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

In an 11-year-old girl with congenital insensitivity to pain, diagnosis depended on three diagnostic features: pain sensation absent from birth; entire body affected; all other sensory modalities and deep tendon reflexes present. The cause of this disease is unknown. Other diseases to be considered when insensitivity to pain is present are diabetes, lues, and syringomyelia. Less common neurologic diseases are congenital sensory neuropathy with or without anhidrosis, familial dysautonomia (Riley-Day syndrome), and sensory radicular neuropathy. The three orthopedic manifestations of congenital insensitivity to pain are recurrent fractures, neuropathic (Charcot's) joints, and osteomyelitis. Management is based on proper appreciation of the disease. Prevention of complications is important. Treatment of fractures and osteomyelitis is straightforward. However, the treatment of neuropathic joints demands caution and is done best nonsurgically.
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PMID:Orthopedic aspects of congenital insensitivity to pain. 618 64

This report describes the experimental design, methods, and baseline characteristics of patients enrolled in a Veterans Administration Cooperative Study on the effect of aspirin (325 mg t.i.d.) and dipyridamole (75 mg t.i.d.) (110 patients), or placebo (121 patients) on major vascular outcome variables in noninsulin-dependent diabetic patients with either a recent amputation for gangrene (n = 207) or active gangrene (n = 24). It also describes the baseline characteristics of the patients. A total of 231 patients of 563 screened (41%) were enrolled at 11 participating V.A. Medical Centers during a 39 month period. The median age at entry was 60 years, the median duration of diabetes was 10 years, and weight was 110% of desirable. All patients were men. Sixty-eight percent were treated with insulin and 32% with diet alone. Only 42% were smokers at entry, 40% had retinopathy, 61% sensory neuropathy, 42% hypertension, and 29% had a history of myocardial infarction, angina, and/or congestive heart failure. Thirteen percent had a history of cerebrovascular disease. Despite randomization, the treatment group had an increased frequency of a history of cerebrovascular disease (p = 0.01), diagnosed as stroke (p = 0.03), a finding suggesting that the treatment group was at a slightly increased risk for vascular disease upon enrollment in the study. Other baseline variables did not differ significantly between the two groups. This study should provide definitive data on the efficacy of these doses of antiplatelet agents in preventing further vascular disease in diabetic men with gangrene or recent amputation for gangrene, using death due to vascular disease and subsequent amputation of the opposite extremity for gangrene as major outcome variables. It should also give useful information on the effect of antiplatelet therapy on vascular outcome variables such as same side amputations, myocardial infarction, stroke, transient ischemic attack, retinopathy, and renal failure. Finally, the study should provide useful data on the natural history and significance of risk factors in this patient population.
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PMID:V.A. Cooperative Study on antiplatelet agents in diabetic patients after amputation for gangrene: I. Design, methods, and baseline characteristics. 637 22

Out of an unselected group of 160 patients with diabetic neuropathy 51 patients were followed up for an average of 5, 6 years by repeated neurological examinations and by means of a questionnaire. The control of the diabetes was requested from the house physicians. The patients were classified as presenting (1) a symmetrical, predominantly sensory neuropathy (2) a mixed syndrome with additional autonomic neuropathy and (3) multiple mononeuropathy. Individual symptoms and objective signs of neuropathy revealed a remarkable variety of changes. The outlook in multiple mononeuropathy and distal paresis was favorable while autonomic failures, in particular of male sexual function, progressed. There seemed to be some beneficial effect of improved glycemic control. However, despite satisfactory metabolic control some progression of diabetic neuropathy occured.
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PMID:The natural course of diabetic neuropathy. A follow-up. 692 85

C57BL/KsJ db/db inbred mice have an hereditary autosomal recessive disease resembling in some respects maturity onset human diabetes mellitus. At 8--11 months of age, they displayed intermittent symptoms suggestive of a mild sensory neuropathy. These symptoms consisted of adduction of their hind limbs and flexing hind paws when raised by the tail, and inability to maintain their position on the roto wheel. Peripheral nerves and sensory ganglia of the diabetic mice were compared with those of the unafflicted littermates and studied with respect to Schwann cell counts and myelinated nerve fiber diameter measurements. In addition, teased fibers of peripheral nerves were compared for obvious changes in internodal distance and demyelination. Chromatolytic neurons were moe abundant in lumbosacral spinal ganglia of diabetic mice than in corresponding ganglia of controls or in more anterior spinal ganglia and trigeminal ganglia of diabetics. Histologic studies showed an increase in Schwann cell counts in longitudinal sections of peripheral nerves. A similar but larger increase was observed in peripheral nerves of mice affected with an hereditary sensory neuropathy, dystonia musculorum. A small but general decrease in myelinated fiber diameter was observed in sensory and motor nerves.
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PMID:Peripheral neuropathy in mouse hereditary diabetes mellitus. I. Comparison of neurologic, histologic, and morphometric parameters with dystonic mice. 696 18

