Recovery Of Neuropathy Research Articles

SPA KAKI DIABETIK EFEKTIF MEMPERBAIKI SENSASI KAKI PADA DIABETESI

Chronic hyperglycemia in diabetes mellitus nonenzymatic glycosylation and excessive glucose to intracellular diffusion leads to structural abnormalities and capillary function as well as peripheral nerve injury. Nerve cell injury and supported by capillary dysfunction lead to neuropathy. Sensory neuropathy results in decreased leg sensation that is easily injured. Recovery of neuropathy is done by improving blood circulation repairing peripheral nerves. The purpose of this study was to determine the effect of diabetic foot spa on foot sensation in diabetics. The study was conducted with pre test post test with control group design on 45 people divided into 25 people into treatment group and 20 men men in the control group taken with simple random technique at Puskesmas II Denpasar Barat 2017. Treatment group given treatment in the form of diabetic foot spa covers gymnastics foot, foot soak and massage with VCO for 4 weeks, while the control group get foot exercises done by puskesmas. Foot sensation data is measured by Semmes-Weinstein monofilament. The results showed that foot spa ektof increase foot sensation in people with diabetes. It is recommended that people with diabetes can do foot spa in the form of foot exercises, soak feet and dimasase with VCO regularly.

Serum micronutrients and prealbumin during development and recovery of chemotherapy-induced peripheral neuropathy.

Chemotherapy-induced peripheral neuropathy (CIPN) is a frequent adverse event. Nutritional status can become impaired in cancer patients, potentially contributing to neuropathy's evolution. Our aim was to evaluate serum micronutrients and prealbumin in a cohort of 113 solid-cancer patients receiving platinum and taxane compounds during the development and recovery of neuropathy, up to 1 year after finishing treatment. CIPN was graded according to Total Neuropathy Score(©) and NCI.CTCv3 at T0 (baseline), T1 (1-3 months), and T12 (12 months) after chemotherapy. CIPN was classified as asymptomatic (< grade 2) or symptomatic (≥2). CIPN recovery was defined as ≥1 grade improvement at T12. Symptomatic CIPN developed in 52% of patients. Symptomatic patients presented a higher increase in TNSc (p < 0.001), in TNSr(©) (p < 0.001), and decrease in sural (p < 0.001) and radial nerve conduction (p < 0.001). No significant differences with any of the micronutrients were observed along T0-T1 period between severity or chemotherapy groups. By T12, symptomatic patients without recovery had a decrease in vitamin E levels (p = 0.019) and prealbumin (p = 0.062) compared with those symptomatic that improved. A correlation between the variation of vitamin E and prealbumin at T0-T1 (r = 0.626, p = 0.001) and T1-T12 (r = 0.411, p = 0.06) was observed. After chemotherapy treatment, the improvement of patients displaying symptomatic neuropathy is related to vitamin E and prealbumin serum levels. Our results suggest that nutritional status can play a role in CIPN recovery.

Relationship between persistent neurotoxicity and long-term platinum exposure after treatment with cisplatin

2546 Background: We aimed to assess relationships between the severity of persistent neuropathy and long-term platinum exposure in patients previously treated with cisplatin. Methods: Twenty patients, treated with a cisplatin containing regimen 18 to 75 months before participating in this study, were included. Sensory nerve function in hands and feet was evaluated using vibration threshold (VT) determination. Platinum levels in plasma and plasma ultrafiltrate were assessed using inductively coupled plasma mass spectrometry (ICP- MS). Possible factors affecting sensory nerve function or platinum retention were collected, including cumulative dose, follow-up time, route of administration, renal function, glutathione S-transferase (GST) genotypes, co-administration of sodium thiosulfate (STS with intra-arterial (i.a.) cisplatin), and co-morbidity (alcoholism and diabetes). Results were evaluated using non linear mixed effects modelling. Results: Patients (9 testis, 8 head-neck, 1 NSCLC, 1 SCLC, and 1 yolk sac) were treated with a cumulative dose of 300–600 mg·m-2. Five patients received STS. Platinum plasma concentrations ranged between 142.4–1154 ng·L-1of which on average14.8% was recovered in ultrafiltrate. Platinum levels decreased with a half-life of 21.7 months and were related to the cumulative dose. Platinum levels were reduced by 60% with i.a. cisplatin and co-administration of STS (p=0.002). The hand-VT decreased with time (t1/2=19.9 months) and was related to cumulative dose and to alcohol use (p=0.06). Moreover, the half-life of recovery of the hand-VT was related to the elimination half-life of platinum, albeit non-significant. In contrast, the feet-VT did not improve over time and did not show an association with cumulative dose or any of the other factors. GST genotypes and renal function were not related to VT and platinum levels. Conclusions: Our data suggest that plasma platinum levels are related to follow-up time, cumulative dose, and STS use. The data show that neuropathy in the feet might be irreversible in contrast to the hand-VT, which was also related to cumulative dose and alcohol use. Whether recovery of neuropathy was related to platinum elimination remains to be established. No significant financial relationships to disclose.