Risk Factors For Polyneuropathy Research Articles

208-OR: Fat Mass and Insulin Resistance Are Independent Risk Factors for Polyneuropathy in Non-DM Subjects Who Underwent Bariatric/Metabolic Surgery

Background: Obesity is an important risk factor for polyneuropathy (PN) in subjects with DM. However, PN can be detected in subjects without overt DM but with risk factors for DM such as metabolic syndrome. Therefore, it is worthy to investigate the prevalence of PN in obese subjects and to discover the underlying mechanisms of the association between obesity and PN. Methods: We analyzed the data of 184 subjects who underwent bariatric/metabolic surgery. PN was diagnosed when a Michigan Neuropathy Screening Instrument score was ≥ 2.5. Total body fat mass and percentage were measured by bioimpedance analysis, and visceral fat area (VFA) was quantified by computed tomography. According to DM status, obesity-related parameters were compared between subjects with PN and those without PN. The association between obesity-related parameters and PN was analyzed using logistic regression models. Results: Of 184 subjects (mean age, 39.1 years; mean BMI, 38.6 kg/m2), 39.7% were diagnosed with DM. The prevalence of PN was 9.0% in non-DM group and 21.9% in DM group. In non-DM group, subjects with PN showed higher HOMA-IR, fat mass, and VFA compared with those without PN. HOMA-IR (OR, 1.492; 95% CI, 1.110-2.005), fat mass (OR, 1.087; 95% CI, 1.008-1.171), and VFA (OR 1.013; 95% 1.001-1.024) were significantly associated with PN even after adjustment of known risk factors of PN. In DM group, subjects with PN showed higher body weight, BMI, waist circumference, and VFA compared with those without PN. However, after adjustment of known risk factors of PN, these obesity related parameters were not significantly associated with PN. Conclusion: Fat mass and insulin resistance might be independent risk factors in development of PN for obese subjects without DM. PN evaluation might be necessary in subjects with morbid obesity even before development of overt DM, and we need to investigate whether weight loss intervention can prevent or delay PN in obese subjects. Disclosure K. Kim: None. T. Oh: None. S. Choi: None. H. Jang: None.

Identification of risk factors for patients with diabetes: diabetic polyneuropathy case study

BackgroundMethods of data mining and analytics can be efficiently applied in medicine to develop models that use patient-specific data to predict the development of diabetic polyneuropathy. However, there is room for improvement in the accuracy of predictive models. Existing studies of diabetes polyneuropathy considered a limited number of predictors in one study to enable a comparison of efficiency of different machine learning methods with different predictors to find the most efficient one. The purpose of this study is the implementation of machine learning methods for identifying the risk of diabetes polyneuropathy based on structured electronic medical records collected in databases of medical information systems.MethodsFor the purposes of our study, we developed a structured procedure for predictive modelling, which includes data extraction and preprocessing, model adjustment and performance assessment, selection of the best models and interpretation of results. The dataset contained a total number of 238,590 laboratory records. Each record 27 laboratory tests, age, gender and presence of retinopathy or nephropathy). The records included information about 5846 patients with diabetes. Diagnosis served as a source of information about the target class values for classification.ResultsIt was discovered that inclusion of two expressions, namely “nephropathy” and “retinopathy” allows to increase the performance, achieving up to 79.82% precision, 81.52% recall, 80.64% F1 score, 82.61% accuracy, and 89.88% AUC using the neural network classifier. Additionally, different models showed different results in terms of interpretation significance: random forest confirmed that the most important risk factor for polyneuropathy is the increased neutrophil level, meaning the presence of inflammation in the body. Linear models showed linear dependencies of the presence of polyneuropathy on blood glucose levels, which is confirmed by the clinical interpretation of the importance of blood glucose control.ConclusionDepending on whether one needs to identify pathophysiological mechanisms for one’s prospective study or identify early or late predictors, the choice of model will vary. In comparison with the previous studies, our research makes a comprehensive comparison of different decisions using a large and well-structured dataset applied to different decision support tasks.

Statins do not increase risk of polyneuropathy: A case-control study and literature review.

