[Systematic review and Meta-analysis of efficacy and safety of Tangmaikang Granules in treatment of diabetic peripheral neuropathy].

This study aimed to explore the efficacy and safety of Tangmaikang Granules in the treatment of diabetic peripheral neuropathy(DPN). PubMed, Cochrane Library, EMbase, SinoMed, CNKI, Wanfang and VIP were retrieved for randomized controlled trial(RCT) of Tangmaikang Granules in the treatment of DPN. Cochrane handbook 5.3 was used to evaluate the quality of the inclu-ded studies, and RevMan 5.4.1 and Stata 15.1 were employed to analyze data and test heterogeneity. GRADEpro was used to assess the quality of each outcome index. Clinical effective rate was the major outcome index, while the improvement in numbness of hands and feet, pain of extremities, sluggishness or regression of sensation, sensory conduction velocity(SCV) and motor conduction velocity(MCV) of median nerve and peroneal nerve, fasting blood glucose(FBG), 2 h postprandial blood glucose(2hPBG), and glycated hemoglobin(HbA1c) and incidence of adverse reactions were considered as the minor outcome indexes. A total of 19 RCTs with 1 602 patients were eventually included. The Meta-analysis showed that the improvements in clinical effective rate(RR=1.45, 95%CI[1.32, 1.61], P<0.000 01), pain of extremities(RR=1.70, 95%CI[1.27, 2.27], P=0.000 3), MCV of peroneal nerve(MD=4.08, 95%CI[3.29, 4.86], P<0.000 01) and HbA1c(SMD=-1.23, 95%CI[-1.80,-0.66], P<0.000 1) of Tangmaikang Granules alone or in combination in the experimental group were better than those in the control group. Compared with the conditions in the control group, numbness of hands and feet(RR=1.42, 95%CI[1.12, 1.80], P=0.003), sluggishness or regression of sensation(RR=1.41, 95%CI[1.05, 1.91], P=0.02), SCV of median nerve(MD=4.59, 95%CI[0.92, 8.27], P=0.01), SCV of peroneal nerve(MD=4.68, 95%CI[3.76, 5.60], P<0.000 01) and MCV of median nerve(MD=5.58, 95%CI[4.05, 7.11], P<0.000 01) of Tangmaikang Granules in combination in the experimental group were improved by subgroup analysis. The levels of FBG(MD=-0.57, 95%CI[-1.27, 0.12], P=0.11) and 2hPBG(MD=-0.69, 95%CI[-1.70, 0.33], P=0.18) in the experimental group were similar to those in the control group after treatment with Tangmaikang Granules alone or in combination. There was no difference in the safety(RR=1.28, 95%CI[0.58, 2.82], P=0.54) of Tangmaikang Granules in the treatment of DPN between the experimental group and the control group. Tangmaikang Granules could significantly increase clinical effective rate and nerve conduction velocity as well as improve symptoms of peripheral nerve and blood glucose level, and no serious adverse reactions were identified yet. Further validation was needed in future in large-sample, multicenter, high-quality RCTs.

Traditional Chinese medicine fumigation as auxiliary treatment of diabetic peripheral neuropathy: A protocol for systematic review and meta-analysis.

BACKGROUND: Diabetic peripheral neuropathy (DPN) is 1 of the most common clinical complications of diabetes, which seriously affects the quality of life of patients and causes a substantial economic burden on diabetes care. The pathogenesis of DPN is complex. There is no targeted treatment method, and mainstream treatment methods have low efficacy and large side effects. Traditional Chinese medicine has rich clinical experience in the prevention and treatment of diabetic peripheral neuropathy, which has dramatically improved the quality of life of patients. It is clinically proven that traditional Chinese medicine fumigants (TCMF) have apparent effects in treating diabetic peripheral neuropathy. Therefore, we aim to systematically review the effectiveness and safety of TCMF for DPN. METHODS: We will search the following databases: PubMed, Embase, Cochrane Library, MEDLINE, the China National Knowledge Infrastructure, the Chinese Biomedical Literature Database, Cqvip Database, and Wanfang Data. Besides, we will also search for clinical trial registrations, potential grey literature, relevant conference abstracts, and reference lists of established studies. The studies published from the inception of the database to November 2020 will be retrieved. The randomized controlled trials on TCMF for DPN will be included. Also, we will search for clinical trial registrations, potential grey literature, relevant conference abstracts, and reference lists of established studies. The main result is clinical efficacy and nerve conduction velocity. Fasting blood glucose, 2 hours postprandial blood glucose, blood lipid, glycosylated hemoglobin, and adverse events are secondary results. We will perform the analyses using RevMan V.5.3 software. RESULTS: This study will provide a high-quality comprehensive evaluation of the efficacy and safety of TCMF in the treatment of DPN. CONCLUSIONS: This systematic review will evaluate the effectiveness and safety of TCMF in the treatment of DPN, and provide the latest evidence for clinical application. INPLASY REGISTRATION NUMBER: INPLASY2020110137.

