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

Vascular and neuropathic complications of diabetes are a significant cause of morbidity and mortality. Symmetric polyneuropathy is the most common diabetic neuropathy. Treatment of the mononeuropathies consists of pain control and physical therapy to maintain muscle tone. Prognosis for recovery is excellent. Renal and retinal microangiopathy produce most of the clinically significant mortality and morbidity in diabetes. Recent advances in chronic hemodialysis and renal transplantation have improved the outlook for diabetics with end-stage nephropathy. The poor prognosis for retention of vision in diabetic malignant retinopathy has led to exploration of various forms of palliative therapy, including pituitary ablation, xenon arc coagulation, and laser treatment. Cardiovascular disease is more prevalent among diabetics than among the general population, according to a recent study, and mortality from this cause is three times higher. Animal studies linking aortic wall metabolism and atherosclerotic changes with hyperglycemia suggest that poor control of diabetes may play a role in the development of vascular lesions.
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PMID:Neuropathic and vascular complications occurring in diabetes. 124 35

Twenty-one patients with familial amyloidosis and polyneuropathy have been examined for the presence of skin lesions, localized to the lower legs and feet. The lesions were classified as atrophic skin lesions, hypertrophic scar-like skin lesions, rubeosis plantarum, spontaneous blisters, necrotic skin lesions, yellow nails, traumatic skin lesions, purpura and abundant pigmented small non-atrophic spots. Skeletal destructions in the feet were also demonstrated. In many respects these lesions are similar to those of long-standing diabetes mellitus. I studied the cutaneous reactions to local thermal trauma with heat and cold to the legs and forearms in 11 patients. Petechiae were observed within the area of traumatization with either heat or cold more often in patients than in controls. Four of the 11 patients developed atrophic circumscribed skin lesions at the site of traumatization.
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PMID:Skin lesions of the legs and feet and skeletal lesions of the feet in familail amyloidosis with polyneuropathy. 125

Disturbances of the peripheral nervous system, summarised under the term "diabetic polyneuropathy", are a well-known complication of long-term diabetes mellitus. However, there is little information about the fact that these conditions may lead to difficulties in monitoring neuromuscular blockade by peripheral nerve stimulation during general anaesthesia. We report two diabetic patients (40 resp. 62 years of age) in whom a total of four ophthalmological operations were performed under general anaesthesia. In all cases monitoring of neuromuscular transmission was attempted by stimulation of the left ulnar nerve slightly proximal to the wrist, but not even the usual calibration could be obtained in either patient. Checks confirmed that the nerve stimulator was functional and the electrodes--in all cases self-adhesive, pregelled surface electrodes--were placed correctly. In order to evaluate the hypothesis that disturbances of peripheral nerve function might be responsible, the patients were examined neurophysiologically in the postoperative period. Both patients showed severe alterations in peripheral nerve conduction: a sensory response could not be evoked in any of the extremities and the ulnar distal motor latency time was pathologically prolonged (5.4 ms in patient 1 and 4.9 ms in patient 2; normal: 1.4-4.0 ms). Therefore, in accordance with the clinical symptoms, the diagnosis of diabetic polyneuropathy was established. These cases demonstrate that severe disturbances of the peripheral nervous system may render neuromuscular monitoring impossible.
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PMID:[Failure of relaxometry in diabetic polyneuropathy]. 132 74

The authors have studied, by biopsy of the tip of the big toe, the histologic changes in microvessels of patients affected by ethylic polyneuropathy. Patients affected by diabetes, hypertension, peripheral arterial or venous diseases, or dermatologic diseases or vasculitides were excluded. The mean of daily drinks was 310 +/- 105 g of alcohol, chiefly wine. Important pathologic modifications were noted; complete narrowing of the arteriovenous anastomosis, regressive changes of the Vater-Pacini corpuscles, and dilatation of the small veins and the capillaries. The findings were compared with those of a patient affected by ulcerans and mutilans acropathy of Bureau and Barriere, a typical disease of alcoholics. The same characteristics appeared: profound changes of the structure of the smallest vessels, with sclerosis, extended to the interstitium. In a previous study of the authors, 3 other patients affected by Bureau-Barriere disease showed the same pattern. These alterations can be explained as the effect of alcohol on the microvessels.
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PMID:Microangiopathy of ethylic polyneuropathy. 133 53

