Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic neuropathy, clinically established, occurs in up to 50% of diabetics, sometimes even prior to detection of diabetes mellitus. Distal symmetric polyneuropathy is the most frequent clinically established lesion of the nervous system. Other clinical entities, however, are not so rare, if they are studied with attention using differential diagnostic procedure. In this paper authors present two patients with sub-types of one of the rare forms of diabetic peripheral neuropathy--so called acute painful neuropathy: the first case associated with unregulated diabetes mellitus and in the second patient it occurred as a consequence of abrupt normalization of glycemic control with so-called insulin neuritis. The authors described the most important clinical characteristics of patients, differential diagnosis, therapy and the course of the disease.
 ...
PMID:[Acute painful neuropathy--2 case reports]. 864 48

Diabetic neuropathy is a debilitating disorder whose causation is poorly understood. A new theory proposes that neuropathy may arise as a consequence of loss of neurotrophic insulin-like growth factor (IGF) activity due to diabetes, superimposed on a slow continual loss due to aging. The prediction that IGF-I and IGF-II gene expression are reduced in diabetic nerves was recently tested and validated. Here we tested the prediction that IGF administration can prevent or reverse diabetic sensory neuropathy. Subcutaneous infusion of IGF-I or IGF-II, but not vehicle, halted (P < 0.01) the progression of hyperalgesia in streptozotocin-diabetic rats. Moreover, impaired sensory nerve regeneration was partially reversed within 2 weeks after treatment of diabetic rats with IGFs (P < 0.01). Impaired regeneration could also be prevented by daily subcutaneous IGF injections. The low replacement doses of IGFs were effective despite unabated hyperglycemia and weight loss. These results show that IGF replacement therapy can reverse or prevent diabetic sensory neuropathy independently of hyperglycemia or weight loss.
 ...
PMID:Insulin-like growth factors reverse or arrest diabetic neuropathy: effects on hyperalgesia and impaired nerve regeneration in rats. 869 62

Diabetic neuropathy is the most common neuropathy in industrialized countries, with a remarkable range of clinical manifestations. The usual pattern is a distal symmetrical sensory polyneuropathy, associated with autonomic disturbances. Less often, diabetes is responsible for a focal or multifocal neuropathy affecting cranial nerves, especially oculomotor nerves, and roots and nerves innervating proximal muscles of the lower limbs. Metabolic abnormalities due to hyperglycaemia, lack of insulin and their consequences and ischaemic phenomena secondary to diabetic microangiopathy account for nerve lesions.
 ...
PMID:Diabetic neuropathy: an update. 880 14

Diabetic neuropathy is characterized by progressive nerve fiber degeneration resulting in nerve fiber loss. In order to examine what role impaired nerve fiber regeneration may play in the progressive net nerve fiber loss, spontaneously diabetic biobreeding Worcester (BB/W) rats were subjected to sciatic nerve axotomy at 6 weeks of diabetes. Myelinated nerve fiber regeneration was examined morphologically and morphometrically at various time points following axotomy. The data were compared with those of axotomized control rats and diabetic rats treated with an aldose reductase inhibitor (ARI) from 1 week after onset of diabetes. Diabetic rats showed a significant attenuation of nerve fiber regeneration during the first 6 weeks following axotomy, which was normalized at 4 months postaxotomy. ARI treatment resulted in an initial burst of supranormal regeneration, which was normalized at 4 months postaxotomy. Impaired nerve fiber regeneration in diabetic rats was associated with a marked delay in preceding Wallerian degeneration and decreased phagocytic activity by macrophages, changes not demonstrated in ARI-treated diabetic rats. We propose that the impaired nerve fiber regeneration in the diabetic BB/W rat may, in part, be the result of impaired recruitment and/or function of macrophages necessary for the initiation of normal nerve fiber regeneration. The corrective effects of ARI treatment on the regenerative ability of diabetic peripheral nerve suggest that an activated polyol pathway may impact on both intrinsic and extrinsic mechanisms governing nerve fiber regeneration.
J Diabetes Complications
PMID:Nerve fiber regeneration following axotomy in the diabetic biobreeding Worcester rat: the effect of ARI treatment. 883 17

