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

The main risk factors for plantar forefoot ulcers are loss of protective sensation due to sensory neuropathy and increased mechanical stress on the sole of the foot. The aim of this study was to find a better parameter than the plantar pressure to explain the occurrence of plantar ulcers under the metatarsalheads (MTHs). Twenty diabetic patients (3 Type 1 and 17 Type 2) each with 1 plantar ulcer and 23 Type 2 diabetic patients without plantar ulceration (controls), were investigated. The parameters of plantar pressure, length of contact time and pressure-time integral (PTI) were determined by pedography at defined foot regions. PTI represents the duration of mechanical stress on the foot. Based on the distribution of ulcers, the ratio of stress on the MTHs to that on the big toe was calculated. In diabetic patients with ulcers the difference of PTI between MTHs and hallux was higher at 153% and hence 3.2 times greater than the difference in plantar pressure between MTHs and hallux of 47.3%. In the control group the ratio of difference had a factor of 2 only because the corresponding difference in PTI was 85.1% and the difference in plantar pressure was 43.1%. These results may indicate that increased stress at the MTHs is responsible for the occurrence of planar ulcers compared with other regions of the sole. Diabetic patients with elevated PTI ratio are at risk of developing foot ulcers and therefore have to be provided with orthopaedic shoes to prevent foot ulceration.
Diabetes Nutr Metab 1999 Jun
PMID:Estimation of risk for plantar foot ulceration in diabetic patients with neuropathy. 1055 1

Foot and ankle sensory neuropathy may result from a variety of pathologic conditions, especially diabetes mellitus. Decreased sensation, particularly on the plantar surface of the feet, leads to obvious risks of cutaneous injury. Less obvious are the risks of fall-related injury associated with changes in other sensory systems of the foot and ankle, such as the receptors involved in joint movement and position perception. The results of a number of studies demonstrate that the neuropathic process affects these receptors in individuals with diabetes mellitus. Associated with the decreased sensory function of the foot and ankle is decreased performance on tests of static and dynamic postural stability. Subjective feelings of instability and an increased incidence of fall-related injuries have also been reported. The reduced postural stability in persons with diabetic neuropathy cannot be attributed exclusively to loss of plantar cutaneous sensation; it appears to be the result of a general loss of peripheral sensory receptor function in the lower legs, including that of the muscle spindles. During the evaluation of an individual with foot and ankle sensory neuropathy, the possibility of balance deficits should be given proper attention. Assessment of balance deficits could be particularly important when planning the course of rehabilitation for individuals with foot and ankle neuropathy who use modified footwear or have an amputation of a section of the foot or lower extremity.
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PMID:Foot and ankle sensory neuropathy, proprioception, and postural stability. 1061 69

Clinical neurological studies, blood pressure measurements and some haematological investigations were performed on a random sample of forty-four patients, at the Diabetes Out-Patient Clinic of the University Hospital of the West Indies (UHWI), to examine some of the factors that predispose to the development of the diabetic foot. Our results revealed that 86% of the patients had elevated glycosylated haemoglobin (HbA1 > 9.0%), 82% had clinical signs of peripheral sensory neuropathy, 29% had signs of autonomic neuropathy in addition to peripheral sensory neuropathy. Sixty-one per cent (61%) of the patients had ankle/arm systolic blood pressure ratio less than 1.0 and were diagnosed as having peripheral vascular disease (PVD). The group with neuropathy was found to have a significantly lower diastolic blood pressure (p < 0.0005) than the group without neuropathy. We believe that hyperglycaemia-induced vasodilation (indicated by a lower diastolic blood pressure) in a significant number of diabetics resulted in compensatory shunting of blood from the deeper tissues, including nerves, to the periphery. The resulting endoneural hypoxia could be responsible for the unusually high incidence of peripheral sensory neuropathy detected in this sample of diabetic patients. Metabolic factors may also play a role.
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PMID:Some clinical factors contributing to the development of the diabetic foot. 1063 45

