The role of calcitonin gene-related peptide and substance P in the pathogenesis of dialysis headache.

AIM: The present study aims to establish the role of serum CGRP and SP levels in the disease pathophysiology in patients with dialysis headache not accompanied by primary or secondary headaches, and also whether there is a correlation between these vasoactive peptides and the severity of headache. METHOD: This study was designed as prospective and multicenter. A total of 30 dialysis headache patients and 30 patients without headache as the control group in the Nephrology outpatient clinics which implement similar dialysis procedures were included in the study. Blood samples were taken from all the patients before hemodialysis, and post-hemodialysis samples were collected. CGRP and SP contents in serum samples were measured using the ELISA method with detection kits. RESULTS: A total of 60 patients were included in the study with 17 female and 13 male patients in the dialysis headache group and 18 female and 12 male patients in the control group, and there were no significant differences in sex and age between the groups. CGRP levels in the headache group were found to be significantly higher compared with the control group both before and after hemodialysis. Furthermore, pre-hemodialysis CGRP levels were significantly higher than post-hemodialysis CGRP levels in both the headache and control groups. Serum SP levels in the headache group were found to be higher compared with the control group both before and after hemodialysis, there was no significant difference between the groups. Even though SP levels in both groups decreased after hemodialysis, there was again no significant difference between the groups. No correlation was found between the patients' severity of headache and serum CGRP and SP levels. CONCLUSION: This study concludes that CGRP and SP, even though the latter is not statistically significant, play a role in the pathophysiology of the dialysis headache, and further studies with a larger and more specific patient population may reveal the relationship between the neuropeptides and dialysis headache more clearly.

The relationship between inflammatory markers and spirometric parameters in ACOS, Asthma, and COPD.

Objective: The inflammatory mechanisms underpinning asthma-chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS) have not been fully elucidated. Here, we examined the levels of cysteinyl leukotrienes (cys-LTs), prostaglandin D2 (PG-D2), prostaglandin E2 (PG-E2), interleukin 5 (IL-5), and a disintegrin and metalloprotease domain (ADAM 33) in ACOS patients to determine the relationship between levels of these inflammatory markers and pulmonary functions.Methods: Blood samples were obtained from asthma, COPD, and ACOS patients who received combined therapy and were stable for the last month to measure cys-LTs, PG-D2, PG-E2, IL-5, and ADAM33 levels. Differences between groups and their correlations with pulmonary function tests were evaluated.Results: In total, 24 ACOS, 27 asthma, and 35 COPD patients were included. . PG-D2 levels were higher in ACOS (120.9 ± 117.2 ng/L) and asthma (119.6 ± 111.7 ng/L) patients than in COPD (82.6 ± 46.7 ng/L) patients (p = 0.036 and p = 0.038, respectively). In ACOS patients, PG-D2, cys-LTs, and ADAM33 levels were negatively correlated with FEV1/FVC% values (p = 0.021, p = 0.008, and p = 0.028, respectively). In COPD patients, a negative correlation was detected between PG-E2 and FEV1/FVC% (p = 0.007), whereas positive correlations were detected between IL-5 and pulmonary function tests, including FVC, FVC%, FEV1, FEV1%, FEF25-75, and FEF25-75% (p = 0.047, p = 0.005, p = 0.002, p = 0.002, p = 0.010, and p = 0.005, respectively). In asthma patients, cys-LTs levels were negatively correlated with FEV1 and FEF25-75 values (p = 0.045 and p = 0.037, respectively).Conclusions: PG-D2 levels may be a valuable biomarker to differentiate COPD in asthma and ACOS patients.

The role of midkine in the inflammatory process and its correlation with other inflammatory markers in renal transplant recipients.

BACKGROUND: Midkine (MK), which is expressed in the proximal tubular epithelial cells of the kidney, is thought to have a role in the pathophysiology of inflammation-related renal diseases. Both immunological and nonimmunological mechanisms may affect renal functions negatively during the early and late post-transplantation periods. We aimed in our study to evaluate the relationship of MK with clinical findings and inflammatory markers, including high sensitivity C-reactive protein (hs-CRP), interleukin (IL-6) and tumor necrosis factor (TNF-α) in the pretransplant and post-transplant period. METHODS: Forty-one consecutive patients transplanted from living related donors were included in this prospective observational study. All patients received the same immunosuppressive treatment protocol. MK, hsCRP, IL-6 and TNF-α levels were measured before and 2 months after renal transplantation. RESULTS: Pretransplant MK levels correlated positively with hsCRP (r = 0.41, p = 0.004) and IL-6 (r = 0.58, p<0.001). The mean post-transplant MK level was found to be higher than the pretransplant level (143 ± 350 pg/mL, 2792 ± 4235 pg/mL respectively, p = <0.001), while the mean hsCRP, IL-6 and TNF-α levels did not change significantly. Post-transplant IL-6 correlated significantly with MK (r = 0.388, p = 0.012), hsCRP (r = 0.41, p = 0.007) and TNF-α (r = 0.348, p = 0.026). There was no significant correlation between clinical findings and inflammatory markers. CONCLUSIONS: MK may be a good inflammatory marker in renal transplant recipients as in other inflammatory diseases. Moreover, it seems that it is not affected by factors other than inflammation during the post-transplantation period.

Serum adenosine deaminase and its isoenzyme activities in pregnancy.

OBJECTIVE: ADA is widely distributed in human tissues, which may contribute to the maturation of the immunological system, especially the proliferation and differentiation of lymphoid cells, and seems to be critical at different stages of the maturation process. The activity of ADA changes in diseases characterized by the alteration of cell-mediated immunity. In this study we examined changes in serum total ADA activity and the patterns of two ADA isoenzymes, ADA-1 and ADA-2, in healthy pregnant women, and evaluated the possible role of the alteration of cell-mediated immunity during pregnancy as causes of changes in ADA activity. MATERIALS AND METHODS: We measured serum activities of total ADA, ADA-1 and ADA-2 in healthy pregnant women (n=129) and age-matched healthy nonpregnant women (n=42). We divided the study group into three different subgroups: first trimester, second trimester and third trimester. RESULTS: Serum ADA, ADA-1 and ADA-2 activities in healthy pregnant women were significantly lower than in nonpregnant women (p<0.001, p<0.001 and p<0.01 respectively). ADA (p<0.001) and ADA-2 (p<0.001) activities in the first trimester were significantly lower than in the control group. However, there were no significant differences between the first trimester and control group according to their ADA-1 activities (p=0.016). ADA (p<0.001), ADA-1 (p<0.001) and ADA-2 (p<0.008) activities in the second trimester were significantly lower than in the control group. Combined trisomy 21 risk, biochemical trisomy 21 risk, age risk and trisomy 18 + Nuchal translucency (NT) risk were calculated using a first trimester screening test in 63 pregnant women. Furthermore, trisomy 21 risk, age risk and trisomy 18 risk were calculated by triple test in 52 pregnant women. ADA, ADA-1 and ADA-2 activities were not significantly correlated with risks in the first trimester screening test. ADA-1 activity was slightly significantly negative correlated with age risk (r= -0.314, p<0.05) and trisomy 18 risk (p<0.05) in the triple test. ADA (p<0.05) and ADA-2 (p<0.05) activities were slightly significantly correlated with gestational age, while there was no significant correlation between ADA-1 activity and gestational age. CONCLUSION: Serum ADA activity may be useful for clinical diagnosis and observation of high-risk pregnancies in which cell-mediated immunity has been altered.