Diabetic neuropathy affects up to 60 percent of the estimated 13 million Americans who have diabetes mellitus. Foot and ankle complications are responsible for more hospital admissions than all other complications of diabetes mellitus combined. Neuropathy is more likely to affect patients who have higher degrees of hyperglycemia and a longer history of diabetes, and those who are older, taller and male. Diabetic neuropathy is usually diagnosed by the loss of ankle reflexes and distal vibratory sensation, but these signs may not always be present. Electromyography is useful in establishing a diagnosis. Treatment is directed toward alleviating the symptoms and correcting the underlying pathogenesis. Strict glycemic control is key in the ultimate prevention of diabetic neuropathy. The family physician can play a significant role in preventing this complication by emphasizing the importance of strict glycemic control.
 ...
PMID:Diabetic neuropathy. 896 47

There is enthusiasm for the application of knowledge concerning neurotrophins and other growth factors to human neurologic disease. New neurotrophins and other growth factors or inflammatory mediators that influence neurons and axons have been recently identified. Diabetic neuropathy may be an ideal testing ground for these substances because specific neurotrophins and growth factors could theoretically prevent loss of diabetic dorsal root ganglion (DRG) cells or enhance regeneration of diabetic nerves. Several of the neurotrophins support DRG cells in culture or prevent their loss during neonatal development, and a few help prevent retrograde loss of adult DRG cells after axotomy. Early Phase I trials suggest that nerve growth factor, brain-derived neurotrophic factor, and neurotrophin-3 are reasonably safe agents as administered in short-term trials to humans, but there are lingering experimental doubts. For example, it has not been established whether DRG cells are targeted by diabetes. Additional work suggests that simultaneous and sequential cocktails of trophins are required to support and rescue neurons and that the use of single agents may not be sufficient. Finally, it in uncertain whether trophins might act as a general tonic for DRG cells to prevent diabetes-related injury or whether they are actually deficient in human diabetic patients.
 ...
PMID:Neurotrophins and other growth factors in diabetic neuropathy. 898 29

Diabetic neuropathy is a common and debilitating complication of diabetes mellitus associated with high health costs. In recent years several clinical trials have been undertaken to test the efficacy of drug intervention in this disorder. The results of these trials have in general been disappointing. In this review we discuss selection criteria, efficacy endpoints, duration of clinical trials, and data collection and analyses. We offer suggestions based on past experiences that might improve trial design and execution in order to achieve improved results from treatment of this silent but common disorder.
 ...
PMID:Design of controlled clinical trials for diabetic polyneuropathy. 898 33

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.
 ...
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

Diabetes mellitus affects over 14 million people in the United States and the number of diabetics is increasing by 5% per year. Diabetic neuropathy (DN) is a common complication of diabetes and occurs in approximately 50% of diabetic patients over time. Clinical trials have proven that hyperglycemia almost certainly conditions the development of DN. Despite this fact, we still do not understand the mechanism(s) underlying DN. Several possible etiologies have been proposed including altered metabolism of polyol, lipids, or amino acids, vascular insufficiency, increased superoxide-induced free radical formation, impaired axonal transport or reduced neurotrophism. Accumulating evidence suggests that these defects are likely interrelated and that their interaction(s) within the diabetic milieu are responsible for the development and progression of DN. In this review we will discuss these theories, their interrelationships and how, collectively, these ideas may begin to explain the etiology of DN.
 ...
PMID:Pathogenesis of diabetic neuropathy. 935 81

Diabetic neuropathy, ranging from reversible mononeuropathies to irreversible and progressive autonomic neuropathy, is the most frequent neurological complication of diabetes. Diabetes also affects the central nervous system and manifestations vary from stroke to paroxysmal disorders related to fluctuations in blood glucose levels.
 ...
PMID:The neurology of diabetes. 950 58


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>