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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nerve biopsies were obtained from 27 patients with diabetic neuropathy. All had a symmetric distal sensory and autonomic neuropathy or a purely sensory neuropathy. Mean age was 39.8 years (range 23-57 years). Two patients had Type 2 (non-insulin-dependent) diabetes mellitus and the remainder Type 1 (insulin-dependent) diabetes. Morphometric observations on endoneurial capillaries were compared with results from organ donor control cases and from patients with type 1 hereditary motor and sensory neuropathy. The area of the lumen of the capillaries did not differ between the three groups. The area occupied by the capillary endothelial cells in transverse section and the number of endothelial cell nuclei were increased both in the patients with diabetic neuropathy and hereditary motor and sensory neuropathy, as was the thickness of the surrounding basal laminal zone. 'Closure' of endoneurial capillaries in diabetic neuropathy, reported in another study, was not confirmed. Capillary density and nearest-neighbour distances were similar in the diabetic and organ donor control cases. Capillary density was reduced in the patients with hereditary motor and sensory neuropathy, this being related to increased fascicular area consequent upon the presence of hypertrophic changes. The presence of thickening of the pericapillary basal laminal zone and endothelial cell hyperplasia both in diabetic and hereditary motor and sensory neuropathy, the latter being a neuropathy in which a vascular basis can be discounted, makes it difficult to use such changes as an argument favouring a vascular cause for diabetic neuropathy. There were differences in the basal laminal zone between the diabetic and hereditary motor and sensory neuropathy cases suggesting that the reduplicated basal lamina was more persistent in the diabetic patients.
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PMID:Morphometry of endoneurial capillaries in diabetic sensory and autonomic neuropathy. 225 98

A 62-year-old woman with chronic lymphatic leukemia (CLL) (RAI stage IV) with multiple organ involvement and diabetes mellitus, three months prior to death presented with a symmetrical sensory neuropathy of the upper extremities with little motor impairment and, two months later, sensory atactic neuropathy of the lower limbs. No cranial nerve or CNS impairment was noted. Clinical diagnosis was predominantly sensory neuropathy, but nerve conduction velocities were normal on upper limbs and moderately abnormal on lower limbs, the latter attributing to long lasting diabetes mellitus. The women died from acute subarachnoid hemorrhage. Autopsy revealed CLL of B-cell type with generalized organ involvement and acute craniospinal subarachnoid hemorrhage from ruptured cerebral aneurysm. There was selective neoplastic infiltration of the dorsal root ganglia and peripheral nerves, particularly the median nerve. Although selective infiltration of peripheral nerves by B-cell lymphoma cells was not associated with myelo-axonal degeneration, the relationship of this case to human neurolymphomatosis is discussed.
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PMID:Human neurolymphomatosis in a patient with chronic lymphatic leukemia. 227 42

The flare response in skin largely depends on an intact primary sensory fiber, the C-fiber. We measured the flare response to the intradermal injection of substance P, histamine, and capsaicin in control subjects and in diabetic patients with and without clinically obvious polyneuropathy. The neuropathic diabetic patients had a reduced flare response to substance P, histamine, and capsaicin, compared with control and nonneuropathic diabetic subjects. The smaller flare response in the neuropathic diabetics after capsaicin administration suggested a dysfunction of the peripheral component of the C-fiber. Alternatively, dysfunction of the mast cell or vascular reactivity may contribute to the diminished flare. Because C-fibers participate in nociception in addition to the flare response, the findings of this study, by a method that permits a quantifiable measurement of the function of peripheral sensory neurons in diabetic subjects, has potential usefulness in evaluating sensory neuropathy in diabetic patients.
Diabetes 1987 Oct
PMID:Diminished flare response in neuropathic diabetic patients. Comparison of effects of substance P, histamine, and capsaicin. 244 7

Peripheral neuropathy is a common and well-studied complication of diabetes mellitus, but the possibility that central neuropathy is also present has received scant attention. Based on recent evidence showing that insulin has a direct effect on axon formation and neuronal survival in vitro, it was predicted that functional neuropathy would be present in the spinal cord of diabetic animals. Although structural lesions are encountered in the spinal cord of diabetic patients at autopsy, the functional corollaries have essentially remained unstudied. We used a new procedure to study evoked spinal cord potentials in the rat, which revealed a significant retardation in conduction velocity in streptozocin (STZ)-induced diabetic animals. This retardation was not due to a toxic effect of STZ on the involved spinal cord sensory pathways, because insulin infusion prevented the development of spinal cord neuropathy. The kinetics and magnitude of decline in conduction velocity were similar in the spinal cord, saphenous nerve, and common peroneal nerve during the first 2 wk, suggesting that a common mechanism was involved. After 10 wk, a spontaneous improvement in function was observed in the spinal cord and common peroneal nerve but not in the saphenous nerve. Our results support the hypothesis that central nervous system dysfunction can occur along with peripheral sensory neuropathy in diabetes.
Diabetes 1989 Jun
PMID:Impairment of spinal cord conduction velocity in diabetic rats. 265 42

