Neuropathic pain is one of the most common symptoms of diabetic neuropathy. It is known than the serum level of many inflammatory cytokines increase especially in the early stages of Diabetes Mellitus. In this study, the role of immunological mechanisms in the neuropathic pain development was investigated by measuring serum cytokine levels in Type2 Diabetes Mellitus patients with neuropathy.
Material and Method: 60 patients followed up with Type 2 Diabetes Mellitus diagnosis for at least five years and detected to have neuropathy based on the electrophysiological examination were included in the study. Control group was formed by 30 healthy volunteers of similar ages and genders. Diabetes mellitus and pain related anamnesis was taken from the patients. Body mass index was measured by measuring height and weight. Fasting blood sugar, HbA1C, C-reactive protein, kidney and liver function tests were registered from the patient files. LANSS, PAINDETECT, VAS and NRS scales were used for neuropathic pain evaluation. While 30 of the patients had neuropathic pain, 30 didn’t. Interleukin-10, Interleukin17, Tumor necrosis factor- α and Transforming growth factor -β levels were measured among the patients who had and didn’t have neuropathic pain and the control group. Information on the operations to be made was given to all cases participating in the study and their consent was taken. Consent of the local ethic board was taken for the study.
Findings: 25 of the patients were female and 35 were male and the mean age was 56.73±9.42. Dorsal sural nerve couldn’t be stimulated in the electrophysiological examination of all patients and symmetrical sensory polyneuropathy was detected. SSR couldn’t be qualified in 4 patients (6.7%). TNF- α and TGF-β levels were significantly lower in the patient group compared to the control group (p<0.001 and p: 0.002 in order). IL-10 and IL-17 levels were found similar in patient and control groups (p: 0.729, p: 0.871 in order). TNF-α and TGF- β levels were lower in NA patients compared to the control group (p: 0.008 and p: 0.001 in order). TGF- β was found lower in the group with NA compared to the group without NA (p: 0.007). IL10 and IL-17 levels were found similar in the control group and the patients with and without NA. Mean LANSS score was 16.00, PAINDETECT score was 19.3 and VAS and NRS score was 5 in patients with NA. When compared to those with NA, a moderate negative correlation was detected among TGF-β level and PAINDETECT scale (p: – 0.361). Mean age of the patients with NA was 57.4 and 15 of these were female and mean BMI value was 30.5, mean HbA1c level was 7 and no statistical relation was detected between NA presence and age (p: 0.588), gender (p: 0,190), BMI (p: 0.965) and HbA1c level (p: 0.982). Duration of the disease was longer in patients with NA (p: 0.02). SSR wasn’t noticed in 13.3% of the patients with NA. No loss was observed in SSR of patients without NA. SSR amplitude was lower in patients with NA (p: 0.015). No relation was detected between NA presence and SSR latency (p: 0.170).
Discussion and Conclusion: It is known that inflammation increases significantly in type 2 DM and diabetes plays an important role in the occurrence of microvascular and macrovascular complications including polyneuropathy. Detection of lower TGF-β and TNF-α levels in our patients compared to the control group supports the importance of inflammation in DM occurrence. The fact that only TGFβ level is low and other cytokine levels are normal in patients with NA may be related to the low number of patients in our study.
As a result, NA Type 2 is a common complication in DM patients and confirming the role of inflammatory mechanisms would be useful in the development of new treatments.
Keywords: Diabetic Neuropathy, Neuropathic Pain, Cytokines.
-Study is made by Lutfiye Asena Binyay