Relationship Of Dyslipidaemia To Diabetic Peripheral Neuropathy

Objective and Background:Diabetic peripheral neuropathy(DPN) is one of the most frequently-occurring microvascular complications of type 2 diabetes mellitus. It lowers the patient's quality of life. Unfortunately, the pathogenesis has not been made out clearly. Different hypotheses have been proposed to explain the various modes of progression of DN but a consensus has not emerged. Since insulin is absolutely or relatively deficient in diabetes, the synthesis of fat reduces and the resolution accelerates, leading to disorders of lipid meta bolism. There is a consensus that dyslipidaemia is a potential risk factors for cardiovascular disease now. However the studies about its effect on microvascular are few and their results are not coincident. Some study suggested hyperlipidemia is associated with the development of DPN and statins has a trend towards slower progression of neuropathy. But others suggested they were not correlative. In this study, we detected and compared the serum lipid and other compositions of metabolic syndrome in type 2 diabetic patients with/without neuropathy to evaluate the possible relationship among the lipid, the other compositions of metabolic syndrome and diabetic peripheral neuropathy.Design and Methods:A retrospective analysis of clinical features of type 2 diabetic patients was conducted based on 112 type 2 diabetic patients. Serum lipid and uric acid levels were examined in 52 patients with DPN and in 63 patients without diabetic peripheral neuropathy(NDPN).1. Physical examination: measure height, weight, waistline, hip circumference, SBP, DBP, BMI, WHR.2. Detection of serum lipid and other clinical parameters: blood was obtained for serum lipid and other clinical parameters(BG0h, Ins0h, CP0h, BG2h, Ins2h, CP2h, HbA1c, TG, TC, LDL-C, HDL-C, VLDL-C, UA, et al). Urine for 24h was obtained for UAE3. Detection of NCV: Median nerve and common peroneal nerve were detected by electrophysiological test to get the motor nerve conduction velocity(MCV); median nerve, ulnar nerve, sural nerve, peronous super nerve were detected to get the sensory nerve conduction velocity(SCV).Results:Disorder of lipid metabolism is hypertriglyceridemia in type 2 diabetes mellitus. Neuropathy was not found to have any significant correlation with lipid profile abnormalities. CP0h, Ins0h, Ins2h, HOMA-IRI of DPN is lower than NDPN, UAE is higher than NDPN. No significant relationships were found between neuropathy and age, gender, quality of diabetes control, duration of disease, BP, hyperlipidemia, cigarette smoking and UA. UA is negatively correlated with HDL-C.Conclusions:Type 2 diabetes mellitus patients have disorders of lipid metabolism such as hypertriglyceridemia. However peripheral neuropathy was not found to have any significant correlation with lipid profile abnormalities. Whether UA can be one of compositions need more researches.Diabetic peripheral neuropathy(DPN) is one of the most frequently-occurring microvascular complications of type 2 diabetes mellitus. The pathogenesis has not been made out clearly up to now. Recently, the study about pathogenesis mianly refers to the following hypothesises: 1. Metabolic aberrations: increased activity of the polyol pathway, abnormalities in inositol metaboism, increased production of non-enzymatic glycation, oxidative stress, increased activity of PKC-β, increased serum lever of homocysteic acid. 2. disfunction of blood vessel: structural change, reduced diastolic function, haemorheology change. 3. Neurotrophy disorders: reduced nerve growth factors and IGFs. 4. autoimmune injury 5. hereditary susceptibility.LADA, a special type of diabetes, is related to slowly progressive β -cell failure, with clinical manifestation similar to type 2 diabetes and auto-antibodies positive at diagnosis. Not only islet organ-specific auto-antibodies such as GADAb4CA,IA-2A, can be found in LADA patients, but also non-specific auto-antibodies such as Anu'-CD38aAbs,and non-islet organ-specific auto-antibodies such as TPOAb and AGAAb can be found. However ,LADA is not completely identical with type 1 diabetes in the epitope, category and titre of antibody which are also different in different LADA patients. That may be correlated to the different clinical manifestation, pathogenesy, degree of β-cell failure and prognosis. Studies on auto-antibodies offer a base to research the pathogenesy of LADA, and the mecessity of insulin therapy at diagnosis and immunol regulation therapy.