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

Diabetes mellitus, which results from a failure of the endocrine system to control blood glucose levels within normal limits, affects approximately 15% of the population over the age of 65 in developed countries. Between 20-50% of people with diabetes for more than 10 years will experience symmetrical distal sensory neuropathy resulting in a progressive, distal to proximal, loss of sensation in the lower extremities. The most common consequence is plantar ulceration that too often results in partial or total amputation of the foot. While neuropathy is a major permissive factor, plantar ulcers occur at locations of high plantar pressures. The measurement of pressure using tools developed and refined in the field of biomechanics has been shown to be a valuable asset to the management of the foot at risk for ulceration. In particular, the use of in-shoe measuring techniques has the potential to revolutionize the prescription of therapeutic footwear. Biomechanical techniques have also helped to evaluate other consequences of diabetic neuropathy on the foot such as callus formation, foot deformity, limited joint mobility and bony abnormalities. The reduction of afferent information from the lower extremities implies a lack of active feedback thought to be necessary for the control of human movements such as posture and gait. Our results show that diabetic neuropathy results in a significant increase in sway during standing that is not compensated for by other sensory systems. The study of the sagittal plane movements of the same individuals walking on a treadmill showed little effect on the kinematic control of gait when compared to age matched nonneuropathic control groups. This may indicate the dominance of efferent input over afferent feedback during gait. We believe that the study of the biomechanical consequences of diabetes can act as a model for many other diseases that have yet to come under the scrutiny of a multidisciplinary team.
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PMID:Ulceration, unsteadiness, and uncertainty: the biomechanical consequences of diabetes mellitus. 850 50

Familial polyneuropathy mimicking Charcot-Marie-Tooth disease associated with parkinsonism and dementia has been reported in literature. We present with similar peroneal muscular atrophy, rigidity of upper extremities, severe peripheral neuropathy, mental retardation and diabetes mellitus. The patient, a 42-year-old man, developed progressive muscle weakness, mental retardation and difficulty in walking in childhood. Because of his pes cavus, he had three surgical operations. At the age of 20 years, he developed distal muscular atrophy of lower limbs. On neurological examination, all limb muscles were atrophic, especially in lower one third of the thigh. Rigidity was noted in the upper extremities. Deep tendon reflexes were hyperactive in the upper and diminished in the lower extremities. Muscle CT revealed low density areas in all the muscles examined, specially in the gastrocnemius and anterior tibial muscles. Needle EMG showed neurogenic change in the forearm, but not in the lower limbs, because of no voluntary contractions obtained due to severe muscle atrophy. Marked slowing of motor conduction velocity with muscle action potentials of very low amplitude was found in the ulnar nerve. Muscle action potentials were not elicited in the median and peroneal nerves. Sensory action potentials were not elicited from the median, ulnar and sural nerves. These findings were consistent with axonal polyneuropathy. In the sural nerve biopsy, the densities of myelinated fibers were markedly decreased. However, unmyelinated fiber densities were relatively preserved. Onion bulb formation was not found. This patient may be classified into hereditary motor-sensory neuropathy (HMSN) type II based on the clinical findings delayed nerve conduction velocities and axonal degeneration in the sural nerve. He has also diabetes mellitus. CT of the brain revealed nothing particular. He is one of members with familial Parkinson's disease (PD) developed in Sagamihara. Peroneal muscular atrophies are not necessarily associated with PD, though it has been occasionally complicated in various neuro-degenerative diseases including parkinsonism. We are now following the patient to detect the symptom of Parkinson's disease for early treatment.
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PMID:[An unusual case of peroneal muscular atrophy with rigidity, polyneuropathy, mental retardation, and diabetes mellitus developed in familial Parkinson's disease]. 866 30

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.
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PMID:Insulin-like growth factors reverse or arrest diabetic neuropathy: effects on hyperalgesia and impaired nerve regeneration in rats. 869 62

We studied the features and frequency of sensory neuropathy among 79 HIV-1-infected individuals participating in a multicenter clinical trial of zalcitabine (2'3'-dideoxycytidine, or ddC) antiretroviral therapy. The trial compared zalcitabine monotherapy (2.25 mg/day) versus combination therapy (2.25 mg/day ddC) with zidovudine (ZDV, formerly AZT) versus monotherapy with ZDV alone. Neuropathy developed in 34% of ddC recipients but in only 4% of comparable patients treated with ZDV alone--a 7.9-fold increase in the attack rate of neuropathy. Using risk factor analysis, we found that diabetes mellitus was significantly associated with the development of toxic neuropathy (p = 0.02), and weight loss may contribute to its appearance. Like HIV-associated sensory neuropathy, ddC-related toxic neuropathy is a predominantly sensory, length-dependent, symmetric, painful neuropathy. Dose reduction lessened the severity of symptoms, although objective signs of neuropathy persisted. Patients with subclinical neuropathies or significant neuropathy risks such as diabetes may be poor candidates for ddC therapy.
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PMID:Low-dose zalcitabine-related toxic neuropathy: frequency, natural history, and risk factors. 878 79