The most common form of neuropathy associated with diabetes mellitus is distal symmetric sensorimotor polyneuropathy, often accompanied by autonomic neuropathy. This disorder is characterized by striking atrophy and loss of myelinated and unmyelinated fibers accompanied by Wallerian degeneration, segmental, and paranodal demyelination and blunted nerve fiber regeneration. In both humans and laboratory animals, this progressive nerve fiber damage and loss parallels the degree and/or duration of hyperglycemia. Several metabolic mechanisms have been proposed to explain the relationship between the extent and severity of hyperglycemia and the development of diabetic neuropathy. One mechanism, activation of the polyol pathway by glucose via AR, is a prominent metabolic feature of diabetic rat peripheral nerve, where it promotes sorbitol and fructose accumulation, myo-inositol depletion, and slowing of nerve conduction by alteration of neural Na(+)-K(+)-ATPase activity or perturbation of normal physiological osmoregulatory mechanisms. ARIs, which normalize nerve myo-inositol and nerve conduction slowing, are currently the focus of clinical trials. Other specific metabolic abnormalities that may play a role in the pathogenesis of diabetic neuropathy include abnormal lipid or amino acid metabolism, superoxide radical formation, protein glycation, or potential blunting of normal neurotrophic responses. Metabolic dysfunction in diabetic nerve is accompanied by vascular insufficiency and nerve hypoxia that may contribute to nerve fiber loss and damage. Although major questions about the pathogenesis of diabetic neuropathy remain unanswered and require further intense investigation, significant recent progress is pushing us into the future and likely constitutes only the first of many therapies directed against one or more elements of the complex pathogenetic process responsible for diabetic neuropathy.
Diabetes Care 1992 Dec
PMID:Complications: neuropathy, pathogenetic considerations. 146 45

Diabetic neuropathy is a common complication of diabetes that may be associated both with considerable morbidity (painful polyneuropathy, neuropathic ulceration) and mortality (autonomic neuropathy). The epidemiology and natural history of diabetic neuropathy is clouded with uncertainty, largely caused by confusion in the definition and measurement of this disorder. We have reviewed various clinical manifestations associated with somatic and autonomic neuropathy, and we herein discuss current views related to the management of the various abnormalities. Although unproven, the best evidence suggests that near-normal control of blood glucose in the early years after diabetes onset may help delay the development of clinically significant nerve impairment. Intensive therapy to achieve normalization of blood glucose also may lead to reversibility of early diabetic neuropathy, but again, this is unproven. Our ability to manage successfully the many different manifestations of diabetic neuropathy depends ultimately on our success in uncovering the pathogenic processes underlying this disorder. The recent resurgence of interest in the vascular hypothesis, for example, has opened up new avenues of investigation for therapeutic intervention. Paralleling our increased understanding of the pathogenesis of diabetic neuropathy, refinements must be made in our ability to measure quantitatively the different types of defects that occur in this disorder. These tests must be validated and standardized to allow comparability between studies and more meaningful interpretation of study results.
Diabetes Care 1992 Dec
PMID:Diabetic neuropathies. 146 46

Aminoguanidine prevents some pathophysiologic changes typical of streptozocin diabetes and, therefore, might be efficacious in prevention or treatment of human diabetic polyneuropathy. In order to evaluate the possible toxicity of aminoguanidine on peripheral nerves, Sprague-Dawley rats received aminoguanidine intraperitoneally in dosages of 0, 50, 100, and 300 mg/kg per day for 3 months. Only rats receiving the highest dosages developed acute and chronic behavioral changes and had decreased weight gain. Minor hepatic dysfunction also was observed in this group. Teased-fiber abnormalities were not significantly more frequent in the highest dosage group than in controls. Likewise, a significant morphometric abnormality was not found for the peroneal nerve. Mild changes were found in the highest dosage group compared to the control group in the sural nerve (increased fiber density, decreased myelin area). We interpret the small morphometric differences for the sural nerve as due to maldevelopment. We found no evidence that aminoguanidine at a high dosage (300 mg/kg per day) caused fiber degeneration or demyelination.
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PMID:Neuropathologic and morphometric effects of aminoguanidine on rat nerves. 146 58

