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

Glycosylated hemoglobin (Hb) concentrations were measured in 50 patients with clinically significant diabetic neuropathy. There were 24 males and 26 females with a mean age of 58.1 years and a mean duration of diabetes of 8.9 years. The glycosylated Hb concentration was not significantly different in these patients (13.9% +/- 2.4 SD) compared with randomly selected diabetic patients matched for age (+/- 5 years), sex and therapy without clinical evidence of neuropathy (13.6% +/- 2.2). There was no significant difference in the duration of diabetes between the two groups. The results would suggest that factors other than the degree of control of diabetes are important in the pathogenesis of diabetic neuropathy.
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PMID:Glycosylated hemoglobin concentrations in patients with diabetic neuropathy. 52 6

Sensory nerve conduction velocity (NCV) and the vibratory sense (biothesiometry) were determined in 67 children and adolescents with insulin dependent diabetes. Age at onset of diabetes varied between 1-14 years (mean +/- S.D. 6.5 +/- 3.6) and the duration of diabetes between 4-17 years (7.7 +/- 3.4). Within +/- 3 months of the nerve function tests blood was drawn for determination of C-peptide and insulin antibodies (IgG and IRI). A low NCV (less than 50 m/s) in the sural nerve and/or an abnormal vibratory sense (greater than or equal to 1.0 microns) were found in 34 patients (50.7%). Measurable fasting serum C-peptide 0.04-0.60 pmol/ml (0.17 +/- 0.15) was found in 16 patients (23.9%). All but one patients had insulin antibodies with IgG 0.130-11.029 mU/ml (2.957 +/- 2.509) and total IRI 10-9120 muU/ml (1204 +/- 1723). In multiple regression analysis we did not find any correlation between nerve function and sex, age, or age at onset of diabetes, and there was only a weak relationship between NCV and duration. However, there was a positive correlation between NCV and C-peptide (p less than 0.001). Vibration sense was also better among patients with C-peptide (p less than 0.05). The results support the view that insulin deficiency contributes to peripheral diabetic neuropathy.
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PMID:Sensory nerve conduction velocity and vibratory sensibility in juvenile diabetics. Relationship to endogenous insulin. 52 41

Diabetic myelopathy occurred in 41% of 75 consecutive, unselected diabetic patients in an autopsy study; clinical peripheral neuropathy occurred in 13%, and histologic radiculopathy in 21%. Infection represented 2.7% of the cord lesions. Posterior column demyelination, seen in 27%, apparently has the same metabolic-toxic origin as diabetic neuropathy and radiculopathy; it is an independent lesion, not a secondary manifestation of peripheral demyelination. It occurs slightly more frequently in those with juvenile-onset diabetes. Spinal cord infarcts, seen in 19%, are related to anteriolar sclerosis of the intrinsic vessels of the spinal cord. They have a higher incidence in diabetics than in a nondiabetic aging population, show a predilection for the white matter, and are usually small. The myelopathy is not related to patient age or duration of diabetes. It is often clinically occult.
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PMID:Diabetic myelopathy. 58 Nov 51

Acute diabetes with ketosis was induced in rats by intraperitoneal streptozotocin and also a milder form of diabetes without ketosis by injecting less of the drug. The acutely diabetic rats were killed 72h after injection and the others after either 2 or 13 weeks. Free and lipid myo-inositol was then measured in various tissues and body fluids by g.l.c. of the trimethylsilyl ether. Serum inositol was increased in the acutely diabetic group, whereas liver inositol was decreased. Brain and kidney inositol concentrations were increased in the mildly diabetic animals at 13 weeks and there was a progressive decrease in sciatic-nerve inositol. Lipid inositol of sciatic nerve was decreased in the acutely diabetic group only. Brain lipid inositol concentration was decreased in mild diabetes at 13 weeks. Possible implications of these findings in relation to diabetic neuropathy was discussed.
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PMID:Free and lipid myo-inositol in tissues from rats with acute and less severe streptozotocin-induced diabetes. 58 54

Myocardial infarction is considered the prime cause of death among adult diabetic patients. In a great number of cases, during myocardial infarction the patients don't feel pain or it is atypical. Diagnosis can be neglected, and mortality increases. In search of an explanation for the absence of pain in these patients, the authors studied the autonomic nerve fibers of the heart muscle with argentic and combined techniques, looking for lesions in the sympathetic or parasympathetic nerve fibers that conduct pain. In the five cases of painless myocardial infarction studied, the nerve fibers showed typical lesions of diabetic neuropathy: beaded thickenings, spindle-shaped thickenings, fragmentation of fibers, and diminution of the number of fibers in the nerves. The patients in the control group (five diabetics with painful infarction, five diabetics with infarction, five nondiabetics with painful infarction, and five nondiabetics without infarction) had no lesions. These facts led us to assume that the absence of pain in diabetics with myocardial infarction could be due to a lesion of the afferent nerves that conduct pain.
Diabetes 1977 Dec
PMID:Autonomic neuropathy and painless myocardial infarction in diabetic patients. Histologic evidence of their relationship. 59 Jun 38

