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

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) may occur in association with diabetes mellitus (DM). We report a case of a poorly controlled diabetic patient who presented with rapid onset of bilateral lower extremity weakness and sensory loss associated with sacral and posterior thigh paresthesias and urinary and bowel incontinence, indicative of cauda equina syndrome (CES). Subsequent evaluation was consistent with CIDP. Monthly infusions with intravenous immunoglobulins (IVIg) with strict glycemic control using insulin resulted in remarkable clinical and electrophysiological recovery. This case report describes a rare presentation of CIDP and emphasizes the importance of early utility of electrodiagnostic (EDX) studies in the clinical evaluation of diabetic patients presenting with rapidly progressive lower extremity weakness and sensory loss associated with diminished reflexes.
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PMID:Chronic inflammatory demyelinating polyradiculoneuropathy presenting as cauda equina syndrome in a diabetic. 1752 74

One hundred consecutive diabetes mellitus patients attending the diabetic clinic of the hospital constituted the study group. One hundred age and sex matched non-diabetics were taken as controls. The majority, 63%, belonged to the 41-60 years age group and 98% had non-insulin dependent diabetes. Among the study group, 64% had one or more cutaneous manifestations as compared to 22% in the controls. This was statistically highly significant (p < 0.001). Infections comprised the largest group affecting 35 of the 64 cases. Among the bacterial infections, pyodermas were observed in 11 and erythrasma in one. Fungal infections were seen in 21, dermatophytoses in 11, and candidiasis in 10. Herpes zoster was seen in 2 cases. Pruritus was observed in 10, neurological abnormalities in the form of paresthesias was seen in 6, mal perforans in one, and meralgia paresthetica in one. Diabetic dermopathy was seen in 6 and rubeosis in 4. Six dermatoses strongly associated with DM were seen, namely one each of waxy skin syndrome, granuloma annulare, eruptive xanthoma, scleredema adultorum, and 2 cases of diabetic bulla. Ten patients exhibited other dermotoses less associated with diabetics: xanthelasmo palpebrarum in 5 patients, acrochordi in 4, and pigmented purpuric dermatoses in one. Likewise syndromes of insulin resistance were seen in 4 patients of whom 3 had aconthosis nigricans and one had congenital lipodystrophy. Furthermore, 9 patients had dermatoses known to be associated with an increased incidence of diabetes; vitiligo in 4, acquired perforating dermatoses in 3, and lichen planus in 2. Four patients had dermatoses known to be associated with diabetes: psoriasis in 3 and diffuse alopecia in one. Three had adverse drug reactions to anti-diabetic therapy.
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PMID:Cutaneous manifestation of diabetes mellitus. 1764 48

A 67-year-old man affected by moderate weight loss, acral paresthesia and plantar burning sensation was admitted to our department. Electromyographic (EMG) and electroneurographic (ENG) studies confirmed a peripheral, asymmetrical, motor-sensorial polyneuropathy (PPN). Hematological data and bone marrow biopsy discovered a non-secerning multiple myeloma (MM). All other probable causes of peripheral neuropathy could be excluded, and the possible relationship between nerve damage and neoplasia was confirmed. Furthermore, all possibilities of association of MM with PPn, namely the osteosclerotic variant, the Crow-Fukase syndrome, and the amyloid one have been evaluated. The only finding of osteolytic bone areas by radiology, the absence of organomegaly, diabetes mellitus, skin alterations, and of amyloid deposition in muscles and nerves, exclude the possible connection of the case to any of the listed possibilities. On the other hand, some clinical aspects differ, in part, to others described in the literature. In conclusion, the association between PPN and MM as the result of multiform clinical variants could be considered.
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PMID:Peripheral neuropathy and multiple myeloma in aging: a case report. 1864 92