To investigate whether there is an association between cholesterol-lowering medication use, specifically statins, and chronic polyneuropathy. A literature study was carried out to assess the current state of evidence on the association between chronic polyneuropathy and cholesterol-lowering medication use. We also conducted a prospective case-control study to compare exposure to cholesterol-lowering medication between patients with cryptogenic axonal polyneuropathy and controls prior to the index date (defined in patients as date of onset of polyneuropathy symptoms, in controls as date of first study survey). Outcomes were adjusted for potential confounders such as cardiovascular history and metabolic syndrome. The 13 studies identified in our literature search showed conflicting results (odds ratios [ORs] ranging from 0.66 to 14.2), but most studies had methodologic limitations. There was insufficient evidence that statin use is a risk factor for polyneuropathy. Our prospective case-control study included 333 patients with cryptogenic axonal polyneuropathy and 283 controls. Patients with polyneuropathy were less likely to have been exposed to statins than controls (OR 0.56, 95% confidence interval 0.34-0.95, p = 0.03). The odds of polyneuropathy decreased as exposure duration to statins increased. Cholesterol-lowering medication consisted almost exclusively of statins; therefore we only draw conclusions on the effect of statin use. Statin use does not increase the risk of chronic polyneuropathy. Therefore, statins should not be routinely withheld from polyneuropathy patients. This study provides Class III evidence that statin use does not increase the risk of polyneuropathy.

The role of nutrition as risk factor for polyneuropathy: a case-control study.

The aim of this case-control study is to investigate the role of nutrition as risk factor for polyneuropathy. Three hundred eighteen patients with chronic idiopathic axonal polyneuropathy and 636 matched controls completed a validated food frequency questionnaire that covered nutrient intake and alcohol consumption. As risk estimates, we calculated adjusted odds ratios for the intake of energy and nutrients. Energy and nutrient intake did not differ between patients and controls, regardless of moderate alcohol consumption. Nutrition is not a risk factor for chronic idiopathic axonal polyneuropathy.

Differential Diagnosis of Quadriparesis in an Otherwise Healthy Adult Male by a Physical Therapist

HISTORY: A 52-year-old male was referred to Physical Therapy (PT) by his primary care physician for progressive quadriparesis related to suspected peripheral neuropathy (PN). The patient was healthy and active until two years prior when he began experiencing weakness and paresthesias in both hands. This progressed to his right lower extremity, then all four extremities, and by the time of the PT evaluation, the patient was no longer able to stand. He also endorsed several episodes of bladder incontinence, constipation, and painful muscle spasms. He was scheduled for imaging of the spine and a follow-up with his physician in two months. Review of the medical record revealed that the patient was evaluated by a physical therapist nine months prior. His presentation then was consistent with the working diagnosis of PN. However, a sinister diagnosis was suspected due to the involvement of all four extremities without risk factors for polyneuropathy. At that time, no further steps were taken as the patient did not follow up in clinic. PHYSICAL EXAMINATION: The patient presented in a wheelchair, though was unable to propel or stand without assistance due to significantly worsening weakness. Neurologic exam revealed several upper motor neuron signs including hypertonicity and hyperreflexia. This presentation was no longer consistent with the working diagnosis of PN (see table).Table: No title available.DIFFERENTIAL DIAGNOSIS: 1. Cervical spine stenosis with myelopathy 2. Space occupying lesion in cervical region 3. Progressive motor neuron disease TESTS AND RESULTS: Cervical/Thoracic spine MRI: 12.4 cm intradural intramedullary mass from C5 to T5, likely related to multiple tumoral cystic areas, with syrinx from T3 to T4 FINAL DIAGNOSIS: Intradural intramedullary ependymoma extending from C5 to T5 with associated syrinx TREATMENT AND OUTCOMES: Based on the examination and presence of multiple red flags, the physical therapist referred the patient to the Emergency Department for further evaluation.

HIV-Associated Polyneuropathy in Resource-Limited Settings: Genetic Predisposition and Vitamin Variations