A new animal model for the study of diabetic neuropathy is presented. The homozygote (db/db) of the mouse strain C57BL/Ks shows severe diabetes with longstanding hyperglycemia. Electrophysiological studies showed severely decreased motor nerve conduction velocity. Morphometric examination of sensory and motor nerves at different levels revealed absence of large myelinated fibers, with morphological features indicative of axonal atrophy.
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PMID:Peripheral neuropathy in mutant diabetic mouse [C57BL/Ks (db/db)]. 63 48

The peripheral nerves of alloxan and streptozotocin diabetes rats six months after the induction of diabetes were morphologically investigated. The effect of insulin treatment was also examined. Prominent segmental demyelination and remyelination were observed in both alloxan and streptozotocin diabetes rats by isolated nerve fiber studies. Axonal degeneration and globular swelling were also recognized in some nerve fibers. Transmission electron microscopic findings were characterized by the figures of destructed myelin sheaths and axons. Reduplication and thickening of basal lamina of vasa nervorum were noted in the diabetes rats. Scanning electron microscopy revealed three dimensional architectures of degenerated nerve fibers and rough surface of Schwann cells in the diabetes rats. Insulin treated diabetes rats showed less structural changes of nerve fibers. It was indicated that the peripheral nerve lesions of experimental diabetes rats were caused by metabolic impairment of both axons and Schwann cells. Insulin treatment seemed to be effective on the experimental diabetic neuropathy.
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PMID:Peripheral nerve structures of experimental diabetes rats and the effect of insulin treatment. 76 Feb 49

Tests of autonomic function were performed on 16 subjects with diabetic neuropathy. Abnormal sweating occurred in 10/10 (100 per cent), postural hypotension in 7/16 (44 per cent), an abnormal Valsalva ratio in 7/11 (64 per cent), and denervation hypersensitivity to phenylephrine in 2/8 (25 per cent) of patients tested. A quantitative assessment of baroreceptor function was made. In diabetics, there was a reduced resting heart period, heart period range and mean gain. Quantitative histological studies were performed on the greater splanchnic nerves removed at autopsy from 9 control subjects and from 8 subjects with diabetic neuropathy. The fibre density was significantly reduced in the greater splanchnic nerve of diabetics. The predominant pathology on teased fibre preparations was that of demyelination. Disordered blood pressure control in diabetes correlated with the pathological abnormalities in the sympathetic nervous system. Light and electronmicroscopic studies were performed on the sural nerves of 2 diabetic subjects with autonomic dysfunction. The predominant change was active axonal degeneration affecting mainly unmyelinated and small myelinated fibres.
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PMID:The sympathetic nervous system in diabetic neuropathy. A clinical and pathological study. 81 Feb 14

Glucagon response to insulin hypoglycemia was tested in diabetics with autonomic neuropathy (N=9), diabetics without neuropathy (N=8), and normals (N=9). With similar levels of hypoglycemia, growth hormone and plasma cortisol increased in all groups. The glucagon response in normals (121+/-19 vs. 308+/-30 pg./ml., mean+/-S.E.M. of baseline vs. hypoglycemia peak) was significantly less in nonneuropathic diabetics than in normals (128+/-13 vs. 209+/-30) and absent in neuropathic diabetes (128+/-23 vs. 115+/-20). Arginine stimulation produced a glucagon response in the neuropathic diabetics (106+/-16 vs. 523+/-103). The data indicate that the capacity to release glucagon during hypoglycemia is lost in diabetic neuropathy while glucagon responsiveness to arginine is retained. Neuropathy in diabetes may contribute to metabolic instability.
Diabetes 1977 Mar
PMID:Lack of glucagon response to hypoglycemia in diabetic autonomic neuropathy. 83 71

The authors present the results of clinico-neurological study on 3976 patients suffering from diabetes with the use of electrophysiological, biochemical and other methods. As revealed, the sex of diabetic patients, particularly at definite age periods produced a significant influence on the time of occurrence and the rate of development of various types of the central and peripheral neuropathy. Thus, at the age of under 30 years almost all the types of diabetic neuropathy originated earlier and developed more rapidly in women, and after the age of 50 years some of these types of neuropathies were more frequent and more pronounced in men. No significant differences in the incidence of many types of diabetic neuropathy were revealed at the age of from 30 to 50 years both in men and in women. The mentioned regularity was most distinctly traced in analysis of distal pelyneuropathy. A hypothesis is put forward on the causes inducing peculiarities of the diabetic neuropathy development depending on the sex factor.
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PMID:[Characteristics of development of diabetic neuropathy depending on sex of diabetic patients]. 92 18


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