Two patients with idiopathic Fanconi syndrome and glucose intolerance were studied from a metabolic perspective. They had fasting hyperglycemia, massive glucosuria, insulinopenia, ketosis, and elevated serum free fatty acids. There was a markedly blunted insulin secretory response to glucagon, tolbutamide, glucose, and arginine. One patient had the findings of diabetic retinopathy and a sensory neuropathy. Neither patient could convert galactose to glucose, but they did not have galactosemia. As a result of these studies, and previous reports in which similar changes were noted, we conclude that diabetes mellitus may occur in patients who have had idiopathic Fanconi syndrome for many years.
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PMID:Metabolic abnormalities in the idiopathic Fanconi syndrome: studies of carbohydrate metabolism in two patients. 701 70

A 16-year-old girl with insulin dependent (Type I) diabetes since age 9 and painful sensory neuropathy for two months was treated with a portable insulin infusion pump, allowing strict control of hyperglycemia. Within 28 days the distal motor latency in all nerves tested had improved and painful incapacitating dysesthesias disappeared. The findings suggest that strict control of hyperglycemia with a portable insulin infusion pump can successfully reverse the changes of recent onset diabetic neuropathy.
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PMID:Improvement of diabetic peripheral neuropathy with the portable insulin infusion pump. 703 57

To determine whether touch acuity is altered in individuals with maturity-onset diabetes, tactile thresholds on the pad of the index finger of 32 diabetic and 27 nondiabetic subjects were compared. A set of modified Von Frey hairs was used to present touch stimuli in a forced-choice tracking procedure that controls for subject response bias. The mean tactile threshold of diabetic patients was significantly higher than that of nondiabetic subjects, although the difference between the two groups is small. Within the diabetic group, decreased tactile acuity was associated with a longer duration of disease diagnosis, presence of insulin therapy, and low-digit temperature. However, reported presence or absence of peripheral sensory symptoms (tingling, numbness, etc.) in diabetic patients did not relate to touch thresholds. The small but significant increase in touch threshold that was observed in diabetic individuals may provide an early indication of sensory neuropathy. Further use of threshold determinations will contribute to our understanding of sensory changes that accompany diabetes.
Diabetes Care
PMID:Light touch thresholds in diabetic patients. 717 99

Biologic gastric emptying time (BGET) was measured in 24 patients with severe diabetes mellitus complicated by vascular damage and peripheral or sensory neuropathy. This population had a BGET of 192 +/- 32.9 min (mean +/- s.e.m. normal 40-85 min). Patients with diabetic gastroenteropathy had prolongation of BGET to 295 +/- 45 (p < 0.05). Metoclopramide significantly shortened BGET in this subgroup to 101 +/- 40 min, with return to normal values in eight of the 12 patients given the drug. The Tc-99m-labeled resin-oatmeal test meal used as described in this study provides a reliable measure of BGET and of the response to metoclopramide.
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PMID:Biologic gastric emptying time in diabetic patients, using Tc-99m-labeled resin-oatmeal with and without metoclopramide. 743 Nov 11

Small fiber sensory neuropathy is one of the most common complications of diabetes mellitus. Currently there is no adequate therapy to prevent this often debilitating problem. Nerve growth factor (NGF) is a protein that promotes the survival and integrity of a large percentage of sensory neurons including the small fiber pain transmitting neurons which are often prominently affected in diabetic neuropathy. We report here that exogenously administered NGF is capable of preventing the behavioral and biochemical manifestations of diabetic sensory neuropathy in a streptozocin induced rat model. NGF administration prevented the elevation of tailflick threshold (a measure of the rat's response to a thermal noxious stimulus) which occurred in streptozocin-induced diabetic rats. Further, it prevented the induced reduction in levels of the neuropeptides substance P and calcitonin gene related peptide measured from cervical dorsal root ganglia. Finally, NGF did not ameliorate the prolonged latency of the compound action potentials measured from the caudal nerve of the tail. In view of these results, a clinical trial of NGF in diabetic neuropathy has now commenced.
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PMID:Nerve growth factor administration protects against experimental diabetic sensory neuropathy. 751 29

Dorsal root ganglion neurons from streptozotocin (STZ)-induced diabetic, genetic diabetic and normal mice were cultured in serum-containing media with or without nerve growth factor (NGF). The immunocytochemical analysis carried out after 1 week in culture revealed that the ratios of neurons immunoreactive to calcitonin gene-related peptide (CGRP) in NGF-free medium in the STZ-diabetic mice (average 23.2%) were significantly lower than those in the normal mice (45.1%). The ratios of neurons immunoreactive to CGRP and substance P (SP) in the NGF-free medium were also lower in the genetic diabetic mice (23.6% and 21.8%) than those in the normal ones (40.7% and 34.2%). However, treatment with NGF restored these reduced immunoreactivities in the diabetic groups in a dose-dependent manner. These results show that NGF can be effective for the diabetes-induced depletion of CGRP and SP in sensory neurons, and suggest its possible role in the prevention and improvement of diabetic sensory neuropathy.
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PMID:Nerve growth factor (NGF) restores depletions of calcitonin gene-related peptide and substance P in sensory neurons from diabetic mice in vitro. 753 Jul 67


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