scholarly journals SP400EFFECT OF CHOLECALCIFEROL SUPPLEMENTATION ON TLR7, TLR9, IL-6 AND IFN-Y EXPRESSION IN B AND T LYMPHOCYTES ON CHRONIC DIALYSIS PATIENTS

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii511-iii511
Author(s):  
Jose Tarcisio Giffoni de Carvalho ◽  
Marion Schneider ◽  
Lilian Cuppari ◽  
Caren Cristina Grabulosa ◽  
Silvia Regina Manfredi ◽  
...  
2017 ◽  
Vol 68 (2) ◽  
pp. 354-357 ◽  
Author(s):  
Andrei Niculae ◽  
Cristiana David ◽  
Razvan Florin Ion Dragomirescu ◽  
Ileana Peride ◽  
Flavia Liliana Turcu ◽  
...  

Once recombinant human erythropoietin (r-HuEPO) was introduced in daily practice, huge steps were made in combating the adverse effects induced by anemia in chronic kidney disease population. Still, r-HuEPO resistance and the doses ensuring the maximum therapeutic benefit remain matters of debate. The aim of our study was to assess the correlation between the presence and the degree of inflammation and the r-HuEPO requirements in chronic dialysis patients. We conducted a 2 years prospective study on 146 patients undergoing chronic dialysis treated with r-HuEPO. Based on their average CRP (C-reactive protein) levels, obtained from repeated samplings at 3 months interval, 3 groups were formed; we noted in each group the average values of r-HuEPO prescribed to achieve the optimum hemoglobin levels according to the dialysis best practice guidelines and all the adverse effects of the therapy. A direct correlation was observed between CRP levels and r-HuEPO requirements in the first 2 groups of patients (CRP under 6 mg/L and CRP values 6-20 mg/L), with significant increase in r-HuEPO doses between groups (p [ 0.001); the third group, CRP values over 20 mg/dL, showed a minor, insignificant increase in average r-HuEPO doses compared to mild inflammation group (p = 0.199) and more adverse effects of the therapy (p [ 0.05). Inflammation is an important determinant of anemia in chronic dialysis patients and can induce an increase in the doses of r-HuEPO. However, prescribing excessive r-HuEPO doses is not the answer in severe inflammatory status, due to lack of response and possible adverse effects.


2021 ◽  
Vol 6 (4) ◽  
pp. S237
Author(s):  
J. SANTACRUZ ◽  
C. Santacruz Tipanta ◽  
A. Vasquez Pérez ◽  
P. Reinoso ◽  
S. Carlotta ◽  
...  

2021 ◽  
Vol 33 (1) ◽  
Author(s):  
Emad M. El-Shebiny ◽  
Enas S. Zahran ◽  
Sabry A. Shoeib ◽  
Eman S. Habib

Abstract Background Autoimmunity is used to cause by impairment of adaptive immunity alone, whereas autoinflammatory was originally defined as a consequence of unregulated innate immunity. So, the pathogenetic mechanisms of autoimmune diseases were well-thought-out to be mediated by B and T lymphocytes. Whereas, autoinflammatory diseases were defined as unprovoked times of inflammation with the absence of a high titre of autoantibodies. Main body of the abstract Autoimmune and autoinflammatory diseases were split into two groups, but considering the similarities, it can be considered as only one group of diseases with a large immune pathological and clinical spectrum which involves at one end pure autoimmune diseases and the other pure autoinflammatory diseases. Conclusions We can safely conclude that there is bridging between autoinflammatory and autoimmune diseases.


2019 ◽  
Vol 209 ◽  
pp. 36-44 ◽  
Author(s):  
Atri Ghods ◽  
Abbas Ghaderi ◽  
Mahmoud Shariat ◽  
Abdol-Rasoul Talei ◽  
Fereshteh Mehdipour

1998 ◽  
Vol 32 (4) ◽  
pp. 629-634 ◽  
Author(s):  
CO Stehman-Breen ◽  
S Emerson ◽  
D Gretch ◽  
RJ Johnson

The Lancet ◽  
1979 ◽  
Vol 314 (8150) ◽  
pp. 1024-1025 ◽  
Author(s):  
A. Caralps ◽  
J. Lloveras ◽  
J. Andreu ◽  
A. Brulles ◽  
J. Masramon ◽  
...  

2011 ◽  
Vol 1217 (1) ◽  
pp. 18-31 ◽  
Author(s):  
Lynn M. Heltemes-Harris ◽  
Mark J. L. Willette ◽  
Kieng B. Vang ◽  
Michael A. Farrar

Hereditas ◽  
2004 ◽  
Vol 119 (2) ◽  
pp. 99-103 ◽  
Author(s):  
Benkt Högstedt ◽  
Anita Karlsson ◽  
Ingrid Bratt ◽  
Anders Holmén

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