Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic neuropathy affects both sensory and autonomic peripheral nerve fibres. Vasoactive intestinal polypeptide (VIP) is present in autonomic fibres which modulate sweat secretion, while calcitonin gene-related peptide (CGRP) is localized to cutaneous sensory fibres. In this study, immunohistochemistry and image analysis were used to assess changes of VIP and CGRP, and of the pan-neuronal marker protein gene-product (PGP)-9.5, in skin biopsies of 18 patients affected by type 1 diabetes (age range 18-46 years) and from seven aged-matched controls. Patients were divided into three groups: group 1 (n = 6), with diabetes for 6 months to 3 years; group 2 (n = 5), with the disease for 5-10 years; and group 3 (n = 7), with diabetes for more than 10 years. VIP immunoreactivity (IR) and PGP-9.5-IR were significantly reduced around sweat glands (P < 0.005) in groups 2 and 3. Epidermal CGRP-IR and PGP-9.5-IR were significantly reduced in group 3 (P < 0.05). Twenty-eight per cent (5/18) of all patients showed high VIP-IR around sweat glands (> 95 per cent confidence limits of controls) and all of these patients had diabetes for less than 3 years. Conversely, 55 per cent (10/18) of patients had low VIP-IR (< 5 per cent confidence limit of controls). The latter, compared with the former, showed a significantly longer duration of diabetes (Fisher exact test P = 0.002), presence of clinical autonomic neuropathy (Fisher exact test P = 0.04), and a reduced sural nerve conduction velocity (Fisher exact test P = 0.04). These results suggest that quantitative immunohistochemical analysis of peptide-containing cutaneous nerves allows an objective evaluation of nerve fibre alterations at early stages of diabetes than is currently possible with neurophysiological functional tests.
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PMID:Early increase precedes a depletion of VIP and PGP-9.5 in the skin of insulin-dependent diabetics--correlation between quantitative immunohistochemistry and clinical assessment of peripheral neuropathy. 844 92

Diabetic neuropathy may cause an alteration of the function of the muscles of the sole of the foot. This is at the origin of the chronic dislocation of the articular heads, mainly of the little metatarsal bones (neuro diabetes arthropathy), with formation of areas of pathological pressure. The tissues below being chronically under pressure are affected by trophic lesions called "plantar perforating disease". Recovery may be obtained by not exposing the injured area of the foot to pressure and through careful local therapy. This doesn't prevent disease from appearing again, even though some specially conceived soles are being used, aiming at a correct weight redistribution on the sole of the foot. The clinical case we are describing applies to a man affected by insulin dependent diabetes mellitus, with relapsing diabetic foot ulcers, in spite of him using a specifically designed sole. Such lesion is aggravated by a serious infection which, by gradually penetrating in depth, leads to osteomyelitis, affecting the 5th Metatarsal head. The bone area, dislocated by neuroarthropathy, was presumably responsible for the persisting plantar lesion. The amputation of this infected necrotic structure, has led to the overcoming of the serious septic problem. By eliminating the bone link responsible for the transmission of the pathological pressure, the plantar lesion the patient had been suffering from for a long time, has consequently disappeared.
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PMID:[Diabetic foot. A clinical case]. 850 59

Diabetic neuropathy is thought to comprise a reversible metabolic and an irreversible structural component of neuronal abnormality. To investigate whether the cardiac sympathetic denervation recently described in newly diagnosed, but metabolically stabilized, diabetic patients without myocardial perfusion abnormalities reflects transient or permanent sympathetic abnormalities, 123-I-metaiodobenzylguanidine (123-I-MIBG) scintigraphy was performed in 16 patients with insulin-dependent (Type 1) diabetes mellitus (IDDM) 1 year after initial assessment and diagnosis. All patients had been treated with an intensified insulin therapy for 1 year. HbA1c had fallen from 11.5 +/- 2.0% to 6.3 +/- 0.9% (p < 0.001). The global myocardial 123-I-MIBG uptake (score 1-6) had improved in 7 patients at 1 year, remained unchanged in 7, and deteriorated in 2 patients. Regionally, the myocardial uptake score of the posterior and septal regions had improved significantly (p < 0.01, p = 0.02) with a mean uptake score in the groups of 3.8 +/- 1.1 and 3.4 +/- 1.2 at diagnosis versus 2.6 +/- 0.5 and 2.5 +/- 0.9 at 1 year. Myocardial uptake scores of the anterior, lateral, and apical regions had also improved in 7, 6, and 9 patients, but the mean changes of these scores did not reach significance. The study demonstrates that scintigraphically assessed cardiac sympathetic denervation in newly diagnosed, but metabolically stabilized, IDDM patients is partially reversed with improved metabolic control after 1 year of intensified insulin therapy. We suggest that even in the early stage of IDDM, cardiac sympathetic dysfunction is composed of reversible and irreversible neuronal abnormalities.
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PMID:Partial restoration of scintigraphically assessed cardiac sympathetic denervation in newly diagnosed patients with insulin-dependent (type 1) diabetes mellitus at one-year follow-up. 901 55

