Introduction: Evaluating small nerve fibers in patients with systemic lupus erythematosus (SLE) using cutaneous silent period (CSP) and skin biopsy and assesssing the relationship between clinical signs, autoantibodies and neuropathic pain score. Objectivemethods: Fifty one SLE patients and 46 healthy volunteers were included in this study. Nerve conduction studies and CSP were performed both on upper and lower limbs in subjects. Skin biopsy was performed and the number of epidermal nerve density and IL-6 staining were evaluated. Results: In SLE patients, CSP latencies were significantly prolonged both in lower and upper limbs and lower and upper extremity CSP durations were significantly shorter when compared to controls (p < 0.001). The number of epidermal nerve was significantly lower in SLE patients when compared to healthy controls (p < 0.001). Conclusion:We detected marked small nerve fiber damage in both lower and upper limbs in SLE patients using CSP. Decreased epidermal nerve density also supports this finding.
The involvement of the autonomic nervous system is less common than that of the central and peripheral nervous system in systemic lupus erythematosus (SLE) patients. However, its involvement can negatively affect the quality of life of the patient and cause life-threatening situations. In this study, autonomic function was evaluated in SLE patients who did not show any sign of autonomic involvement using R-R interval variation (RRIV) and sympathetic skin response (SSR) electrophysiological tests. SSR was used to evaluate the sympathetic nervous system, whereas RRIV was used for the parasympathetic nervous system. We included 23 SLE patients and 21 healthy volunteers in the study. Of the 23 SLE patients, 20 (86.9 %) were female and 3 (13.1 %) were male. The age range of the patients was between 19 and 52 years, with a mean age of 32.5 ± 9.1 years. Routine nerve conduction studies and autonomic tests were performed on patients in the electromyography (EMG) laboratory. Lower extremity SSR latencies were prolonged and a significant loss of amplitude was observed in comparison to the control group. Furthermore, deep-breath RRIV values for the patient group were significantly lower than that of the control group. Both sympathetic and parasympathetic nervous system involvement was seen in our study. In conclusion, EMG can reveal a possible underlying involvement in the absence of signs of autonomic involvement.
IntroductionIn this study, we aimed to investigate the histological and clinical effect of angiotensin-converting enzyme (ACE) and ACE gene polymorphism in nonalcoholic fatty liver disease (NAFLD) and their roles in the progression of the disease.Materials and methodsLiver function tests, body mass index, waist circumference, lipid parameters, fasting blood glucose (FBG), hemoglobin A1c (HbA1c), homeostasis model assessment-IR (HOMA-IR), ACE, and ACE gene polymorphism were evaluated in the NAFLD group and control group. The study group was evaluated by dividing the group into four subgroups by ACE gene polymorphism (D/D homozygous, I/I homozygous, D/I heterozygous, I/D heterozygous). Liver biopsies were evaluated according to Brunt Classification.ResultsA total of 31 patients who were diagnosed with NAFLD and 40 healthy individuals were included in the study. The ACE level was found to be 11.69 ± 1.99 in the NAFLD group and 11.52 ± 1.72 in the control group (p = 0.70). There was a negative correlation between ACE levels and HOMA-IR levels (p = 0.008, r= −0.512). Biochemical parameters were not different among ACE gene polimorphism subgroups, except FBG (between D/D, I/D and D/I, I/D; p = 0.02). When the ACE levels were compared in terms of grade and stage, no significant difference was found (for stage and grade p = 0.68). The ACE gene polymorphism subgroups did not differ by histopathologic findings; grade and stage (for grade p = 0.42, for stage p = 0.92).ConclusionIn this study, we could not find a correlation of ACE and ACE gene polymorphism with metabolic risk factors and the disease severity in NAFLD.How to cite this articleTekatas DD, Bahcecioglu IH, Ispiroglu M, Sahin A, Ilhan N, Yalniz M, Demirel U. Role of Renin–Angiotensin-converting Enzyme Level and ACE Gene Polymorphism in Patients with Nonalcoholic Fatty Liver Disease. Euroasian J Hepato-Gastroenterol 2016;6(2):137-142.
Background Small fiber neuropathy (SFN) is a peripheral nerve disorder affecting specifically small myelinated A Delta fibers and unmyelinated C fibers. SFN is one of the common causes of neuropathic pain syndrome, however it can not be shown in conventional nerve conduction studies, making it difficult to diagnose. It was suggested that Cutaneous Silent Period (CSP) can be used as an objective method for evaluating small nerve fibers. Objectives Evaluating small nerve fibers in patients with systemic lupus erythematosus (SLE) using CSP and assesssing the relationship between clinical signs, autoantibodies and neuropathic pain score. Methods 51 SLE (48 female, 3 male, mean age:39.9±9.4), and 46 healthy control subjects (42 females, 4 males, mean age: 40±9.2) were included the study. Patients having risk factors for peripheral neuropathy were excluded. Electrophysiologic recordings were performed both on patients and the control group using nerve conduction studies and CSP. Values (latency and duration) gahered by using CSP from lower and upper extremities were recorded. Clinical features were extracted from medical charts. Results The mean level of upper and lower extremity latencies were significantly higher in patients with SLE than in healthy control subjects (p<0.001). In addition, the mean duration of upper and lower extremity were significantly shorter in SLE patients than in controls (p<0.001). The mean upper latency is significantly higher in active SLE patients (SLEDAI score ≥6) when compared to inactive patients (85.4±14.9 vs. 78.6±8.4, p=0.023). The mean level of upper latency of active SLE patients tended to be higher (117.3±22 vs. 108.3±13.9, p=0.08). In SLE patients with nephritis, the mean level of lower extremity latency was significantly higher than in SLE patients without nephritis (119.4±20.2 vs. 107.6±14.3, p=0.028). Other EMG measures (NCS) were similar in patients with and without nephritis (all p values >0.05). When patients with anti-dsDNA positive were compared to the anti-dsDNA negative, it was observed that there was a tendency a lower duration of upper extremity in former group (31.2±8.2 vs. 35.2±7.5, p=0.08). Other measures were similar in patients with and without anti-dsDNA (all p values >0.05). The mean level of latency and duration were similar in SLE patients with and without hypocomplementemia, arthritis, photosensitivity, serositis, CNS involvement and other ENA antibodies. Age, treatment with antimalarials, steroids, immunsuppressives (azathioprine, cyclophosphamid), hemogram parameters had no effect on the NCS or CSP results. Also, LANNS score was not associated with any clinical parameters and NCS or CSP measure.In SLE patients, SLEDAI scores correlated with upper (r=0.36, p=0.009) and lower extremity latency (r=-0.38, p=0.008). The level of lower extremity latency also correlated with ESR (r=0.34, p=0.01) and disease duration (r=0.30, p=0.03). Conclusions We detected marked small nerve fiber damage in both lower and upper extremities in SLE patients using CSP. Howe...
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