Evaluation of the effect of N-acetylcysteine on the prevention and amelioration of paclitaxel-induced peripheral neuropathy in breast cancer patients: a randomized controlled study.

PURPOSE: The aim of the current study was to evaluate the effect of N-acetylcysteine (NAC) on the incidence and severity of paclitaxel-induced peripheral neuropathy (PIPN) in breast cancer patients. METHOD: A prospective randomized controlled open label study was conducted on 75 breast cancer patients receiving adjuvant paclitaxel 80 mg/m2 weekly for 12 weeks. Eligible patients were randomized to either the low dose group; 1200 mg daily NAC, the high dose group; 1200 mg NAC twice daily or the control group; received paclitaxel only. The primary endpoint was the incidence of different grades of PIPN using National Cancer Institute's common toxicity criteria for adverse event (NCI-CTCAE) while secondary endpoints were the severity of PIPN using modified total neuropathy score (mTNS), quality of life (QOL) using Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity (FACT-GOG-NTX) subscale, serum nerve growth factor (NGF), and serum malondialdehyde (MDA). RESULTS: At the end of the 12-week period, the incidence of grade (2, 3) peripheral neuropathy was significantly lower in the high dose group (28.6%) compared to the low dose group (61.9%) and the control group (100%), p value < 0.001. A significant improvement in the mTNS and QOL scores was observed after 6 and 12 weeks in the high dose group and the low dose group compared to the control, p value < 0.001. Significantly higher levels of serum NGF in the high dose group and lower level of serum MDA in the high dose and the low dose group were observed. CONCLUSION: Oral NAC (1200 mg once and twice daily) might reduce the incidence and severity of PIPN and improve the patients' QOL. TRIAL REGISTRY: Clinical Trial.gov registration number: NCT03492047.

Correlation between serum vitamin B12 level and peripheral neuropathy in atrophic gastritis.

AIM: To explore the correlation between serum vitamin B12 level and peripheral neuropathy in patients with chronic atrophic gastritis (CAG). METHODS: A total of 593 patients diagnosed with chronic gastritis by gastroscopy and pathological examination from September 2013 to September 2016 were selected for this study. The age of these patients ranged within 18- to 75-years-old. Blood pressure, height and weight were measured in each patient, and the body mass index value was calculated. Furthermore, gastric acid, serum gastrin, serum vitamin and serum creatinine tests were performed, and peripheral nerve conduction velocity and Helicobacter pylori (H. pylori) were detected. In addition, the type of gastritis was determined by gastroscopy. The above factors were used as independent variables to analyze chronic gastritis with peripheral neuropathy and vitamin B12 deficiency risk factors, and to analyze the relationship between vitamin B12 levels and peripheral nerve conduction velocity. In addition, in the treatment of CAG on the basis of vitamin B12, patients with peripheral neuropathy were observed. RESULTS: Age, H. pylori infection, CAG, vitamin B9 and vitamin B12 were risk factors for the occurrence of peripheral nerve degeneration. Furthermore, CAG and H. pylori infection were risk factors for chronic gastritis associated with vitamin B12 deficiency. Serum vitamin B12 level was positively correlated with sensory nerve conduction velocity in the tibial nerve (R = 0.463). After vitamin B12 supplementation, patients with peripheral neuropathy improved. CONCLUSION: Serum vitamin B12 levels in patients with chronic gastritis significantly decreased, and the occurrence of peripheral neuropathy had a certain correlation. CAG and H. pylori infection are risk factors for vitamin B12 deficiency and peripheral neuropathy. When treating CAG, vitamin B12 supplementation can significantly reduce peripheral nervous system lesions. Therefore, the occurrence of peripheral neuropathy associated with vitamin B12 deficiency may be considered in patients with CAG. Furthermore, the timely supplementation of vitamin B12 during the clinical treatment of CAG can reduce or prevent peripheral nervous system lesions.

