Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of acute motor and sensory neuropathy during a flare of ulcerative colitis. A 28-year-old male presented with a flare of distal ulcerative colitis despite treatment with mesalamine enemas and suppositories simultaneously with rapidly deteriorating weakness and needle sensation in both legs. Neurological assessment showed axonal sensorimotor polyneuropathy affecting mainly the lower limbs and to a lesser extent the upper limbs. Colonoscopy revealed moderately to severe active ulcerative colitis with a patchy distribution involving the rectum and the right colon. Vitamin and folic acid levels were normal. Virological, immunological and other laboratory tests were negative except for positive anti-ganglioside antibodies (anti-GM1). Ulcerative colitis and polyneuropathy improved when patient was treated with immunosuppressive therapy (corticosteroids, immunoglobulin and azathioprine). Peripheral polyneuropathy is a rare extraintestinal manifestation of ulcerative colitis and it is probably associated with an autoimmune pathogenetic mechanism.
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PMID:Acute motor sensory polyneuropathy (AMSAN) complicating active ulcerative colitis with a patchy distribution. 1771 40

The World Health Organization (WHO) predicts there will be 300 million people world-wide with diabetes mellitus by 2025. Currently it is estimated that there are 20 and 60 million people suffering from diabetes mellitus in North America and Europe, respectively. Within this huge population of diabetic persons approximately 50% will develop some form of sensory polyneuropathy, which involves the dying back of distal axons and a failure of axons to regenerate. This leads to incapacitating pain, sensory loss and poor wound healing. The end result is lower extremity amputation with approximately 90,000 diabetes-related amputations occurring each year in North America and the expectation of a 5-fold increase over the next 10 years due to increased incidence of type 2 diabetes. Abnormal neuronal Ca(2+) homeostasis and impaired mitochondrial function have been implicated in numerous CNS and PNS diseases including diabetic sensory neuropathy. The endoplasmic reticulum (ER), in part, regulates cellular Ca(2+) homeostasis and this process is linked to regulation of mitochondrial function and activity of anti-apoptotic signal transduction pathways. Here we review the current state of research regarding role of Ca(2+) dyshomeostasis and mitochondrial physiology in neuronal dysfunction in diabetes. The central impact of diabetes-induced alteration of Ca(2+) handling on sensory neurone function is discussed and related to abnormal ER performance. New results are presented showing suboptimal Ca(2+) concentration in the ER lumen in association with reduced SERCA2 expression in sensory neurones from type 1 diabetic rats. We hypothesize that deficits in neurotrophic factor support, specifically linked to diabetes-induced lowered expression of insulin and neurotrophin-3, triggers alterations of sensory neurone phenotype that are critical for the development of abnormal Ca(2+) homeostasis and associated mitochondrial dysfunction. The role of hyperglycaemia in diabetes is also discussed and we propose that high glucose concentration may impact at other sites to contribute to the heterogeneous aetiology of nerve damage in diabetes.
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PMID:Mitochondrial malfunction and Ca2+ dyshomeostasis drive neuronal pathology in diabetes. 1819 Nov 98

Nucleoside analog-associated sensory neuropathy (NRTI-SN) attributed to stavudine, didanosine, or zalcitabine (the dNRTIs) and distal sensory polyneuropathy (DSP) attributed to HIV are clinically indistinguishable. As inflammatory cytokines are involved in DSP, we addressed a role for inflammation in NRTI-SN by determining the alleles of immune-related genes carried by patients with and without NRTI-SN. Demographic details associated with risk of various neuropathies were included in the analysis. Alleles of 14 polymorphisms in 10 genes were determined in Australian HIV patients with definite NRTI-SN (symptom onset <6 months after first dNRTI exposure, n = 16), NRTI-SN-resistant patients (no neuropathy despite >6 months on dNRTIs, n = 20), patients with late onset NRTI-SN (neuropathy onset after >6 months of dNRTIs, n = 19), and HIV-negative controls. Carriage of TNFA-1031*2 was highest in NRTI-SN patients, suggesting potentiation of NRTI-SN. Carriage of IL12B (3' UTR)*2 was higher in NRTI-SN-resistant patients than controls or NRTI-SN patients, suggesting a protective role. BAT1 (intron 10)*2 was more common in NRTI-SN than resistant patients, but neither group differed from controls. This marks the conserved HLA-A1, B8, DR3 haplotype. Of the demographic details considered, increasing height was associated with NRTI-SN risk. A model including cytokine genotype and height predicted NRTI-SN status (p < 0.0001, R(2) = 0.54). Late onset NRTI-SN patients clustered genetically with NRTI-SN-resistant patients, so these patients may be genetically "protected." In addition to patient height, cytokine genotype influenced NRTI-SN risk following dNRTI exposure, suggesting inflammation contributes to NRTI-SN.
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PMID:Cytokine genotype suggests a role for inflammation in nucleoside analog-associated sensory neuropathy (NRTI-SN) and predicts an individual's NRTI-SN risk. 1824 Sep 60