Diabetic neuropathy is thought to comprise a reversible metabolic and an irreversible structural component of neuronal abnormality. To study whether cardiac sympathetic dysinnervation in poorly controlled longer-term Type 1 Diabetes Mellitus (DM) without myocardial perfusion abnormalities is partially reversible with improved metabolic control, 123-I-metaiodobenzylguanidine (123-I-MIBG) scintigraphy (myocardial uptake score 1-6) was performed in 11 Type 1 DM patients (HbA1c 12.0 +/- 1.8%, duration of diabetes 10 +/- 4 yrs) one year after initial assessment. During follow-up, all patients had been treated with intensive insulin therapy and at one year, HbAlc had fallen to 8.4 +/- 1.4% (p < 0.01). The global myocardial 123-I-MIBG uptake score had improved in 5 patients at one year, remained unchanged in 5 patients, and deteriorated in 1 patient. Cardiac sympathetic dysinnervation (123-I-MIBG myocardial uptake (MU) score >2), initially observed in 10 patients, was detectable in 8 patients at follow-up. Myocardial uptake scores of the anterior, lateral, posterior, septal and apical region had improved in 6, 6, 6, 7 and 6 patients, but the mean changes of these scores did not reach significance. In patients with substantial improvement of metabolic control (HbAlc 7.3 +/- 0.6% at one year, mean HbA1c of months 2-12: 7.8%, n = 6), global myocardial uptake had improved from 4.3 +/- 1.0 to 3.2 +/- 1.0 (p < 0.05). Respectively, myocardial uptake score of the anterior, posterior and septal region had ameliorated: 3.8 +/- 1.3 vs 2.3 +/- 0.8 (p < 0.05), 4.0 +/- 1.7 vs 2.5 +/- 1.0 (p < 0.05), 4.3 +/- 1.2 vs 3.2 +/- 1.5 (p < 0.05). In conclusion, cardiac sympathetic dysinnervation in poorly controlled longer-term Type 1 DM patients is dominated by irreversible neuronal abnormalities. Substantial metabolic improvement, however, partially restores cardiac sympathetic dysinnervation, indicating the presence of a reversible component of cardiac sympathetic dysfunction in longer-term Type 1 DM.
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PMID:Scintigraphically assessed cardiac sympathetic dysinnervation in poorly controlled type 1 diabetes mellitus: one-year follow-up with improved metabolic control. 1048 43

Diabetic neuropathy encompasses various disturbances concerning somatic and autonomic nervous system and has significant impact on prognosis and course of diabetes mellitus. The aim of the work is an evaluation of vestibulo-spinal reflexes in children and young adults suffering from diabetes mellitus type 1. Material--95 children and young adults aged from 6 to 28 years with diabetes mellitus type 1 diagnosed. The control group consisted of 44 otoneurologically healthy subjects aged from 6 to 28 years. After detailed medical history collection and physical ENT examination stato-posturography was performed in each case. Posturographer PE 62 Model 04 was applied in the studies. Static posturography as well as dynamic one (one leg standing test) was performed in each case. 6 patients belonging to diabetic group complained about vertigo or dizziness. There were worse stabilograms parameters in diabetic group in comparison to control one, statistically significant in younger children. There were better stabilogram parameters in diabetic patients with longer history of the disease. The parameters analysed were significantly worse in the subgroup with not compensated diabetes. The parameters were slightly better in relation to the presence of hypoglycaemic incidents. No apparent differences in stabilograms parameters were present in relation to the presence of diabetic complications. Diabetes mellitus type 1 with slight or without complications does not have significant influence on vestibulo-spinal reflexes and posture stability of the patients. Balance organ disturbances in diabetes mellitus type 1 in children and young adults despite their presence have subclinical course. Perhaps one should consider monitoring of those disturbances in the course of the disease.
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PMID:[The influence of metabolic disturbances present in diabetes mellitus type I on vestibulo-spinal reflexes in children and young adults]. 1237 5