Therapeutic Implications of Peripheral Nerve Hyperexcitability in Muscle Cramping: A Retrospective Review.

PURPOSE: Muscle cramping due to peripheral nerve hyperexcitability (PNH) is poorly characterized. This retrospective study examines the prevalence of PNH and response to treatment. METHODS: The Duke EMG Database was queried to identify patients with muscle cramping tested for PNH from 2010 to 2015. Peripheral nerve hyperexcitability was defined by compound muscle action potential after-discharges on repetitive nerve stimulation. Response to treatment was determined by the treating physician's clinical impression 6 months after diagnosis or last documented visit. RESULTS: Seventy-two patients met inclusion criteria. Twenty-three (32%) patients had electrodiagnostic evidence of PNH. Of the patients with PNH, 74% had a good response to treatment whereas 37% of treated patients in the PNH-negative group (P = 0.0258). Carbamazepine and gabapentin were the most frequently used treatments with response rates of 70% and 77%, respectively. CONCLUSION: Muscle cramps associated with PNH respond well to symptomatic treatment, particularly with carbamazepine and gabapentin.

Determination of the coenzyme Q10 status in a large Caucasian study population.

Coenzyme Q10 (CoQ10 ) exists in a reduced (ubiquinol) and an oxidized (ubiquinone) form in all human tissues and functions, amongst others, in the respiratory chain, redox-cycles, and gene expression. As the status of CoQ10 is an important risk factor for several diseases, here we determined the CoQ10 status (ubiquinol, ubiquinone) in a large Caucasian study population (n = 1,911). The study population covers a wide age range (age: 18-83 years, 43.4% men), has information available on more than 10 measured clinical phenotypes, more than 30 diseases (presence vs. absence), about 30 biomarkers, and comprehensive genetic information including whole-genome SNP typing (>891,000 SNPs). The major aim of this long-term resource in CoQ10 research is the comprehensive analysis of the CoQ10 status with respect to integrated health parameters (i.e., fat metabolism, inflammation), disease-related biomarkers (i.e., liver enzymes, marker for heart failure), common diseases (i.e., neuropathy, myocardial infarction), and genetic risk in humans. Based on disease status, biomarkers, and genetic variants, our cohort is also useful to perform Mendelian randomisation approaches. In conclusion, the present study population is a promising resource to gain deeper insight into CoQ10 status in human health and disease.

Peripheral systems: neuropathy.

Long-term, excessive consumption of alcoholic beverages produces a peripheral neuropathy with symptoms of decreased superficial sensation, hyperalgesia, and weakness. Alcoholic neuropathy is characterized by axonal degeneration with reduced density of both small and large fibers and axonal sprouting. Electrophysiologic studies reveal a marked reduction in the amplitude of sensory potentials and moderate slowing of nerve conduction, mainly in the lower extremities. Dietary deficiency of vitamins, which are often associated with chronic alcoholism, can contribute to the pathogenesis. Recent studies using animal models have identified several mechanisms by which ethanol impacts peripheral nerve function. Ethanol can exert direct neurotoxic effects on peripheral nerves via its metabolite acetaldehyde and by enhancing oxidative stress. Ethanol activation of protein kinase Cε signaling in primary afferent nociceptors plays an important role in lowering nociceptive threshold. Further, ethanol causes cytoskeletal dysfunction and inhibits both anterograde and retrograde axonal transport. Alcoholic neuropathy is potentially reversible and treatments include abstinence from alcoholic beverages and consumption of a nutritionally balanced diet supplemented with B vitamins. However, response to these treatment strategies can be variable, which underscores the need for novel therapeutic strategies. In this review, we provide an overview of the clinical findings and insights on molecular mechanisms from animal models.

Prevalence and features of peripheral neuropathy in Parkinson's disease patients under different therapeutic regimens.