Necrotizing fasciitis can be a devastating infectious process when diagnosis and early aggressive therapy is delayed. The etiologic factors that may play a role in or affect this necrotizing infectious process are reviewed. An interesting case is presented of bilateral, lower extremity, necrotizing fasciitis in a patient with diabetes mellitus, peripheral vascular disease and profound sensory neuropathy.
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PMID:Necrotizing fasciitis. 266 36

Studies on erythrocyte insulin receptors were performed in a family with hereditary motor sensory neuropathy (Charcot-Marie-Tooth) with superimposed type I diabetes mellitus. The maximum specific insulin binding of the erythrocytes was high and the increase was shown to be due to increased affinity of the insulin receptor to erythrocytes.
Diabetes Res 1989 Jan
PMID:Erythrocyte insulin binding in a family with hereditary motor sensory neuropathy (Charcot-Marie-Tooth) with superimposed insulin-dependent type I diabetes mellitus. 266 41

In vivo urinary bladder function was examined in BB rats after 4 and 6 mo of diabetes, and the data were correlated with morphometric changes in the pelvic and hypogastric nerves, which constitute the micturition reflex arc. After controlled bladder distension, diabetic animals revealed irregular bladder contractions at frequencies that were reduced to 33% of normal values and with significantly increased amplitudes. The abnormal micturition in diabetic animals was elicited at moderately elevated threshold volumes. These functional abnormalities of the diabetic bladder were associated with a progressive axonopathy of afferent myelinated sensory fibers and later-occurring axonal atrophy of unmyelinated efferent preganglionic fibers. These data suggest that diabetic urinary bladder dysfunction is initiated by a visceral sensory neuropathy involving the afferent limb of the micturition reflex arc.
Diabetes 1989 Aug
PMID:Autonomic neuropathy in BB rats and alterations in bladder function. 275 32

Detailed clinical neurological examinations were conducted on 44 nondiabetic volunteers and 59 diabetic subjects. The examinations focused particularly on sensory symptomatic and physical evaluation. Standardized assessment of symptoms and physical testing of light touch, pain, vibratory, and thermal sensation was performed at the hand, wrist, elbow, foot, ankle, and knee. A total symptom score and physical score were defined by summing test scores at each site. Current perception threshold (CPT) testing that used constant sine-wave-alternating current was conducted at the same anatomic sites. CPT correlations with the physical score gave r values of .55 for 5 Hz, .60 for 250 Hz, and .62 for 2000 Hz (n = 618). Correlations with the symptom score were not as strong: r = .45 for 5 Hz, .46 for 250 Hz, and .51 for 2000 Hz. The correlation with symptom score was due primarily to a strong relationship for the symptom of numbness (r = .53 for all 3 frequencies). Correlations with pain and paresthesia were much lower. CPTs for diabetic subjects at the three frequencies were higher at most locations than for the nondiabetic volunteers. However, CPTs were no different from normal values in diabetic subjects without evidence of neuropathy. CPT testing appears to be a useful technique for assessment of diabetic sensory neuropathy.
Diabetes Care 1989 Oct
PMID:Mapping diabetic sensory neuropathy by current perception threshold testing. 279 26

The purpose of this study was to determine the occurrence and severity of diabetic retinopathy and to clarify its association with the duration of diabetes and several other factors in an outpatient diabetic population. The material consisted of 328 diabetics, mainly (77%) C-peptide negative, type 1 diabetics. The mean age of the patients was 45 years, and the mean duration of diabetes was 15 years. Retinal changes were assessed by ophthalmoscopy and widefield fundus photography. All retinopathy was confirmed in 59% and proliferative retinopathy (PR) in 20% of the patients. The frequency of diabetic retinopathy was 15% in patients with diabetes for less than five years but 100% in those with diabetes for 30 or more years. In type 1 diabetics PR was seen only after 10 or more years' duration but, after 20 years' duration it was seen in half of the patients with type 1 and in one-third of the patients with type 2 diabetes. The patients with diabetic nephropathy often had PR. In type 1 diabetics with onset of the disease less than 30 years peripheral sensory neuropathy, coronary disease, hypertension and leg-vessel disease were also often associated with PR. Because one reason for visual handicapping in diabetes is the delay of the diagnosing of vision-threatening lesions screening for treatable retinopathy should be intensive after 10 years' duration and in poorly-controlled diabetics even earlier.
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PMID:Predicting diabetic retinopathy. 283 48

We have studied risk factors for diabetic foot ulceration by comparing diabetic patients who had active foot ulcers (n = 86) with diabetic patients who had no history of foot ulcers (n = 49). Whereas there was a strong association of diabetic foot ulceration with abnormal vibratory perception (Odds Ratio = 10.77; p less than 0.001, which increased with worsening vibratory perception), there was little association with abnormality of the ankle-pressure index (Odds Ratio = 2.84, p = n.s.). Although foot ulceration and limited joint mobility were associated (Odds Ratio = 3.57, p less than 0.001), this relation was not significant when allowances for abnormal vibratory perception and diabetes duration were made. These data suggest that sensory neuropathy is of greater aetiological importance than peripheral vascular disease in the development of diabetic foot ulceration. The measurement of the vibratory perception threshold is clinically useful in identifying those diabetic patients at high risk of foot ulceration.
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PMID:Impaired vibratory perception and diabetic foot ulceration. 294 22


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