Vitamin D in RA

Published: 18 May 2026| Version 1 | DOI: 10.17632/hy5nxwpxhn.1
Contributors:
Thikra Hasan Mathkor,

Description

Research Hypothesis In patients with Rheumatoid Arthritis (RA), systemic autoimmune inflammation and reduced mobility disrupt the bone-mineral axis. We hypothesized that severe vitamin D depletion significantly stimulates parathyroid hormone (PTH) secretion, causing secondary hyperparathyroidism and secondary fluctuations in serum calcium, phosphorus, and albumin levels across different age and sex groups. What the Data Shows & Notable Findings The dataset tracks 653 retrospective RA cases from Al-Zahraa Hospital, Iraq (January 2023–August 2025). Key findings include: • Female Predominance: Vitamin D deficiency disproportionately affects women, who constitute 81.69% of the severely deficient group. The female-to-male prevalence ratio peaks at 5.2 in the 31–60 age group. • Strong Inverse Axis: A significant negative correlation (r = -0.630, p < 0.001) exists between Vitamin D and PTH. As Vitamin D status improves from severe deficiency to sufficiency, mean PTH drops from 62.80 to 43.18 pg/dL in females and 51.91 to 34.40 pg/dL in males. • Mineral Depletion: Serum phosphorus and calcium levels significantly decline alongside worsening vitamin D status. Data Gathering & Methodology Demographic and laboratory metrics were extracted from medical files. Patients with diabetes, renal failure, or those taking vitamin D supplements were excluded to prevent confounding results. Vitamin D and PTH were measured via electrochemiluminescence on a Roche Cobas analyzer, while minerals and albumin were measured via colorimetric assays on an Abbott Architect clinical system. Interpretation & Reuse The data demonstrates classical secondary hyperparathyroidism, where the body elevates PTH to preserve serum calcium when intestinal absorption fails due to low Vitamin D. Researchers can reuse this rigorous, supplement-excluded data for global meta-analyses, epidemiological bone-loss mapping, or targeted therapeutic optimization models for high-risk autoimmune cohorts.

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Biochemistry, Rheumatology

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