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Status unknownNCT01623024Updated Jun 21, 2012

Effect on Liver Histology of Vitamin D in Patients With Non-alcoholic Steatohepatitis

A Phase 3 interventional study of Vitamin D and Lifestyle counseling in Non.Alcoholic Fatty Liver Disease, sponsored by University of Palermo. Status unknown at 1 site in Italy. Open to participants aged 18 Years and older. Per ClinicalTrials.gov, last updated 2012-06-21.

Sponsored by University of Palermo · Phase 3, Interventional, and Treatment

The sponsor has not verified this record recently (last verified Jun 2012), so the status shown — last known as Not yet recruiting — may be out of date.
Phase
Phase 3
Study type
Interventional
Enrollment
200
Allocation
Randomized
Ages
18 Years and older
Sex
All
01

Study summary

Non-alcoholic fatty liver disease (NAFLD) represents a spectrum of disorders characterized by predominantly macrovesicular hepatic steatosis occurring in individuals in the absence of significant alcohol consumption. In this context it is possible to distinguish a condition of simple fatty liver, where the only histologic finding is the presence of steatosis, from a state of non-alcoholic steatohepatitis (NASH), characterized by hepatocellular injury/inflammation with or without fibrosis. The prevalence of NAFLD is around 20-30% in the general population. With a rapid increase in the risk factors for metabolic syndrome, NAFLD has become the most common cause of liver disease in Western countries. The clinical relevance of NAFLD arises from the fact that a considerable proportion of subjects (20-30%) develop NASH, and this condition can progress to cirrhosis in up to 15% of patients. In addition NAFLD, and particularly NASH, represents a cardiovascular risk factor, independent of other well-known conditions contributing to heart and vascular diseases.

Lifestyle modification is the effective medical treatment recommended for NASH, while there is currently no pharmacologic therapy of proven benefit in these patients. Several pilot studies, using insulin sensitizers (thiazolidinediones or metformin), and antioxidants, like vitamin E, have provided inconclusive evidence that these drugs may improve clinical and histological features of NASH.

In the complex and not completely understood pathogenic puzzle of NAFLD and NASH, also vitamin D might have an important role. Vitamin D deficiency is associated with many common pathological conditions frequently observed in NAFLD, like cardiovascular disease, and insulin resistance. A recent paper by Targher and colleagues showed low vitamin D serum levels in NAFLD patients, identifying an inverse relation between vitamin D levels and the severity of liver disease. In keeping with the above data, recent experimental evidence also suggested the potential ability of vitamin D, through interaction with its nuclear receptor (vitamin D receptor - VDR), to interfere with inflammatory response, T cell function and fibrogenesis. Therefore considering the link between vitamin D serum levels, severity of NAFLD, and risk factors for NAFLD, we speculate that vitamin D might represent a new therapeutic target in the management of NASH patients.

02

Conditions studied

03

In context

Liver Diseases

2,081 studies on the registry are indexed under Liver Diseases; 390 are open to participants now.

This study's planned enrollment of 200 is above the median of 50 across 1,323 interventional studies indexed under Liver Diseases.

Browse Liver Diseases studies →

Lead sponsor

University of Palermo is the lead sponsor of 142 studies on the registry; 28 are open to participants now.

Counted across the registry records on this site, refreshed daily.

04

Who can participate

Ages eligible
18 Years and older
Sexes eligible
All
Accepts healthy volunteers
No

Inclusion criteria

  1. Patients older 18 years
  2. Histological diagnosis of possible or definite NASH, according to Kleiner score, within 6 months before randomization.

Exclusion criteria

Exclusion Criteria:

  1. Average alcohol consumption exceeding 20 g per day in women and 30 g per day in men for at least 3 consecutive months during the previous 5 years, as evaluated by self-administrated questionnaires, 7-day recall tests rand confirmed by a family member.
  2. Other causes of chronic liver disease: Wilson's disease (normal serum ceruloplasmin); alpha-1-antitrypsin deficiency (normal serum alpha-1-antitrypsin); viral hepatitis (anti-HCV and HBsAg negativity); primary biliary cirrhosis (ANA\<1:160 and AMA negativity); autoimmune hepatitis (ANA, SMA and LKM \<1:160 and absence of histological features of autoimmune hepatitis); HIV infection (anti-HIV negativity); hypo or hyperthyroidism (normal TSH).
  3. History of or planned gastrointestinal bypass or any additional bariatric surgery/intervention.
  4. Hepatic cirrhosis with a Child-Pugh score of B or C, and/or concomitant hepatocellular carcinoma
  5. Recent significant weight loss (>5% TBW within previous 6 months)
  6. Recent (within 6 months of baseline liver biopsy and screening visit) or concomitant use of agents known to cause hepatic steatosis (corticosteroids, amiodarone, methotrexate, tamoxifen, tetracycline, high dose estrogens (with the exclusion of standard HRT and oral contraceptive treatment), valproic acid)
  7. Recent (within 6 months of baseline liver biopsy and screening visit) change in dose/regimen or first treatment with vitamin E, Vitamin C, betaine, s-adenosyl methionine, ursodeoxycholate, sylimarin, fibrate, statin, pentoxyfilline, angiotensin II inhibitors, orlistat, sibutramine. Oral hypoglycaemic agents and insulin will be allowed, provided they had been initiated at least 6 months before enrollment and are maintained at stable doses.
  8. Ongoing or recent therapy (within 6 months of baseline liver biopsy and screening visit) with vitamin D or with medications known to affect vitamin D3 metabolism, including vitamin/mineral supplements.
  9. Any additional condition that might interfere with optimal participation in the study, according to Investigators opinion.
  10. Be pregnant or breastfeeding.
05

