sharp_razor a scris:
La ce fel de vitamina "D" se refera (D, D2, D3) si in ce cantitate (U.I.)? Multumesc!
Din ce am inteles eu se refera la D3 - sunt mai multe studii care coreleaza probleme la ficat cu deficienta de vitamina D3.
Referitor la UI, nu se specifica, deoarece studiul a fost facut pe soareci :) ... dar o testare a vitaminei D poti sa faci si in functie de rezultat medicul va putea stabilii doza de d3 necesara.
tot la AASLD este un articol care contrazice articolul precedent si spune ca nu este o corelatie intre problemele la ficat si vit d3 " Vitamin D Deficiency In Cirrhosis Relates To Severity And Not Etiology Of Liver Disease"
mai jos dau copy/paste pe ambele articole (oricum daca cauti pe linkul indicat dupa Vitamin D (in cimpul Abstract/Presentation Body Search) vei gasii o gramda de prezentari - dar in acest moment nu exista nici o recomandare ferma, oricum e preferabil sa ne tinem nivelul e vitamina D3 in liminte normale)
1
Vitamin D has a protective antifibrotic effect in rat model of liver fibrosis
S. Reif1, 2; A. Bentov1, 2; E. Sharvit1, 2; E. Brazowski3; Y. Weisman1; S. Abramovitch1, 2
1. Department of Pediatrics, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel.
2. Pediatric Gastroenterology, Tel-Aviv Sourasky Medical Center, Tel Aviv, Israel.
3. Pathology, Tel-Aviv Sourasky Medical Center, Tel Aviv, Israel.
Background and Aim: In our previous In vitro study, we showed that HSCs proliferation induced by PDGF was suppressed by vitamin D. In addition, collagen Iα1 promoter activity, mRNA and protein expression levels were all down-regulated after treatment with vitamin D. Furthermore, exposure to vitamin D led to up-regulation of MMP-9 activity and suppression of TIMP1 mRNA levels. Therefore, in the present study, we investigate the potential of vitamin D treatment to prevent development of liver fibrosis in in vivo model.
Methods: Rats were divided into four groups: no treatment (control), TAA treatment, vitamin D treatment and TAA with vitamin D treatment. Liver fibrosis was induced in rats by administration of thioacetamid (TAA) (200mg/Kg, i.p., twice weekly) for 10 weeks. Treatment with vitamin D (5μg/Kg i.p., twice weekly) was simultaneously given with TAA. Hepatic fibrosis scores were determinate after staining with hematoxylin & eosin and sirius-red. Collagen I deposition was determent following sirius-red staining. αSMA expression was detected by western blotting
Results: Macroscopically, TAA treated group developed cirrhosis. However, rats received TAA with vitamin D treatment, showed almost normal morphology. Microscopically, the hepatic fibrosis score of the TAA treatment group was 3.9 + 0.1, while rats treated with TAA and vitamin D demonstrated only mild fibrosis and scored of 2.3 + 0.3 (P<0.05). No fibrosis was observed in the control rats or the group received vitamin D alone. Quantification of collagen content, following sirius-red staining demonstrated increased collagen deposition in rats treated with TAA by 16-fold compared to the untreated group. However, administration of TAA with vitamin D significantly decreased collagen levels by 4-fold compared to the TAA group. TAA treatment increased αSMA expression to ~160%, while addition of vitamin D suppressed αSMA expression to the control level. Neither hypercalcemia nor renal toxicity was found in rats receiving vitamin D treatment.
Conclusions: These results suggest that treatment of vitamin D can inhibit the development of cirrhosis in a rat model. Hence, vitamin D may play an important role in preventive treatment for liver fibrosis, and may have a potential therapy.
2
Vitamin D Deficiency In Cirrhosis Relates To Severity And Not Etiology Of Liver Disease
J. D. Nusbaum1; H. C. Wright1; J. Smirniotopoulos1; C. Dash2; R. Satoskar1; J. Laurin1; T. Fishbein1; K. Shetty1
1. Transplant Institute, Georgetown University Hospital, Washington, DC, DC, United States.
2. Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, United States.
Background and Aims:The association of vitamin D deficiency(VDD)with non-cholestatic liver disease is not well-defined. Vitamin D (VD) is an important mediator not only of bone health in liver disease, but also of cell differentiation, proliferation and immunomodulation. We therefore examined the prevalence and risk factors for VDD in patients with cirrhosis of various etiologies. Methods : Consecutive patients with cirrhosis being evaluated at our liver transplant center had their 25-OH vitamin D measured. Severity of VDD was categorized as mild (20-32 ng/ml), moderate(7-19ng/ml) or severe( <7 ng/ml), normal being > 32 ng/ml. Univariate and multivariate logistic regression models were used to investigate the association of severe VDD with hepatocellular cancer (HCC) status, and Model for End Stage Liver Disease( MELD) scores. Results: The study group comprised 160 patients with cirrhosis diagnosed by clinical, radiological, laboratory and/or histological features. Of these, 149 (92%) had some degree of VDD with 34%, 38%, and 20% in the mild, moderate and severe VDD groups respectively. Table 1 summarizes characteristics of the study group according to vitamin D level. MELD score was significantly associated with VD level (p=0.0007). For each unit increase in MELD score, log (VD) decreased by 0.04. In pts with MELD >19 vs <9,odds ratio of severe VDD was 6.03 (1.70-21.3). HCC patients were less likely to have VDD than non-cancer patients, but this effect was attributable to lower MELD score in HCC patients. Underlying etiology of cirrhosis was not associated with VDD. Conclusions:1.VDD is highly prevalent in patients with cirrhosis of various etiologies.2.VDD is associated with severity of liver disease – patients with advanced cirrhosis (MELD > 19) were 6 times as likely to have low VD levels as compared to those with less advanced cirrhosis).3.Given the multiple anti-inflammatory and anti-proliferative effects of VD, this study accentuates the need to screen for VDD in all patients with cirrhosis,and provide adequate supplementation.
Table 1 VD >20 ng/ml
(n=61)VD 7-19 ng/ml
(n=72)VD < 7 ng/ml
(n=27)P valueAge, mean (SD)56.3(11.1)55.8(8.1)55.6(9.5)0.9Male, %(n)62(38)64(46)60(16)0.9Race,%(n)
Caucasian62(37)54(39)36(10)0.01BMI,mean(SD)28.9(5.9)28.7(6.5)29(8.5)0.9HCC,%(n)36(22)33(24)7(2)0.01MELD,mean (SD)11.9(5.7)13(4.2)17.2(5.6)<0.0001Etiology
HCV44(27)52(37)43(12)0.8Alcohol11.5(7)18(13)14(4) HBV8(5)6(4)7(2) NAFLD11.5(7)10(7)11(3) Other25(15)14(10)25(7)
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