Undiagnosed chronic Lyme disease caused by Borrelia burgdorferi is considered a differential diagnoses in medically unexplained symptoms like arthralgias, distal paresthesias, depressive symptoms, lack of concentration and fatigue. The aims of the study were to assess the association of mental and physical complaints with seropositivity for anti-Borrelia IgG in a general population sample. Seropositivity indicated an infection with Borrelia in the past. The Study of Health in Pomerania was conducted in a community living in a region with endemic Lyme disease. Mental and physical complaints were assessed on 38 items with the von Zerssen's complaint scale. IgG antibodies to Borrelia were determined by ELISA in 4264 individuals. Seropositivity was analyzed applying two cut-off scores (>5 and >10 IU/ml). IgG antibodies to Borrelia were found positive in 388 subjects (9.1%) applying the >5 IU/ml cut-off and in 130 subjects (3.0%) applying the >10 IU/ml cut-off. In multivariate analyses (MANCOVA), both definitions of seropositivity were not associated with increased mental or physical complaints while adjusting for gender, age, employment status, rural residency, physical activity, diabetes mellitus and number of chronic diseases. In the general population, seropositivity for anti-Borrelia IgG antibodies was not associated with an increase of self-rated mental or physical complaints or impairments. Therefore, clinicians should not overvalue seropositivity for anti-Borrelia IgG as a medical cause for unexplained mental or physical complaints.
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PMID:No association of seropositivity for anti-Borrelia IgG antibody with mental and physical complaints. 1875 3

The study was designed to investigate effect of alpha-lipoic acid (alphaLA) and mexidol on clinical manifestations of diabetic neuropathy (DN) and the associated changes of the affective status in patients with diabetes mellitus at early stages of diabetic foot syndrome (DFS). Integral indicator of clinical symptoms of distal symmetric sensorimotor polyneuropathy (according to the neuropathic signs and symptoms scale) significantly decreased within 14 days after the onset of the treatment with alphaLA (600 mg/day) and mexidol (300 mg/day). Antineuropathic effect of alphaLA was associated with a rise in the left ventricular ejection fraction. Mexidol reduced the severity of DN-related depression and was more efficacious than alphaLA in terms of beneficial effect on spasms and paresthesia (pricking and burning sensation, numbness) in distal segments of the lower extremities. The above clinical effects of alphaLA and mexidol were unrelated to changes of glycemia, lipidemia amd lipid peroxidation.
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PMID:[Effect of alpha-lipoic acid and mexidol on neuro- and the affective status in patients at early stages of diabetic foot syndrome]. 1906 61

Undiagnosed and untreated neuropathy may lead to disability and poor quality of life. Ordering every possible test to find the cause of polyneuropathy can waste time and resources. In this study, we investigated what could be used as a routine neuropathy screen. A retrospective audit of all charts of patients diagnosed to have polyneuropathy by nerve conduction studies from November 2001 to November 2002 were carried out. Demographics, background history, type of neuropathy and investigations done were documented. The charts of 61 patients were audited. 12 patients had a background history of diabetes mellitus. 2 patients had history of alcohol abuse. 23 patients presented with paraesthesia and 33 with weakness of limbs. We found a cause of polyneuropathy in 79% of cases. In most patients with polyneuropathy where a cause can be identified, this can be achieved by the medical history, neurological examination, nerve conduction studies and the baseline blood tests. We suggest a 3-step approach to the diagnostic workup of polyneuropathy.
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PMID:How to work up a patient with polyneuropathy? 1928 14

Progressive external ophthalmoplegia (PEO) can be caused by a disorder characterized by multiple mitochondrial DNA (mtDNA) deletions due to mutations in the TWINKLE gene, encoding a mtDNA helicase. We describe a 71-year-old woman who had developed PEO at age 55 years. She had cataracts, diabetes, paresthesias, cognitive defects, memory problems, hearing loss, and sensory ataxia. She had muscle weakness with ragged red fibers on biopsy. MRI showed static white matter changes. A c.908G>A substitution (p.R303Q) in the TWINKLE gene was identified. Multiple mtDNA deletions were detected in muscle but not blood by a PCR-based method, but not by Southern blot analysis. MtDNA copy number was maintained in blood and muscle. A systematic literature search was used to identify the genotypic and phenotypic spectrum of dominant TWINKLE-related disease. Patients were adults with PEO and symptoms including myopathy, neuropathy, dysarthria or dysphagia, sensory ataxia, and parkinsonism. Diabetes, cataract, memory loss, hearing loss, and cardiac problems were infrequent. All reported mutations clustered between amino acids 303 and 508 with no mutations at the N-terminal half of the gene. The TWINKLE gene should be analyzed in adults with PEO even in the absence of mtDNA deletions in muscle on Southern blot analysis, and of a family history for PEO. The pathogenic mutations identified 5' beyond the linker region suggest a functional role for this part of the protein despite the absence of a primase function in humans. In our patient, the pathogenesis involved multiple mtDNA deletions without reduction in mtDNA copy number.
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PMID:Finding twinkle in the eyes of a 71-year-old lady: a case report and review of the genotypic and phenotypic spectrum of TWINKLE-related dominant disease. 1935 76

