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  • Author: Paweena Susantitaphong x
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Pakkapon Rattanachaisit, Paweena Susantitaphong, Kessarin Thanapirom, Roongruedee Chaiteerakij, Piyawat Komolmit, Pisit Tangkijvanich and Sombat Treeprasertsuk



Non-alcoholic fatty liver disease (NAFLD) is one of the major causes of chronic liver disease. The primary treatment of NAFLD by statins has not been clearly elucidated.


To evaluate the effectiveness of statin use in patients with biopsy-proven NAFLD or non-alcoholic steatohepatitis on the change in liver histology.


We searched MEDLINE, Scopus, Google Scholar, and the Cochrane Central Register of Controlled Trials for clinical trials and observational studies investigating the effects of statins on histological change regardless of type or dosage from inception to December 2015. Random-effect model meta-analyses were used to compute changes in outcomes of interest. The study protocol was registered in advance with the International Prospective Register of Systematic Reviews (PROSPERO 2016 CRD42016033132).


We identified 6 studies (111 patients), representing 5 cohort studies and 1 randomized controlled clinical trial. There was significant decrease in steatosis grading with a standardized mean difference of –2.580 (95% confidence interval [CI] –4.623 to –0.536; P = 0.013) and NAFLD activity score standardized mean difference of –1.488 (95% CI –2.506 to –0.471; P = 0.004). However, there was no significant change in fibrosis stage (0.156; 95% CI –0.553 to 0.865; P = 0.667).


Statin use can possibly reduce the extent of steatohepatitis but not the stage of fibrosis. Further randomized controlled studies to assess histological evidence with adequate sample size and duration are required in order to establish the role of statin as a primary treatment of NAFLD.

Open access

Paweena Susantitaphong, Khajohn Tiranathanagul, Pisut Katavetin, Kearkiat Praditpornsilpa, Marc E. De Broe, Patrick C. D’Haesec and Somchai Eiam-Ong


Background: T`he prevalence of aluminum (Al)-related toxicity in hemodialysis (HD) patients has declined. However, some HD patients continue to receive Al-based phosphate binders, in part because of the expense of Al-free binders.

Objective: To explore the effect of Al-based binders and their discontinuation on iron status, and markers of bone formation resorption in HD patients.

Methods: Following an initial screen of serum Al levels in 37 HD patients, a second screening was performed after discontinuation of Al-based binders in a 2-year follow-up. A desferrioxamine (DFO; 5 mg/kg) test, and assessment of iron status and bone markers were conducted in the second screening.

Results: Mean serum Al level was initially 27.8 ± 10.3 μg/L. Thirteen patients had a serum Al >30 μg/L, a level considered possibly toxic. There was a positive correlation between serum Al levels, HD duration, and cumulative dose of Al-based binder. At the second screening, the mean serum Al level decreased to 12.5 ± 7.4 μg/L. The mean serum Al level increased to 26.0 ± 14.7 μg/L post-DFO, but in none of the patients did the change in serum Al exceed the 50 μg/L threshold associated with Al-induced bone disease. The decrease in serum Al level was associated with a significant increase in intact parathyroid hormone (iPTH) whereas total alkaline phosphatase did not change.

Conclusions: We recommend that if Al-based phosphate binders are used in HD patients, serum Al level, iron, and markers of bone formation resorption be closely monitored to ensure safe use of these drugs.