To determine the prevalence of micro vascular and macro vascular complications in Asian Indian Type 1 diabetic subjects. There has been no major report on the prevalence of vascular complications in Type 1 diabetic patients in India. This study was done in Type 1 diabetic patients, aged < or =20 years at diagnosis of diabetes (n=617, M:F 322:295) with a minimum of 3 year follow-up. Standard diagnostic methodologies were used to test for micro vascular and macro vascular complications of diabetes. Retinopathy was detected in 13. 4% (background diabetic retinopathy 11.2%, proliferative diabetic retinopathy 1.9%, preproliferative 0.31%, maculopathy was seen in 13.3% of retinopathy cases), nephropathy in 7.1%, sensory neuropathy in 3.0%, ischaemic heart disease in 0.5% and peripheral vascular disease in 0.5% of the study subjects. Duration of diabetes showed positive association with retinopathy, nephropathy and neuropathy. Average glycosylated haemoglobin values, at follow up showed an association with retinopathy. Although the glycaemic control was suboptimal in the study group, prevalences of all complications, especially macro vascular complications were lower in Type 1 diabetic patients in this ethnic group, in comparison with the European or American counterparts.
Diabetes Res Clin Pract 2000 Apr
PMID:Vascular complications in young Asian Indian patients with type 1 diabetes mellitus. 1070

Chronic hyperglycemia results in a large deficit in nerve blood flow. Both autoxidative- and ischemia-induced lipid peroxidation occurs, with resultant peripheral sensory neuropathy in streptozotocin-induced diabetes in the rat. Free radical defenses, especially involving antioxidant enzymes, have been suggested to be reduced, but scant information is available on chronic hyperglycemia. We evaluated the gene expression of glutathione peroxidase, catalase, and superoxide dismutase (cuprozinc and manganese separately) in L4,5 dorsal root ganglion (DRG) and superior cervical ganglion, as well as enzyme activity of glutathione peroxidase in DRG and sciatic nerve in experimental diabetic neuropathy of 3 months and 12 months durations. We also evaluated nerve electrophysiology of caudal, sciatic-tibial, and digital nerves. A nerve conduction deficit was seen in all nerves in experimental diabetic neuropathy at both 3 and 12 months. Gene expression of glutathione peroxidase, catalase, cuprozinc superoxide dismutase, and manganese superoxide dismutase were not reduced in experimental diabetic neuropathy at either 3 or 12 months. Catalase mRNA was significantly increased in experimental diabetic neuropathy at 12 months. Glutathione peroxidase enzyme activity was normal in sciatic nerve. We conclude that gene expression is not reduced in peripheral nerve tissues in very chronic experimental diabetic neuropathy. Changes in enzyme activity may be related to duration of diabetes or due to post-translational modifications.
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PMID:Gene expression of antioxidant enzymes in experimental diabetic neuropathy. 1078 Jun 78

Diabetic subjects still have a reduced life expectancy despite many potential advances in patient care. Furthermore, population-based studies in well-defined cohorts of patients, to investigate the reduced life expectancies, are generally lacking. Computerized baseline data on a cohort of diabetic patients first attending our clinic during 1982-1985 were used to identify risk factors for increased mortality. This was carried out using an accelerated failure time (ACF) model. Out of 794 patients entered into the model, 201 (25.3%) patients died between 1982 and 1995. Baseline microvascular diabetic complications (peripheral sensory neuropathy and nephropathy) were found to be associated with increased mortality in patients, indicating that these are important, often overlooked, markers for those at greatest risk. Patients with type I (insulin dependent) diabetes mellitus were also identified as being at greater risk.
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PMID:Showing neuropathy is related to increased mortality in diabetic patients - a survival analysis using an accelerated failure time model. 1081 25

Trigeminal hyperalgesia frequently appears in diabetic neuralgia altering the transmission of orofacial sensory information. This study was designed to explore the effects of trigeminal hyperalgesia in streptozotocin-induced diabetes monitoring the expression of nitric oxide synthase in the trigeminal ganglion cells. The threshold to heat noxious stimuli decreased in diabetic animals. The number of NADPH-diaphorase (NADPH-d)-positive neurons significantly decreased in the diabetic rats compared with controls. Insulin treatment prevented the decreased nociceptive threshold and reduction of the number of NADPH-d-positive neurons. These findings point out that there is a relationship between the trigeminal nociceptive perception and NADPH-d neuronal expression suggesting that NO may play a role in the pathogenesis of trigeminal sensory neuropathy.
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PMID:Nitric oxide involvement in the trigeminal hyperalgesia in diabetic rats. 1081 40