BACKGROUND: Recent reports suggest increased frequency of peripheral neuropathy (PN) in Parkinson's disease (PD) patients on levodopa compared with age-matched controls particularly during continuous levodopa delivery by intestinal infusion (CLDII). The aim of this study is to compare frequency, clinical features, and outcome of PN in PD patients undergoing different therapeutic regimens. METHODS: Three groups of consecutive PD patients, 50 on intestinal levodopa (CLDII), 50 on oral levodopa (O-LD) and 50 on other dopaminergic treatment (ODT), were enrolled in this study to assess frequency of PN using clinical and neurophysiological parameters. A biochemical study of all PN patients was performed. RESULTS: Frequency of PN of no evident cause was 28% in CLDII, 20% in O-LD, and 6% in ODT patients. Clinically, 71% of CLDII patients and all O-LD and ODT PN patients displayed a subacute sensory PN. In contrast, 29% of CLDII patients presented acute motor PN. Levodopa daily dose, vitamin B12 (VB12) and homocysteine (hcy) levels differed significantly in patients with PN compared to patients without PN. CONCLUSIONS: Our findings support the relationship between levodopa and PN and confirm that an imbalance in VB12/hcy may be a key pathogenic factor. We suggest two different, possibly overlapping mechanisms of PN in patients on CDLII: axonal degeneration due to vitamin deficiency and inflammatory damage. Whether inflammatory damage is triggered by vitamin deficiency and/or by modifications in the intestinal micro-environment should be further explored. Proper vitamin supplementation may prevent peripheral damage in most cases.

An unusual case of peripheral neuropathy possibly due to arsenic toxicity secondary to excessive intake of dietary supplements.

A 74-year-old woman presented to the neurology clinic with worsening of her longstanding peripheral neuropathy of unknown cause. There was below knee loss of spinothalamic sensation, reduced joint position of toes, absent below hips vibration sensation and absent ankle jerks. Neurophysiology studies showed further progression of her axonal sensory neuropathy. Urine and blood analysis previously carried out in Australia suggested elevated levels of arsenic. After abstinence from seafood, a random urine sample was collected and this confirmed the elevation in urine arsenic (622.1 nmol/L, reference range <534 nmol/L). The household water was found to be uncontaminated and the patient had no occupational or environmental exposure to arsenic. On questioning the patient admitted to taking fish oils, omega-3 oils and glucosamine sulphate dietary supplements in excess of the recommended dosage. These supplements were identified as possible sources of arsenic and the patient was asked to stop all supplements. One month later the urine arsenic had reduced to 57.5 nmol/L. There was an improvement in patient wellbeing, she no longer required Gabapentin for pain relief and the neurophysiology studies also showed improvement. Clinicians should consider heavy metal toxicity as a cause of peripheral neuropathy of unknown cause. A detailed patient history including all dietary supplements is essential to help elucidate the source of heavy metal toxicity.

Peripheral neuropathy in cystic fibrosis: a prevalence study.

BACKGROUND: Information on peripheral neuropathy in children with cystic fibrosis is scanty. The etiology can be multifactorial (micronutrient deficiency, chronic hypoxia, impaired glucose tolerance, immunological, vasculopathic, critical illness). METHODS: Forty five cystic fibrosis children aged 1-18 years on vitamin E supplementation for at least 6 months underwent detailed neurological examination, serum vitamin E, vitamin B12, folate, copper levels and detailed nerve conduction studies. RESULTS: The mean age of the study population was 8.35 years (±4.9 years) with 62.2% being males. Overall 22 out of 45 (48.88%,CI: 33.7-64.2) had electrophysiological evidence of peripheral neuropathy which was predominantly axonal (86.4%), sensory (50%), and polyneuropathy (95.45%). There was no significant association between status of serum micronutrients and electrophysiological evidence of peripheral neuropathy. CONCLUSION: Patients with cystic fibrosis have electrophysiological evidence of peripheral neuropathy (predominantly axonal, sensory and polyneuropathy). There is significant association of higher chronological age with occurrence of peripheral neuropathy.

Pancytopenia complicated with peripheral neuropathy due to copper deficiency: clinical diagnostic review.

Only a dozen cases of pancytopenia caused by copper deficiency have been reported. We report the case of an 81-year-old man who underwent total gastrectomy for gastric cancer. He received total parenteral nutrition without trace element supplementation for 6 months. Serum levels of copper and ceruloplasmin were low, but serum zinc was normal. The administration of copper into TPN led to rapid improvement in anemia and neutropenia. We review 11 previous cases of copper-deficient cytopenia, categorized into two groups according to etiology, and define the characteristic symptom of copper malabsorption caused by excess Zn as peripheral neuropathy.

Omega-6 and omega-3 fatty acids predict accelerated decline of peripheral nerve function in older persons.