Human immunodeficiency virus-related polyneuropathy remains a painful condition resulting from damaged nerve endings. HIV infection strongly associates with a predominantly polyneuropathy that is attributed to HIV infection itself, or a toxic neuropathy associated with combination antiretroviral therapy (CART). In non-HIV-infected individuals, both deficiency and high intake of vitamins have been associated with polyneuropathy. For that reason, clinicians recommend vitamin supplements before and during CART. Although some, but not all, HIV-related vitamin deficiencies may replete during treatment with CART, it is predictable that high vitamin supplement intakes may contribute to nerve disorders. In resource-limited settings where the diagnosis of polyneuropathy heavily relies on symptoms, data on risk factors for polyneuropathy including vitamin status, alcohol consumption, and co-infections are limited. In addition, studies on genetic influence on the concentration of micronutrients in the blood of long-term users of CART are scarce. Possible sources of high intakes of vitamins could arise from the fact that a number of HIV-infected persons self-medicate. In addition, since HIV-infected individuals have an increased lifespan, relying on symptoms alone to specifically diagnose HIV-associated neuropathies could be a barrier to effective treatment in recourse-poor settings. This paper reviews evidence on single nucleotide polymorphisms (SNPs) with the potential to influence bioavailability of vitamins in HIV-infected patients. Genome-wide association studies have reported SNPs in alkaline phosphatase, fucosyltransferase 2, cubilin, transcobalamin 1, and tumor necrosis factor as potential determinants of various blood levels of vitamin B-6, B-12 and E. As long term CART increasingly become, personalized, future research should focus on SNPs, which influence vitamin blood levels, and with potential to augment long-term treatment with CART.

Metabolic syndrome is related to polyneuropathy and impaired peripheral nerve function: a prospective population-based cohort study

ObjectiveDiabetes mellitus is a known risk factor for polyneuropathy, but the role of pre-diabetes and metabolic syndrome remains unclear. We aimed to investigate the role of these factors in a...

Chronic obstructive pulmonary disease is not a risk factor for polyneuropathy: A prospective controlled study.

Polyneuropathy has been observed in patients with chronic obstructive pulmonary disease (COPD). If polyneuropathy occurs as a complication or extrapulmonary manifestation of COPD, one would expect an increased prevalence among patients with a cryptogenic axonal polyneuropathy. This case-control study aimed to investigate the association between COPD and polyneuropathy. We prospectively included 345 patients with cryptogenic axonal polyneuropathy and 465 controls. A standardized questionnaire assessed the presence of COPD and we verified this diagnosis by contacting the family physician. The severity of COPD was based on the Global Initiative for Chronic Obstructive Lung Disease classification. The prevalence of COPD did not differ between patients with polyneuropathy and controls (15/345 vs. 12/465 respectively; odds ratio (OR) 1.7; 95% confidence interval (CI) [0.8-3.7]). Adjusting for age, gender and possible confounders did not affect these results (adjusted OR 1.7, 95% CI 0.7-4.1). The severity of COPD was similar between patients with polyneuropathy and controls. This study does not support the hypothesis that COPD is a risk factor for polyneuropathy.

Correlation Between the Severity of Diabetic Peripheral Polyneuropathy and Glycosylated Hemoglobin Levels: A Quantitative Study.

ObjectiveTo investigate risk factors for diabetic peripheral polyneuropathy and their correlation with the quantified severity of nerve dysfunction in patients with diabetes mellitus (DM).MethodsA total of 187 diabetic patients with clinically suspected polyneuropathy (PN) were subclassified into 2 groups according to electrodiagnostic testing: a DM-PN group of 153 diabetic patients without electrophysiological abnormality and a DM+PN group of 34 diabetic patients with polyneuropathy. For all patients, age, sex, height, weight, duration of DM, and plasma glycosylated hemoglobin (HbA1c) level were comparatively investigated. A composite score was introduced to quantitatively analyze the results of the nerve conduction studies. Logistic regression analysis and multiple regression analysis were used to evaluate correlations between significant risk factors and severity of diabetic polyneuropathy.ResultsThe DM+PN group showed a significantly higher HbA1c level and composite score, as compared with the DM-PN group. Increased HbA1c level and old age were significant predictive factors for polyneuropathy in diabetic patients (odds ratio=5.233 and 4.745, respectively). In the multiple linear regression model, HbA1c and age showed a significant positive association with composite score, in order (β=1.560 and 0.253, respectively).ConclusionIncreased HbA1c level indicative of a state of chronic hyperglycemia was a risk factor for polyneuropathy in diabetic patients and a quantitative measure of its severity.