Prescription of aerobic exercise for Type 2 diabetes mellitus (Type 2 DM) in clinical practice is frequently based on exercise intensity at maximum heart rate (60<HR(max)<79%), heart rate reserve (50<HR(reserve)<74%), and rating of perceived exertion (12<RPE<13). We examined these parameters in Japanese males with Type 2 DM at ventilatory threshold (VT) to investigate the exercise capacity of Type 2 DM patients and re-evaluate the exercise prescription. Fifty-six Japanese Type 2 DM males without autonomic neuropathy [age, 53.5+/-7.7 years; body mass index (BMI), 23.7+/-3.6 kg/m(2)] were enrolled and compared with 56 age- and BMI-matched healthy Japanese males. VT was determined breath by breath during exercise test using a ramp protocol and rates of oxygen consumption (VO(2)), work rate (WR), HR, DeltaHR, %HR(max), %HR(reserve), and RPE were measured at VT. Type 2 DM patients had significantly lower VO(2) (3.6+/-0.4 metabolic equivalents (METs)) and WR (62+/-14 W) than controls (VO(2), 3.9+/-0.6 METs; WR, 74+/-13 W). %HR(reserve), (32.6+/-7.7%) was also significantly lower compared with controls (37.6+/-8.3%), while %HR(max), was not different. RPE was also similar in diabetics (12.4+/-1.5) and controls (12.9+/-1.2), however, it was significantly lower in diabetic patients aged 60-69 years (11.8+/-2.0) and those with distal symmetric sensory neuropathy (12.2+/-1.0). Our results indicate reduced exercise capacity in Japanese Type 2 DM males and the exercise intensity of 60%HR(max), 30%HR(reserve), and RPE 12 is recommended in elderly diabetics and those with diabetic sensory neuropathy.
Diabetes Res Clin Pract 2000 Oct
PMID:Re-evaluation of exercise prescription for Japanese type 2 diabetic patients by ventilatory threshold. 1096 Jul 21

The diabetic Charcot foot is a major limb-threatening complication of long-term diabetes mellitus and neuropathy. Although first described over 100 years ago, we are still lacking definitive studies regarding its prevalence in this population, precise etiology, or most effective treatments. Trauma in the presence of peripheral sensory neuropathy and abundant arterial perfusion seem to be the primary causal factors leading to this severe foot deformity. Misdiagnosis or delayed diagnosis of osteoarthropathy allows the destructive phase of this disorder to continue with resultant further destruction of the foot architecture. The authors discuss the natural history of this entity as well as potential treatment options and recommendations. Through a better understanding of the underlying pathogenesis, Charcot arthropathy can be more effectively managed and thereby limit the development of severe deformity, ulceration, infection and limb loss.
Diabetes Metab Res Rev
PMID:Management of the diabetic Charcot foot. 1105 91

We hypothesized that diabetic sensory neuropathy is associated with activation of apoptosis and concomitant mitochondrial dysfunction. Studies were performed in excised intact and acutely dissociated dorsal root ganglion (DRG) neurons from control and streptozotocin-induced diabetic rats with decreased peripheral nerve conduction velocities (NCV). Apoptosis was increased in acutely dissociated DRG neurons from 3- to 6-week-old diabetic rats. Basal mitochondrial membrane potential (deltapsi) was significantly more positive in DRG neurons from diabetic rats. Depolarization with glutamate resulted in significantly more positive deltapsi and delayed recovery of deltapsi in neurons from diabetic rats. Restoration of euglycemia for 2 weeks with insulin implants normalized NCV, deltapsi, and apoptosis. Intact and acutely dissociated neurons from diabetic rats demonstrated decreased Bcl-2 levels and translocation of cytochrome C from the mitochondria to the cytoplasm. Neither levels of Bax nor levels of Bcl-XL were altered in diabetic neuropathy. Apoptosis associated with mitochondrial dysfunction may contribute to the pathogenesis of diabetic sensory neuropathy.
Diabetes 2000 Nov
PMID:Diabetic peripheral neuropathy: evidence for apoptosis and associated mitochondrial dysfunction. 1107 62


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