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ASPEK IMUNOLOGI SLE -, Yuriawantini; Suryana, Ketut
journal of internal medicine Vol. 8, No. 3 September 2007
Publisher : journal of internal medicine

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (468.325 KB)

Abstract

Systemic Lupus Erythematosus (SLE) is autoimmune disease characterised by the production ofautoantibodies to component of the cell nucleus in association with a diverse array of clinical manifestations.The patho-aetiology of systemic Lupus Erythematosus probably involves multifactorial interaction amongvarious genetic and environmental factors. Multiple genes contribute to disease susceptibility, including genesencoding complement and other components of the immune response. The interaction of sex, hormonal millieuand the hypothalamus-pituitary-adrenal axis modifies this susceptibility and the clinical expression of thedisease. Defective immune regulatory mechanism, such as the clearance of apoptotic cells and immunecomplexes, are important contributors to the development of SLE. The loss of immune tolerance, increaseantigenic load, excess T cells helper, defective B cell suppression, and the shifting of T helper 1 (Th1) to Th2immune responses leads to the B cell hyperactivity and the production of pathogenic autoantibodies. ANAs areantibodies against both functional and structural in the cell nucleus. ANA is early detection of autoantibodies forthe patient with clinical features that suggest SLE. Positive test for antinuclear antibodies may support thediagnosis, especially if more spesific autoantibodies are present, such as anti-double-stranded DNA, anti-Sm,anti-RNP or anti-Ro. Understanding the value of autoantibody testing in patient care requires clinical judgmentand experience.
PENGARUH SPIRONOLAKTON SEBAGAI TERAPI TAMBAHAN ACE INHIBITOR DAN/ATAU ANGIOTENSIN RECEPTOR BLOCKERS TERHADAP ALBUMINURIA PADA PENYAKIT GINJAL KRONIK PRADIALITIK STUDI KLINIS ACAK TERKONTROL BUTA GANDA -, Yuriawantini; Suwitra, Ketu; Raka Widiana, I Gde; Sidharta Loekman, Jodi; Sudhan, Wayan; Kandarini, Yenny
journal of internal medicine Vol. 9, No. 3 September 2008
Publisher : journal of internal medicine

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Recently studies suggest that aldosterone contributes to progressive kidney disease. This has raised the possibility ofusing aldosterone antagonist in CKD. To evaluate effects of spironolactone 25 mg/day on albuminuria in CKD patients, thirtyCKD patients were enrolled in randomized double blind placebo controlled study. Permutted block randomization was done toreceive spironolactone 25 mg/day or placebo as control in addition to ACE inhibitors and/or ARBs. Albuminuria and bloodpressure were examined at baseline and 12 weeks. Albuminuria was measured as urinary albumin:creatinine ration and comparedas primary out come. During this study 15 patient were received conventional therapy and spironolactone 25 mg/day and 15patient were received placebo. One of patient dropped-out after 4 weeks due to hiperkalemia in spironolactone group and one ofpatient in the control group lost to follow-up. After 12 weeks of therapy, in spironolactone group albuminuria was decreased from510 (180.0 ? 798.0) to 254.0 (40.3 ? 491.8) mg/g, MD, 187.0 (29.0 ? 332.3) mg/g, p= 0.035 and in control group from 804.0 (52.0? 1126.0) to 637.0 (99.0 ? 1098.8) mg/g MD -10.5 (-186.5-86.0) mg/g, p= 0.490. There was significant difference of decreamentof albuminuria in both groups (Z=-0.69, p=0.046). There were no statistically different of serum potassium levels and bloodpressure in both groups after treatment. Baseline aldosterone levels were not significantly correlated with albuminuria (r = -0.128,p = 0.499). As Conclusion in this study is spironolactone reduces albuminuria in pradialytic CKD patients
Co-Authors I Gde Raka Widiana Jodi Sidharta Loekman Ketu Suwitra Ketut Suryana Wayan Sudhan Yenny Kandarini