Neuropathy in Parkinson’s Disease Patients with Intestinal Levodopa Infusion versus Oral Drugs

BackgroundSevere polyneuropathy has been observed in a number of patients treated for Parkinson’s disease with Levodopa/Carbidopa intestinal gel infusion. This may reflect a rare individual complication or a systematic side effect.ObjectiveTo investigate whether peripheral nerve function differed between patients with oral treatment versus Levodopa/Carbidopa intestinal gel infusion.MethodsIn an observational design, data from median, tibial, and peroneal neurography were prospectively assessed and compared between patients with conventional drug treatment (n = 15) and with Levodopa/Carbidopa intestinal gel infusion (n = 15). The groups were matched for age and disease duration. In view of the medical risk profile for polyneuropathy, comorbidity and basic serological parameters were assessed.ResultsAxonal neuropathy was common in both patient groups. However, although group differences in risk factors for polyneuropathy were not evident, neurographic abnormalities were more severe in the patients treated with Levodopa/Carbidopa intestinal gel infusion than in the orally treated patients. In the group with Levodopa/Carbidopa intestinal gel infusion, the degree of neuropathic change correlated with weight lost since therapy initiation and with the drug dose. In contrast to the axonal abnormalities, conduction velocity was found normal in both groups.ConclusionThe results are compatible with the promotion of axonal neuropathy by Levodopa/Carbidopa intestinal gel infusion. This could be due to the intrinsically high levodopa doses associated with the therapy and/or malnutritional effects from intestinal drug application. The results should be corroborated by a larger longitudinal and controlled trial.

Apply Awaji-shima Consensus Conference Criteria Before Diagnosing Amyotrophic Lateral Sclerosis

Objectives:ALS may be diagnosed although affection of other organs suggests another pathogenetic back-ground. Case report:In a 72yo non-smoking male progressive gait disturbance with recurrent falls since 2y was initially attributed to axonal polyneuropathy. Additionally, he had arterial hypertension, diabetes, hyperlipidemia, hyperuricemia, hyper-CK-emia, hepatopathy, atrial fibrillation, recurrent heart-failure, pulmonary hypertension, mitral insufficiency, and restrictive cardiomyopathy. Possible causes of polyneuropathy were diabetes, long-standing alcoholism, folate-deficiency, or hereditary disease. Later the patient was re-diagnosed as ALS despite absence of upper motor-neuron or bulbar signs, the presence of multiple risk factors for polyneuropathy, of stocking-type sensory disturbances, and of cardiac abnormalities, which could explain dyspnea. Misdiagnosing polyneuropathy as ALS stigmatized the patient and prevented him from further diagnostic work-up for cardiac disease and adequate treatment for heart-failure. Though the diagnosis of ALS was withdrawn, he was put on comfort care and opiates were given when dyspnea acutely deteriorated to death without further cardiac or pulmonary investigations or specific cardiac treatment. Conclusions:ALS should be diagnosed only if the Awaji-shima criteria are fulfilled and if all differential diagnoses were profoundly excluded. Respiratory insufficiency should not be attributed to bulbar involvement in ALS as long as cardiac, pulmonary, or myopathic causes were excluded.

Erythropoietin and polyneuropathy in older persons

Introduction Recent studies demonstrated that erythropoietin (EPO) have a number of non-erythropoietic effects including neuroprotection and vascular protection. Materials Using data from a representative sample of older persons, we tested the hypothesis that EPO levels are correlated with peripheral nerve parameters (NVC and CMAP) assessed by surface ENG and with clinically diagnosed polyneuropathy. We selected 972 participants (aged 60–98 years) with complete data for the analyses. Results We found a significant association between EPO and age-adjusted NCV and CMAP (for NCV: 0.57 ± 0.26; p = 0.03 and for CMAP: 0.54 ± 0.23; p = 0.02). In logistic regression models adjusting for age, sex and multiple potential confounders, higher EPO levels were associated with a significantly lower probability of having a clinical diagnosis of polyneuropathy (OR = 0.43; 95% CI: 0.22–0.84). Discussion These findings suggest that EPO is implicated in the pathogenesis of polyneuropathy in older persons. Whether low EPO is a risk factor for polyneuropathy should be tested in future longitudinal analyses.

