Abstract
Objective: To evaluate neuropathic pain (NP), its intensity, and complications in people with type 2 diabetes mellitus (T2DM) in a city of eastern São Paulo. Method: Cross-sectional study conducted with 96 individuals with T2DM served by primary health units in São João da Boa Vista-SP. The following instruments were used to screen NP: Michigan Neuropathy Screening Instrument, Leeds Assessment of Neuropathic Symptoms and Signs, Douleur Neuropathique 4, and Brief Pain Inventory. The data were analyzed using descriptive and inferential statistics, with a 5 % significance level. Results: Of the 96 people with T2DM for longer than five years, 22.9 % had pain. NP was related to high levels of fasting blood glucose (mean = 214 ± 65.58 mg/dl; p = 0.0002), glycated hemoglobin (mean = 8.8 ± 0.11 %; p < 0.001), absence of a balanced diet (p = 0.0066), obesity (p = 0.023), and high blood pressure (p < 0.001). Conclusion: Higher values of glycated hemoglobin rates increased three times the chance of NP. The screening and management of painful diabetic neuropathy is a challenge but adopting a screening protocol supports the secondary prevention of this manifestation.
Highlights
Diabetic peripheral neuropathy (DPN) is prevalent in about 50 % of diabetes mellitus (DM) cases
We investigated variables related to sociodemographic characteristics, laboratory, clinical aspects, and complications related to type 2 diabetes mellitus (T2DM), lifestyle habits, comorbidities, treatments, hospitalization for the disease, treatment satisfaction in primary health units, and assessment of neuropathic pain (NP) and its intensity
In our research, the main complications associated with NP in T2DM were the most referred to, i.e., allodynia, poor sleep quality, and night-time worsening of symptoms
Summary
Diabetic peripheral neuropathy (DPN) is prevalent in about 50 % of diabetes mellitus (DM) cases. Among DPN cases, 75 % had distal symmetric polyneuropathy (DSP) of multifactorial pathogenesis, caused by a metabolic dysfunction It results in oxidative stress and inflammation of peripheral nerves, in addition to variations in voltage-dependent sodium channels that worsen DSP and NP [4,5]. NP, the most incapacitating clinical complication of DSP among DPNs, is caused by extensive lesions in fine Aβ-, Aδ-, and C-type nerve fibers that adversely affect the sensory and motor nerve components. It has different clinical manifestations, pathophysiological mechanisms, development, and evolution. The latter is induced by chronic hyperglycemia that causes mitochondrial damage and neural apoptosis [11,12]
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