Adverse effects of vitamin D deficiency on outcomes of patients with chronic hepatitis B

Grace Lai-Hung Wong1, Henry Lik-Yuen Chan1, Hoi-Yun Chan1

  • 1Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China; Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China; State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China.

Insights

Vitamin D deficiency is prevalent in chronic hepatitis B patients and linked to worse health outcomes. Addressing low vitamin D levels may improve long-term prognosis for individuals with CHB.

Area of Science:

  • Hepatology
  • Immunology
  • Endocrinology

Background:

  • Vitamin D acts as an immunomodulator, potentially influencing viral hepatitis pathogenesis.
  • Chronic hepatitis B (CHB) is a significant global health concern requiring investigation into contributing factors for adverse outcomes.

Purpose of the Study:

  • To examine the association between vitamin D deficiency and long-term clinical outcomes in patients diagnosed with chronic hepatitis B.
  • To determine if low serum vitamin D levels predict the occurrence of major adverse events in CHB patients.

Main Methods:

  • A prospective cohort study involving 426 patients with CHB, with serum 25-hydroxycholecalciferol (25(OH)D3) levels measured at baseline.
  • Long-term follow-up (159 ± 46 months) to record clinical events, including hepatocellular carcinoma, cirrhosis complications, and mortality.
  • Statistical analysis to identify independent predictors of adverse outcomes, adjusting for relevant clinical variables.

Main Results:

  • A high prevalence of vitamin D deficiency (82%) was observed at baseline (mean 25(OH)D3: 24.3 ± 9.4 ng/mL).
  • Patients experiencing clinical events had significantly lower baseline 25(OH)D3 levels compared to those without events (23.2 ± 10.4 vs. 28.2 ± 9.3 ng/mL, P < .001).
  • Vitamin D deficiency was an independent risk factor for adverse clinical events, with an adjusted hazard ratio of 1.90 (P = .04).

Conclusions:

  • Vitamin D deficiency is a common condition among patients with chronic hepatitis B.
  • Low serum vitamin D levels are significantly associated with adverse long-term clinical outcomes in CHB patients.
  • These findings suggest a potential role for vitamin D supplementation in managing CHB patients.
Abstract

Related Concept Videos

Vitamins01:30

Vitamins

Vitamins, derived from the Latin word for life, are essential organic substances required in small quantities for optimal growth and overall well-being. Unlike other organic nutrients, vitamins don't act as sources of energy or building materials but rather facilitate these nutrients' utilization by the body. Vitamins are predominantly coenzymes, assisting enzymes in specific chemical actions, like the oxidation of glucose for energy involving B vitamins. Most vitamins are not produced...
3.2K
Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test01:22

Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test

In clinical practice, the direct measurement of hepatic blood flow to evaluate liver function presents significant challenges due to the intricate and specialized nature of the necessary techniques. Consequently, healthcare professionals often rely on empirical estimates derived from thorough patient examinations and liver function tests to gauge liver health. Among the tools at their disposal, the Child–Pugh and MELD scoring systems stand out for their ability to categorize and assess...
266
Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow01:26

Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow

Chronic liver disease significantly impacts drug metabolism due to alterations in hepatic blood flow and enzyme accessibility. This disruption affects the body's pharmacokinetics—the movement and processing of drugs within the system. Key enzymes crucial for metabolizing medications become less accessible, changing how drugs are processed and utilized. Furthermore, liver disease influences the synthesis of plasma proteins, such as albumin and globulins, which play critical roles in drug...
365
Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...
1.1K
Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment01:08

Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment

Hepatic impairment, characterized by decreased liver function, does not uniformly mandate adjustments in drug dosage. Whether dosage modifications are necessary depends on various factors related to the drug's metabolism and elimination pathways. If a drug is primarily excreted via the kidneys and bypasses significant hepatic processing, if it undergoes minimal metabolic transformation in the liver, or if it is volatile and primarily expelled through the lungs, dose adjustments may not be...
367
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
47