shows that epineurial nutrient vessel anatomy is abnormal in subjects with acute painful neuropathy of rapid glycaemic control, a condition previously thought to be purely metabolic in origin. The presence of epineurial arterio-venous shunting and a fine network of vessels resembling the new vessels of the retina, may lead to a 'steal' effect rendering the endoneurium ischaemic. This process may be important in the genesis of neuropathic pain, and further supports the importance of vascular factors in the pathogenesis of diabetic neuropathy.
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