In a group of 46 consecutive outpatients attending the diabetic clinic of our Metabolic Department, 30 insulin-dependent and 16 non-insulin-dependent diabetic patients in stable metabolic control, and in 38 age-matched controls, we measured vibration perception threshold with biothesiometer and autonomic function, by means of the five classical cardiovascular tests: R-R interval variations during deep breathing, Valsalva ratio, lying-to-standing, postural hypotension, and sustained handgrip. None of the patients complained of symptoms related to diabetic autonomic neuropathy (DAN) or sensory polyneuropathy. Vibration perception threshold positively correlated with Valsalva ratio (p < 0.05) and deep breathing (p < 0.01), and all of them correlated with age (p < 0.001), but not with duration of diabetes and metabolic control. Patients scored significantly lower than controls in vibration perception threshold and all of the autonomic function tests. According to the outcomes of cardiovascular tests ["Autonomic Score" (AS)] patients were divided into two different groups: presence (DAN+ = AS > or = 3) or absence (DAN- = AS < 3) of autonomic neuropathy. The DAN- group (n = 28, 60.9%) showed no significant differences from the DAN+ group (n = 18, 39.1%) in age, duration of diabetes, glycated hemoglobin, or body mass index. DAN+ patients had vibration perception threshold measured at the first toe tip and at external malleolus significantly higher than DAN- patients (p < 0.01 and p < 0.001, respectively) and controls (p < 0.005), as well as all the other cardiovascular tests except sustained handgrip. No difference in any of these items was observed between DAN- patients and controls.(ABSTRACT TRUNCATED AT 250 WORDS)
J Diabetes Complications
PMID:Measurable deficit of autonomic and sensory nerve function in asymptomatic diabetic patients. 147 40

Present-day methods of treatment of insulin-dependent diabetes mellitus (IDD) fail to prevent the development of complications in the majority of patients in 5-10 years after the disease manifestation. There are no radical methods for the treatment of this condition, therefore any new treatment modality that may help delay the development of complications and deterioration of the quality of life should be used along with the traditional methods. Deportalization of the pancreatic blood outflow was carried out in 148 IDD patients and its remote (up to 5 years) results analyzed. The surgery was carried out in patients with medium-severe and grave conditions. Under study were carbohydrate and lipid metabolism, liver, kidney, and heart functions, retinal vessel status, and painful manifestations of distal polyneuropathy, as well as changes of the quantity of functioning capillaries and the rheovasographic index. Surgery resulted in reduced insulin requirement, disappearance of hypoglycemic comas, reduced peripheral resistance of the vessels, increased cardiac output index and a higher working capacity of the patients, disappearance of paroxysms and pains in the lower limbs, etc. The authors suppose that changed course of the disease is connected with recovery of the insulin-glucagon coefficient in the liver in glucagon-containing blood shunting into the total blood stream and with the pharmacologic effect of glucagon getting into the systemic blood stream.
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PMID:[Late results of pancreatic blood outflow deportalization and its significance in the combined modality treatment of diabetes mellitus]. 148 May 92

Gastrointestinal dysfunction due to autonomous neuropathy is a complication described in various diseases such as diabetes mellitus, multiple sclerosis, and familial amyloidosis with polyneuropathy. We present the results of a prospective investigation of bile acid malabsorption in 17 patients with familial amyloidosis by means of 75Se-labelled homocholic-tauro acid (SeHCAT). The diagnosis was in all cases verified by the DNA test for mutation of transthyretin in position 30. Small-intestinal biopsy specimens were examined for deposits of amyloid, and the presence of gastric retention was evaluated by gastroscopy. In addition, the patients were investigated for bacterial overgrowth by means of the bile acid breath test (BABT). A high frequency of abnormal BABT results (44%) was encountered. However, 65% also had abnormal low SeHCAT values, indicating bile acid malabsorption. Only two patients had abnormal BABT and normal SeHCAT results, indicating bacterial contamination of the small intestine. Bile acid losses increased with the duration of gastrointestinal symptoms. Significantly lower SeHCAT values were encountered in patients with gastric retention, whereas the occurrence of amyloid deposits in small-intestinal biopsy specimens was without effect on SeHCAT retention. Bile acid malabsorption is frequently encountered in familial amyloidosis with polyneuropathy and seems to be more closely associated with gastrointestinal motility dysfunction than with amyloid deposits in the intestinal mucosa.
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PMID:Bile acid malabsorption caused by gastrointestinal motility dysfunction? An investigation of gastrointestinal disturbances in familial amyloidosis with polyneuropathy. 150 82


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