Pre-clinical studies suggest that both omega-6 and omega-3 fatty acids have beneficial effects on peripheral nerve function. Rats feed a diet rich in polyunsaturated fatty acids (PUFAs) showed modification of phospholipid fatty acid composition in nerve membranes and improvement of sciatic nerve conduction velocity (NCV). We tested the hypothesis that baseline plasma omega-6 and omega-3 fatty acids levels predict accelerated decline of peripheral nerve function. Changes between baseline and the 3-year follow-up in peripheral nerve function was assessed by standard surface ENG of the right peroneal nerve in 384 male and 443 female participants of the InCHIANTI study (age range: 24-97 years). Plasma concentrations of selected fatty acids assessed at baseline by gas chromatography. Independent of confounders, plasma omega-6 fatty acids and linoleic acid were significantly correlated with peroneal NCV at enrollment. Lower plasma PUFA, omega-6 fatty acids, linoleic acid, ratio omega-6/omega-3, arachidonic acid and docosahexanoic acid levels were significantly predicted a steeper decline in nerve function parameters over the 3-year follow-up. Low plasma omega-6 and omega-3 fatty acids levels were associated with accelerated decline of peripheral nerve function with aging.

Sequential changes in plasma selenium concentration after cadaveric renal transplantation.

BACKGROUND: Previous investigations have shown that plasma selenium concentrations are significantly lower in patients with established chronic graft nephropathy (CGN) than in healthy transplant controls. The aims of this study were to determine when in the transplant process low selenium concentrations become apparent and to explore the relationship between selenium levels and risk factors for CGN. METHODS: Plasma selenium concentrations were measured in 40 patients (20 receiving cyclosporin, 20 receiving tacrolimus) undergoing transplantation. Samples were obtained immediately before transplantation and at 3, 6 and 12 months after transplantation. RESULTS: A low plasma selenium concentration was found in 30 patients at the time of transplantation but this had normalized in the majority of patients by 3 months. Plasma selenium concentrations at 3, 6 and 12 months were significantly higher than baseline values for both treatment arms, but were significantly lower at 3 months in patients who experienced either clinical acute rejection (CAR) or cytomegalovirus (CMV) infection during the preceding months. CONCLUSION: Low plasma selenium concentrations are common at the time of transplantation but appear to normalize thereafter. The identification of low selenium levels in patients who experience CAR or CMV (two important risk factors for clinically apparent CGN) suggests that the relationship between selenium and CGN warrants further investigation.

A pilot study on the relation between cisplatin neuropathy and vitamin E.

Peripheral sensory neuropathy is the main non-hematological side-effect related to cisplatin chemotherapy. The strong similarity between clinical and neuropathological aspects in peripheral neuropathy induced by cisplatin and neurologic syndromes due to vitamin E deficiency, prompted us to investigate the relationship between cisplatin neuropathy and plasmatic level of vitamin E (alpha-tocopherol). We measured vitamin E in the plasma of 5 patients (Group 1) which developed severe neurotoxicity after cisplatin treatment and in another group of 5 patients (Group 2) we analyzed the plasmatic level of vitamin E before and after 2 or 4 cycles of cisplatin treatment. The results showed that the patients of group 1 presented low plasmatic levels of vitamin E and that the patients of group 2 presented significantly lower levels of vitamin E after 2 or 4 cycles of cisplatin than before treatment. Our preliminary data suggest that an inadequate amount of the antioxidant vitamin E due to cisplatin treatment could be responsible of the peripheral nerve damage induced by free-radicals. Given the lack of toxicity of vitamin E, we need to systematically assess the possible neuroprotective role of vitamin E supplementation in patients treated with cisplatin chemotherapy.

Folate deficiency, anticonvulsant drugs, and psychiatric morbidity.

The folic acid (FOA) level was determined in serum and erythrocytes in 100 epileptic patients and 100 control patients using a luminescence assay. A lowered FOA concentration in serum, erythrocytes, or both was observed in 15% of the epileptic patients and in 2% of the control group. In the epileptic patients, the FOA in the serum and in the erythrocytes was significantly lower than that in the control group. Patients receiving carbamazepine monotherapy had a significantly lower FOA level in the erythrocytes than did patients receiving phenytoin monotherapy. The FOA level showed a negative correlation to the duration of epilepsy. None of the patients with lowered FOA had a normal mental status. The course of the supplementation treatment with 5 mg folinic acid (or FOA) of four patients with FOA deficiency could be monitored psychopathometrically. All four patients showed an improvement in their well-being and the majority of measured variables of the cognitive performance.