Small fiber neuropathy is increasingly being recognized as a major cause of painful burning sensations in the feet, especially in the elderly. Although strength remains preserved throughout the course of the disease, the pain and paresthesias are often disabling. Diabetes mellitus is the most common identifiable cause of small fiber neuropathy, and impaired oral glucose tolerance and individual components of the metabolic syndrome are often associated with it. Some cases, however, are idiopathic. Skin biopsy (with an evaluation of the density of intraepidermal nerve fibers) and tests of autonomic nerve function are useful for the diagnosis. Management involves controlling pain and identifying and aggressively treating the underlying cause.
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PMID:Small fiber neuropathy: A burning problem. 1941 45

Advanced peripheral diabetic neuropathy (PDN) is associated with elevated vibration and thermal perception thresholds that progress to sensory loss and degeneration of all fiber types in peripheral nerve. A considerable proportion of diabetic patients also describe abnormal sensations such as paresthesias, allodynia, hyperalgesia, and spontaneous pain. One or several manifestations of abnormal sensation and pain are described in all the diabetic rat and mouse models studied so far (i.e., streptozotocin-diabetic rats and mice, type 1 insulinopenic BB/Wor and type 2 hyperinsulinemic diabetic BBZDR/Wor rats, Zucker diabetic fatty rats, and nonobese diabetic, Akita, leptin- and leptin-receptor-deficient, and high-fat diet-fed mice). Such manifestations are 1) thermal hyperalgesia, an equivalent of a clinical phenomenon described in early PDN; 2) thermal hypoalgesia, typically present in advanced PDN; 3) mechanical hyperalgesia, an equivalent of pain on pressure in early PDN; 4) mechanical hypoalgesia, an equivalent to the loss of sensitivity to mechanical noxious stimuli in advanced PDN; 5) tactile allodynia, a painful perception of a light touch; and 5) formalin-induced hyperalgesia. Rats with short-term diabetes develop painful neuropathy, whereas those with longer-term diabetes and diabetic mice typically display manifestations of both painful and insensate neuropathy, or insensate neuropathy only. Animal studies using pharmacological and genetic approaches revealed important roles of increased aldose reductase, protein kinase C, and poly(ADP-ribose) polymerase activities, advanced glycation end-products and their receptors, oxidative-nitrosative stress, growth factor imbalances, and C-peptide deficiency in both painful and insensate neuropathy. This review describes recent achievements in studying the pathogenesis of diabetic neuropathic pain and sensory disorders in diabetic animal models and developing potential pathogenetic treatments.
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PMID:Diabetic painful and insensate neuropathy: pathogenesis and potential treatments. 1978 69

A 35-year-old morbidly obese man, diagnosed with type 2 diabetes in 2006, lost nearly 100 kg extremely rapidly soon after the diagnosis, with dramatic painful paraesthesia and autonomic neuropathy, and poor diabetes control. Investigations to find a tumour, or an infectious, endocrinological or digestive disease, to explain his clinical features were all negative. However, with insulin and analgesic treatment, the patient's symptoms improved markedly within a few months; the patient gained 50 kg, while insulin was tapered and then withdrawn, to be replaced by metformin, which maintained perfect diabetes control. Also, the analgesic therapies could be discontinued. This case report is typical of diabetic neuropathic cachexia, first described by Ellenberg in 1974.
Diabetes Metab 2009 Nov
PMID:Profound weight loss in a type 2 diabetic patient with diabetic neuropathic cachexia: a case report. 1983 86


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