Diabetic neuropathy (DN) represents a major complication of type 1 diabetes mellitus (T1DM) but there is considerable uncertainty as to its incidence, prevalence, diagnosis and prognosis in pediatric population. Generally, DN is classified as polyneuropathy, focal neuropathy and autonomic neuropathy. The latter seems to be detectable even in asymptomatic children and adolescents with diabetes and is associated with the most serious consequences, such as hypoglycemia unawareness and cardiovascular dysfunction. A near-normal control of blood glucose in the early years after onset of diabetes may delay the development of clinically significant nerve impairment and, therefore, children and adolescents with diabetes represent a critical target for primary prevention of this complication. The aim of this review is to focus on the main clinical, epidemiological and prognostic aspects of DN in children and adolescents with T1DM. Etiopathogenetic theories and diagnostic tools are also reviewed from in a pediatric perspective.
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PMID:Diabetic neuropathy in children and adolescents. 1504 90

Diabetic neuropathy is a common complication of diabetes mellitus. Effective blood glucose control retards changes in nerve conduction velocity in type 1 diabetes. This study examined the relationship between glycemic control and electrophysiologic changes in diabetic neuropathy in 57 type 2 diabetic patients. Nerve conduction in the peroneal motor nerve, tibial motor nerve, and sural nerve were measured at study entry and at follow-up 24+/-3.12 months later. Changes in individual nerves are expressed as a percentage change (PC) and overall electrophysiologic changes are expressed as the sum of individual PCs. The PCs for peroneal motor nerve velocity, tibial motor nerve velocity, and sural nerve velocity were all lower in patients with a mean HbA1c of 8.5% or less compared with those in patients with a mean HbA1c of more than 8.5%, and SPCV (sum of PC in velocity) was significantly inversely correlated with mean HbA1c. However, there was no significant difference in SPCV in subjects with or without hypertension, hypertriglyceridemia, or low high-density lipoprotein cholesterol concentration. In conclusion, hyperglycemia is the most important etiology for electrophysiologic progression in type 2 diabetic patients. Furthermore, a mean HbA1c of more than 8.5% will result in significant deterioration in electrophysiology.
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PMID:Effect of glycemic control on electrophysiologic changes of diabetic neuropathy in type 2 diabetic patients. 1575 84

Diabetic neuropathy is a debilitating disorder that occurs in nearly 50 percent of patients with diabetes. It is a late finding in type 1 diabetes but can be an early finding in type 2 diabetes. The primary types of diabetic neuropathy are sensorimotor and autonomic. Patients may present with only one type of diabetic neuropathy or may develop combinations of neuropathies (e.g., distal symmetric polyneuropathy and autonomic neuropathy). Distal symmetric polyneuropathy is the most common form of diabetic neuropathy. Diabetic neuropathy also can cause motor deficits, silent cardiac ischemia, orthostatic hypotension, vasomotor instability, hyperhidrosis, gastroparesis, bladder dysfunction, and sexual dysfunction. Strict glycemic control and good daily foot care are key to preventing complications of diabetic neuropathy.
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PMID:Evaluation and prevention of diabetic neuropathy. 1595 41

Diabetic neuropathy (DN) is a debilitating complication of type 1 and type 2 diabetes. Rodent models of DN do not fully replicate the pathology observed in human patients. We examined DN in streptozotocin (STZ)-induced [B6] and spontaneous type 1 diabetes [B6Ins2(Akita)] and spontaneous type 2 diabetes [B6-db/db, BKS-db/db]. Despite persistent hyperglycemia, the STZ-treated B6 and B6Ins2(Akita) mice were resistant to the development of DN. In contrast, DN developed in both type 2 diabetes models: the B6-db/db and BKS-db/db mice. The persistence of hyperglycemia and development of DN in the B6-db/db mice required an increased fat diet while the BKS-db/db mice developed severe DN and remained hyperglycemic on standard mouse chow. Our data support the hypothesis that genetic background and diet influence the development of DN and should be considered when developing new models of DN.
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PMID:Mouse models of diabetic neuropathy. 1780 49

Diabetic neuropathy and its underlying pathogenesis are reviewed. It has been documented for some time that diabetic neuropathy differs in both human and experimental type 1 versus type 2 diabetes. Such differences are accounted for by impaired insulin action and signal transduction in type 1 diabetes, whereas hyperglycemia per se contributes equally to neuropathy in the two types of diabetes. Such differences in basic initiating factors and pathogenesis translate into differences in the functional and structural expressions of neuropathy in type 1 and type 2 diabetes. Type 1 neuropathy shows a more rapid progression with more severe functional and structural changes. Several experimental mono-therapies have been tested over the last decades which unfortunately have not been efficacious. Therefore discrepancies in underlying pathogenetic mechanisms in the two types of diabetic neuropathy will have to be taken into account in the design of future therapies, which should target several key pathogenetic mechanisms. Therapies that meet these criteria include replacement of acetyl-L-carnitine and replenishment of C-peptide in type 1 diabetic neuropathy.
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PMID:The heterogeneity of diabetic neuropathy. 1850 46


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