Study design

Phase
Phase 3
Primary purpose
Treatment
Allocation
Randomized
Intervention model
Parallel assignment
Masking
None (open label)
Enrollment
200 participants (estimated)

Study arms

  • Experimental
    Vitamin D and Lifestyle counseling

    Drug: Vitamin D

  • Active comparator
    Lifestyle counseling

    Behavioral: Lifestyle counseling

Interventions

  • DrugVitamin D

    20.000 UI/week for 96 weeks

  • BehavioralLifestyle counseling

    Lifestyle counseling for 96 weeks

06

What researchers measure

Primary outcomes

  1. (a) improvement in NAS by at least 2 points spread across at least 2 of the NAS components or post-treatment NAS of 3 points or less, (b) at least 1 point improvement in the score for ballooning degeneration and (c) no worsening of the fibrosis score.

    Time frame: 96 weeks

Secondary outcomes

  1. Changes in individual components of NAS score

    Time frame: 96 WEEKS

  2. Changes in intima-media thickness

    Time frame: 96 WEEKS

  3. Changes in liver fibrosis

    Time frame: 96 weeks

  4. Changes in insulin resistance

    Time frame: 96 weeks

07

Study locations

1 site
  • Sezione di Gastroenterologia, Di.Bi.M.I.S. AOUP Paolo Giaccone, University of Palermo, Italy
    Palermo, 90127, Italy
    • Antonio Craxì, Professor · Contact · antonio.craxi@unipa.it · 00390916552280
    • Antonio Craxì, Professor · Principal investigator
08

References and documents

Publications

  • Targher G, Bertolini L, Scala L, Cigolini M, Zenari L, Falezza G, Arcaro G. Associations between serum 25-hydroxyvitamin D3 concentrations and liver histology in patients with non-alcoholic fatty liver disease. Nutr Metab Cardiovasc Dis. 2007 Sep;17(7):517-24. doi: 10.1016/j.numecd.2006.04.002. Epub 2006 Aug 22. PubMed 16928437 ↗
  • Petta S, Camma C, Scazzone C, Tripodo C, Di Marco V, Bono A, Cabibi D, Licata G, Porcasi R, Marchesini G, Craxi A. Low vitamin D serum level is related to severe fibrosis and low responsiveness to interferon-based therapy in genotype 1 chronic hepatitis C. Hepatology. 2010 Apr;51(4):1158-67. doi: 10.1002/hep.23489. PubMed 20162613 ↗
  • von Essen MR, Kongsbak M, Schjerling P, Olgaard K, Odum N, Geisler C. Vitamin D controls T cell antigen receptor signaling and activation of human T cells. Nat Immunol. 2010 Apr;11(4):344-9. doi: 10.1038/ni.1851. Epub 2010 Mar 7. PubMed 20208539 ↗
  • Abramovitch S, Dahan-Bachar L, Sharvit E, Weisman Y, Ben Tov A, Brazowski E, Reif S. Vitamin D inhibits proliferation and profibrotic marker expression in hepatic stellate cells and decreases thioacetamide-induced liver fibrosis in rats. Gut. 2011 Dec;60(12):1728-37. doi: 10.1136/gut.2010.234666. Epub 2011 Aug 4. PubMed 21816960 ↗
09

Updates

Tracking since Sep 25, 2026
No changes since tracking began. The registry record was last updated on Jun 21, 2012, before this site started recording changes on Sep 25, 2026. Its history is on ClinicalTrials.gov ↗
10

Registry details

Key details

Study ID
NCT01623024
Lead sponsor
University of Palermo
Responsible party
Antonio Craxi (Full Professor of Gastroenterology, University of Palermo) — Principal investigator
First posted
Jun 19, 2012
Start date
Sep 2012
Primary completion
Sep 2014 (estimated)
Last update
Jun 21, 2012

Study contacts

Antonio Craxì, MD
Contact
antonio.craxi@unipa.it
00390916552280
Antonio Craxì, Professor
principal investigator · Sezione di Gastroenterologia, Di.Bi.M.I.S. University of PALERMO, ITALY

Oversight

Data monitoring committee
No
View the source record on ClinicalTrials.gov ↗

Not currently enrolling

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