The purpose of this study is to prospectively evaluate skin temperatures at the site of neuropathic ulceration before, during, and after wound healing using the contralateral extremity as a physiologic control and to evaluate variables that may influence skin temperature gradients. We studied 17 male and 8 female diabetics with mean age and duration of diabetes of 52.4 +/- 11.6 years and 13.8 +/- 7.8 years with grade I (Meggitt-Wagner) plantar ulcers. All patients received weekly cast changes with wound and skin temperature assessments. After healing, all patients were fitted with prescription shoe gear. Temperatures on the ulcerated foot were higher than those on the contralateral foot on initial presentation (91.1 vs. 84.2 degrees F, t = 8.9, p < 0.0001, 95% Cl 5.3 to 8.5), but the same following healing. Patients with vibration perception thresholds greater than 45 V had wider skin temperature gradients than those with lesser degrees of sensory neuropathy (8.8 +/- 4.1 vs. 4.9 +/- 2.5 degrees F, p = 0.007). Additionally, subjects with toe brachial indices below 0.60 had greater skin temperature gradients at the site of ulceration than those with higher indices (9.4 +/- 4.0 vs. 5.8 +/- 3.4 degrees F, p = 0.01). There was not a significant difference in initial skin temperature gradients by duration of wound prior to treatment, duration of wound healing, sex, maximum plantar pressure, or hemoglobin A1C level.
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PMID:Monitoring neuropathic ulcer healing with infrared dermal thermometry. 887 57

Vascular perfusion and neuropathologic evaluation of the lumbar spinal roots and dorsal root ganglia (DRG) were studied in rats with longstanding (duration 12-15 months) streptozotocin-induced diabetes and age- and sex-matched control rats. We also undertook nerve conduction studies including F-wave recordings and measured blood flow in sciatic nerve, DRG, and superior cervical ganglion (SCG). Light microscopically, changes of the myelin sheath in the dorsal and ventral roots and vacuolated cells in the DRG were the major findings, being significantly higher in diabetic rats than in control rats. The effects of the diabetic state on myelin splitting were greater in the dorsal than ventral roots. Electron microscopic studies revealed a gradation of changes in myelin from mild separation to severe ballooning of myelin with relative axonal sparing. DRG cells showed vacuoles of all sizes with cristae-like residues, suggestive of mitochondria. These findings suggest that diabetes mellitus has a dual effect: it accelerates the normal age-related degenerative changes in the spinal roots and DRG, and it also has a selective effect on the sensory neuron. Nerve conduction studies showed markedly reduced conduction velocities in the distal nerve segments and prolonged F-wave latency and proximal conduction time despite the shorter conduction pathway in diabetic rats. Blood flow, which was measured using iodo[14C]antipyrine autoradiography, was significantly reduced in the sciatic nerves, DRG, and SCG of diabetic rats. We suggest that the combination of hyperglycemia and ischemia results in oxidative-stress and a predominantly sensory neuropathy.
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PMID:Neuropathology and blood flow of nerve, spinal roots and dorsal root ganglia in longstanding diabetic rats. 903 58

Plantar ulcers that do not heal in patients with diabetes and peripheral sensory neuropathy have been shown to be precursors of lower extremity amputation. The total contact cast is considered by many authorities to be the most effective technique for healing of wounds in the neuropathic extremity, yet it still is not widely used in clinical practice. Use of the total contact cast allows mobilization and results in diminished edema and decreased pressure over the ulcerated area. Complete healing usually occurs in eight weeks or less. Total contact casting with careful follow-up should be considered as a useful modality for healing plantar ulcers in diabetic patients with neuropathy of the extremities.
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PMID:The total contact cast: a method for treating neuropathic diabetic ulcers. 905 12

We describe two patients with diabetes mellitus and associated neuropathy, who presented with painless foot swelling and no history of trauma. X-Rays revealed recent underlying fractures-in one of a metatarsus, and the other of a proximal phalanx. These were assumed to be 'stress' fractures unassociated with pain because of the severe sensory neuropathy. Though spontaneous fractures in neuropathic feet have been previously described, they almost always occur in association with Charcot joints, and are usually painful. The differential diagnosis of acute swelling in the foot of a diabetic patient with sensory neuropathy should include stress fracture.
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PMID:Painless stress fractures in diabetic neuropathic feet. 915 30

The purpose of the study was to assess the prevalence of foot (pre-)ulcers and their determinants in type II diabetic patients in a primary health care setting. Six hundred and nine patients (246 men, mean age 64.8 (range, 40-94) years, diabetes duration, 4.3 (0-44.9) years) from 22 general practices attended a regional shared care project in Amsterdam. At first visit all patients were examined by a podiatrist. Amputations, active fool ulcers (Wagner stage 1 or 2) and pre-ulcers (Wagner stage 0, hard skin with or without macerating changes) were recorded in 0 (0%), 11 (1.8%) and 79 (12.9%) patients, respectively. In multivariate logistic regression analysis, after adjustment for age and gender, diabetes duration, cigarette smoking, peripheral vascular disease (assessed by calculating ankle/brachial index), sensory neuropathy (by Semmes-Weinstein monofilament 5.07), dry feet and severe hammer toes were independently and significantly associated (pre-)ulceration. In conclusion, one of every seven type II diabetic patients in primary health care has a foot (pre-)ulcer. Patients at risk for foot ulceration can be identified by inspection and the use of simple instruments.
Diabetes Res Clin Pract 1997 Mar
PMID:The prevalence and determinants of foot ulceration in type II diabetic patients in a primary health care setting. 917 71

The combination of sensory neuropathy, ischemia and direct adverse effect on host defense mechanisms makes patients with diabetes vulnerable to foot infections. A high degree of clinical suspicion and vigilance is necessary for early diagnosis of soft tissue infections and their differentiation from noninfected ulcers. Diagnosis and assessment depend primarily on clinical history and physical examination, although radiographs, scans and laboratory tests may also provide useful clinical data. The ability to detect bone in the base of an ulcer with a blunt sterile probe may be particularly useful in assisting the recognition of osteomyelitis. Most non-limb-threatening infections are caused by Gram-positive cocci, but more serious infections are often polymicrobial. Effective treatment is based on a comprehensive strategy of wound care, avoidance of weight bearing, optimal metabolic control, appropriate antibiotic use and, possibly, surgical intervention.
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PMID:Foot infections in patients with diabetes. 922 75


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