Clinical information regarding 3 patients diagnosed with acute thallium poisoning was collected and retrospectively analyzed. All 3 patients presented with severe burning pain in the lower limbs and the abdomen. Diffuse alopecia, hepatic dysfunction and Mees' lines in the digits of each limb were observed between 2 and 3 weeks after onset. A physical examination demonstrated paresthesia of all 4 limbs, but normal deep tendon reflexes. Blood and urine thallium concentrations were significantly elevated. Treatment was initiated using hemoperfusion, hemodialysis, potassium supplementation, oral laxatives and B complex supplementation. Clinical symptoms improved as blood and urine thallium concentrations decreased, although a residual sensory neuropathy remained. This study demonstrated that the primary clinical manifestations of acute thallium poisoning include gastrointestinal symptoms, polyneuropathy and dermatological changes. Hemoperfusion and hemodialysis may be effective treatments for acute thallium poisoning.
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PMID:Clinical manifestations and management of acute thallium poisoning. 1882 57

This article proposes a strategy for the diagnosis and treatment of neuropathic pain due to diabetic peripheral sensory neuropathy, based on 15 years of experience in French pain-management centres and on the available literature. In the diabetic patient with chronic pain in the lower limbs, the first step in the diagnostic process is to identify the neuropathic origin of the pain. The second step is to evaluate the patient's medical history and make a rigorous baseline assessment of the neuropathic pain symptoms to determine an effective pain-management strategy. In the third step, adequate and well-tolerated treatment directed towards a variety of painful symptoms is selected, taking into account other co-morbidities such as anxiety and depression. This report reports on the clinical aspects of neuropathic pain exhibited by patients with diabetic sensory polyneuropathy, and the key factors in their diagnosis and treatment, based on the results of meta-analyses and on a recent expert consensus.
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PMID:Strategies for the diagnosis and treatment of neuropathic pain secondary to diabetic peripheral sensory polyneuropathy. 1904 17

Summary of Neuromuscular Presentations at the 57 Annual AAN 2005 meeting in Miami Florida on topics of Facioscapulohumeral muscular dystrophy (FSHD), Duchenne muscular dystrophy (DMD), Diabetic Neuropathy, Charco Marie Tooth disease (CMT), Comparison of injected steroids versus Surgery for carpal tunnel syndrome, Rituximab in Anti-MAG associated polyneuropathy, Cannabis based medicine (CBM) in the treatment of neuropathic pain, utility of skin biopsy with intraepidermal nerve fiber density (IENFD) in sensory complaints, comparing sympathetic skin responses (SSRs) and skin biopsy in diagnosing small fiber sensory neuropathy, Chronic inflammatory demyelinating polyneuropathy (CIDP) clinical and electrophysiologic predictors, affect of limb warming in mild ulnar nerve conduction study (NCS) abnormalities, Tamoxifen affect in ALS, open label study of 3,4 DAP, Pyridostigmine and Ephedrine in fast channel syndrome, Mexilitine as an antimyotonia treatment in myotonic dystrophy (DM1), frontal lobe impairment evaluation in DM1 and DM2 patients and phenotype-genotype correlation in patients with dysferlinopathy.
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PMID:Neuromuscular Highlights-AAN 2005. 1907 9