[Role of neuropeptides in the pathogenesis of pain syndrome in autonomic and sensory polyneuropathy of occupational etiology and their role in the therapeutic action of laser acupuncture]. / Rol neiropeptidov v geneze bolevogo syndroma pri vegetosensornoi polinevropatii professionalnoi étiologii i ikh uchastie v mekha- nizme terapevticheskogo deistviia lazernoi akupunktury.

Biochemical studies of opiate system in patients with occupational diseases showed the role of the central pain regulating system inducing the pain syndrome in autonomic and sensory polyneuropathy caused by occupational factors. Increased production of the pain-reducing endogenic neuropeptides such as endorphin and leucine enkephalin was found one of the He-Ne laser acting principles which restore the pain adaptation in human. A repeated course of laser therapy would normalize the content of both neuropeptides. Blood levels of neuropeptides may serve for evaluating the pain syndrome and estimating of laser therapy effects.

Prospective study of nerve conduction parameters and serum magnesium following cisplatin therapy.

This study evaluated the effects of cisplatin on 18 nerve conduction parameters of median, ulnar, peroneal, and sural nerves in relation to age, magnesium nadir, average magnesium, and magnesium replacement in gynecologic oncology patients. The 37 patients in this study received cisplatin (70 mg/m2) at 4-week intervals either as a single agent (17 patients) or in combination with doxorubicin and cyclophosphamide (20 patients) following inpatient hydration. The patients were placed randomly on either magnesium supplementation (intravenous plus oral) or placebo. For all patients, nerve conduction studies were performed before and after cisplatin therapy in the same EMG laboratory. Statistical analysis revealed that postcisplatin nerve conduction parameters were significantly predictable based upon pretherapy nerve conduction parameters, magnesium supplementation, total cisplatin, age, magnesium nadir, and average magnesium. Total cisplatin, age, and serum magnesium level were significant predictors in 8, 2, and 2 of the 18 nerve conduction parameters, respectively. Following cisplatin therapy, there was a significant decrease in sensory nerve action potential amplitude of median, ulnar, and sural nerves, whereas sensory latency of median and ulnar nerves was significantly increased. Cisplatin therapy had no effect on motor nerve conduction parameters of median, ulnar, and peroneal nerves. Factors responsible for the decrease in sural sensory action potential amplitude were not identified. Sensory nerve action potential amplitude and sensory latency of ulnar nerve are the two best objective parameters that can be utilized to monitor patients for adverse nerve conduction side effects of cisplatin.

Levels of arsenic in Indian opium eaters.

Intake of opium is very common in India. The contraband material is generally contaminated with arsenic. Most often opium eaters present with neuropathy and hepatomegaly. Arsenic was estimated in serum, urine, nails and hair of opium eaters with and without neuropathy. Arsenic was also estimated in various opium samples. Arsenic was significantly higher in serum, urine, nails and hair of opium addicts when compared to controls. The opium samples analysed showed varyingly high amounts of arsenic.

Pyridoxine metabolism in carpal tunnel syndrome with and without peripheral neuropathy.

The role of insufficient pyridoxine as an etiologic factor in the development of carpal tunnel syndrome (CTS) has been reported and has led to the empirical use of pyridoxine to treat CTS. Previous studies have not employed standardized electrodiagnostic criteria to objectively determine the presence of CTS or to rule out peripheral neuropathy (PN). The present study categorized subjects with symptoms suggestive of CTS into four groups by standardized electrodiagnostic criteria: (1) CTS, (2) PN, (3) CTS and PN, (4) normal. At least seven subjects were in each group. Erythrocyte glutamine oxaloacetic acid transaminase (EGOT) activity with and without in vitro enhancement with pyridoxal phosphate was used as a means of identifying subjects with and without pyridoxine metabolic abnormalities. A significant difference in pyridoxine metabolic activity (PMA) was found between groups by both chi square (p less than 0.05) and analysis of variance (p less than 0.05). Further evaluation showed that this difference was associated with the presence or absence of PN (p less than 0.05). There was no difference in PMA when groups were separated on the basis of CTS. Results showed that a PMA abnormality was a factor highly correlated with the presence of PN but not CTS. This finding suggested that the positive response reported previously in subjects with CTS taking supplemental pyridoxine may actually be related to an unrecognized PN, which was compounding the symptomatology.