Prevalence of Polyneuropathy in Pre-Diabetes and Diabetes Is Associated With Abdominal Obesity and Macroangiopathy

It is controversial whether there is a glycemic threshold above which polyneuropathy develops and which are the most important factors associated with polyneuropathy in the general population. The aim of this study was to determine the prevalence and risk factors of polyneuropathy in subjects with diabetes, impaired fasting glucose (IFG), impaired glucose tolerance (IGT), or normal glucose tolerance (NGT). Subjects with diabetes (n = 195) and control subjects matched for age and sex (n = 198) from the population-based MONICA (Monitoring Trends and Determinants on Cardiovascular Diseases)/KORA (Cooperative Research in the Region of Augsburg) Augsburg Surveys 1989/1990 (S2) and 1994/1995 (S3) aged 25-74 years were contacted again and assessed in 1997/1998 by the Michigan Neuropathy Screening Instrument using a score cut point >2. An oral glucose tolerance test was performed in the control subjects. Among the control subjects, 46 (23.2%) had IGT, 71 (35.9%) had IFG, and 81 had NGT. The prevalence of polyneuropathy was 28.0% in the diabetic subjects, 13.0% in those with IGT, 11.3% in those with IFG, and 7.4% in those with NGT (P <or= 0.05 for diabetes vs. NGT, IFG, and IGT). In the entire population studied (n = 393), age, waist circumference, and diabetes were independent factors significantly associated with polyneuropathy, whereas in the diabetic group polyneuropathy was associated with age, waist circumference, and peripheral arterial disease (PAD) (all P < 0.05). The prevalence of polyneuropathy is slightly increased in individuals with IGT and IFG compared with those with NGT. The association with waist circumference and PAD suggests that the latter and abdominal obesity may constitute important targets for strategies to prevent diabetic polyneuropathy.

Chronic Symmetric Symptomatic Polyneuropathy in the Elderly: A Field Screening Investigation of Risk Factors for Polyneuropathy in Two Italian Communities

A total of 4191 patients 55 years and older were screened for clinical features and risk factors of polyneuropathy by 27 general practitioners (GPs) in two areas of Italy (Varese and San Giovanni Rotondo). Polyneuropathy was diagnosed in the presence of two or more symptoms associated with bilateral impairment of at least two of the following: strength, sensation, tendon reflexes. A risk factor for polyneuropathy (associated disease or neurotoxic agent) was recorded based on its presence in the GP’s records, the presence of specific treatments, or an affirmative answer to the interviewer’s question. The prevalence of polyneuropathy among patients with no recognized exposure to diseases or neurotoxic agents was 1.6% (Varese 1.6%; San Giovanni Rotondo 1.8%). The corresponding values were 11.8% (Varese 11.8%; San Giovanni Rotondo 11.9%) for patients with one risk factor, and 17.3% (Varese 19.2%; San Giovanni Rotondo 13.0%) for patients with two risk factors. Combining the two populations, the prevalence of polyneuropathy was highest in diabetics (18.3%), followed by patients with a diagnosis of alcoholism (12.5%), non-alcoholic liver disease (10.9%), and tumor (7.1%). Diabetes was the commonest independent risk factor for polyneuropathy (odds ratio 11.3), followed by alcoholism (7.4), non-alcoholic liver disease (4.9), and tumor (2.6).

Critical illness polyneuropathy in multiple organ dysfunction syndrome and weaning from the ventilator.

Acute axonal polyneuropathy has been found in patients with multiple organ dysfunction syndrome. This 'critical illness polyneuropathy' (CIP) has been associated with difficult weaning from the ventilator in retrospective studies. To test the hypothesis that CIP is related to the degree and number of organ dysfunctions, and to weaning problems. Prospective study of 18 months. A multidisciplinary intensive care unit in a general hospital Thirty-eight patients under 75 years of age who had been mechanically ventilated for more than 7 days, without previous signs of or risk factors for polyneuropathy. Organ dysfunctions were quantified using a dynamic scoring system (0-12 points). Electromyography studies were performed during mechanical ventilation to identify patients with and without CIP. CIP was present in 18 out of 38 patients and associated with an increased organ dysfunction score (5.3 +/- 1.8 vs. 3.6 +/- 1.5; p = 0.003) and number of organs involved [median (range): 4 (3-5) vs. 2 (1-4); p = 0.009], in particular cardiovascular (p = 0.003), renal (p = 0.04), and hematopoietic failure (p = 0.04). Patients with polyneuropathy were ventilated longer, but this was not clearly due to more difficult weaning [median: 16.5 (1-48) vs. 9.5 (1-38) days; p = 0.26]. Polyneuropathy was present in 2 of 4 patients with normal weaning. Axonal polyneuropathy is related to the severity of multiple-organ-dysfunction syndrome. Its presence does not necessarily implicate difficult weaning from artificial ventilation.