Paraneoplastic syndromes (PNS) represent the clinical manifestation of the remote and indirect effects produced by tumor metabolites or other products. Paraneoplastic effects are not directly mediated by tumor invasion of normal tissue, or by the disruption of normal function of the involved organ, or by distant metastases. More than 260 cases of nasopharyngeal carcinoma (NPC) associated with PNS have been reported in the literature. These syndromes can be divided into six main groups: cutaneous or dermatologic, endocrine, hematologic, osteoarticular or rheumatologic, neurologic, and ocular. The most common dermatologic manifestation is dermatomyositis, while the syndrome of inappropriate secretion of antidiuretic hormone and occasionally Cushing's syndrome due to ectopic ACTH production are the endocrinologic manifestations. Tumor fever and leukemoid reaction, osteoarticular or rheumatic syndromes, including clubbing of the fingers and toes, sensory neuropathy and demyelinating motor polyneuropathy, and rarely optic neuritis represent the most prominent examples of the other groups of syndromes. PNS may occur before the NPC is manifest, or while it is in an occult stage, and thus the possibility of NPC should be considered in patients with these various disorders. While some PNS will respond to direct treatment, most often the PNS subsides in parallel to response of the NPC, and thus may be useful for monitoring tumor response or recurrence.
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PMID:Paraneoplastic syndromes in patients with nasopharyngeal cancer. 1911 98

Paclitaxel is a microtubule-stabilizing chemotherapeutic agent used in ovarian and breast cancer; its principal adverse effect is sensory neuropathy. We describe the occurrence of sensory polyneuropathy after multiple paclitaxel-eluting stents in a patient who may have sub-clinical Sjogrens syndrome.
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PMID:Sensory polyneuropathy associated with paclitaxel-eluting coronary stent. 1935 99

If a sensory neuropathy appear from an autoimmune disease, it was important to precise the type with clinical and electrophysiological characteristic features (distal symmetric polyneuropathy, chronic inflammatory demyelinating polyneuropathy, Sensory mononeuritis multiplex, sensory neuronopathy, small-fiber neuropathy). The type of neuropathy have an influence on the complementary explorations. It was very important to determine the mechanism between the neuropathy and the autoimmune disease for the treatment. We present a young patient with systemic lupus erythemathosus and sensory neuropathy. This case illustrates this diagnosis strategy.
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PMID:[Sensory neuropathy and autoimmune diseases]. 1952 98

PURPOSE To assess efficacy and safety of single-agent bortezomib in previously untreated patients with multiple myeloma, investigate prevalence of baseline and treatment-emergent polyneuropathy, and identify molecular markers associated with response and neuropathy. PATIENTS AND METHODS Patients received bortezomib 1.3 mg/m(2) on days 1, 4, 8, and 11, for up to eight 21-day cycles. A subset of patients underwent neurophysiologic evaluation pre- and post-treatment. Bone marrow aspirates were performed at baseline for exploratory whole-genome analyses. Results Among 64 patients, 41% had partial response or better, including 9% complete/near-complete responses; median duration of response was 8.4 months. Response rates did not differ in the presence or absence of adverse cytogenetics. After median follow-up of 29 months, median time to progression was 17.3 months. Median overall survival had not been reached; estimated 1-year survival was 92%. Thirty-two patients successfully underwent optional stem-cell transplantation. Bortezomib treatment was generally well tolerated. At baseline, 20% of patients had sensory polyneuropathy. Sensory polyneuropathy developed during treatment in 64% of patients (grade 3 in 3%), but proved manageable and resolved in 85% within a median of 98 days. Neurologic examination, neurophysiologic testing, and measurements of epidermal nerve fiber densities in 35 patients confirmed pretreatment sensory neuropathy in 20% and new or worsening neuropathy in 63%. Pharmacogenomic analyses identified molecular markers of response and treatment-emergent neuropathy, which will require future study. CONCLUSION Single-agent bortezomib is effective in previously untreated myeloma. Baseline myeloma-associated neuropathy seems more common than previously reported, and bortezomib-associated neuropathy, although a common toxicity, is reversible in most patients.
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PMID:Single-agent bortezomib in previously untreated multiple myeloma: efficacy, characterization of peripheral neuropathy, and molecular correlations with response and neuropathy. 1994 24


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