Dept. Paediatrics, Leicester Royal Infirmary, Leicester Are we adequately managing Vitamin D deficiency in HIV positive children? (Retrospective audit) P. Sharma, S. Bandi Dept. Paediatrics, Leicester Royal Infirmary, Leicester INTRODUCTION Vitamin D (25-OHD) deficiency is high amongst children with peri-natally acquired HIV infection1, which may be a consequence of antiretroviral therapy2. Advancement in HIV treatment has resulted in increased life expectancy, and this requires more focus on long-term bone health. Early diagnosis and treatment of Vitamin D deficiency aids prevention of diseases such as rickets and osteomalacia3. We aim to audit the management of Vitamin D deficiency in HIV positive children at Leicester Royal Infirmary (LRI). Fig 1: Number of patients with 25-OHD levels monitored in the last 12 months METHOD HIV positive children attending the LRI Infirmary Family Clinic were included. Clinic letters and electronic blood result software were used to collect details of serum 25-OHD (Vitamin D) concentration and prescribed treatment. Other risk factors including BMI, ethnicity, bone profile and antiretroviral treatment were noted. Results were compared to trust guidelines4. RESULTS 93% had 25-OHD concentration monitored within the last 12 months Of these, 53% had 25-OHD concentration <50mmol/L 75% of 25-OHD deficient patients were treated 30% had post-therapeutic levels monitored None had winter maintenance doses prescribed 1 patient with 25-OHD insufficiency was also hypocalcaemic (Ca2+ <2.1mmol/L) All patients not on antiretroviral therapy had 25-OHD concentration <50mmol/L No patients were hypophosphataemic Fig 2: Treatment outcome of 25-OHD deficient patients Table 1: Cohort demographics Measure (n=30) Mean age 12.8 years Afro-Caribbean ethnicity 83% Female 40% BMI >25 10% No antiretroviral therapy 16% DISCUSSION AND CONCLUSION The biggest obstacle to data collection proved to be inconsistent documentation of outpatient blood tests and prescription of treatment. It was assumed that 25-OHD deficiency had not been treated if it was not explicitly documented in clinic letters. Given the ethnicity of patients, 25-OHD deficiency is fairly common and at times severe. Rates of identification and treatment were high, with cholecalciferol (Vitamin D3) as the main choice of treatment. Following up post-treatment and providing a winter maintenance dose were areas where the department fell short. RECOMMENDATIONS Introduction of prophylactic winter dose of Vitamin D regardless of antiretroviral therapy. Monitor 25-OHD level as part of Family Clinic annual review Formal documentation of levels and treatment Table 2: Vitamin D status of audit cohort Vitamin D status % (n=30) Deficient (<25mmol/L) 30% Insufficient (25-50mmol/L) 23% Sufficient (>50mmol/L) 37% No levels monitored in last 12 months 6% Meyzer C et al. Vitamin d deficiency and insufficiency in HIV-infected children and young adults. Paediatr Infect Dis J 2013;32(11):12404-4 Fox J et al. Improvement In Vitamin D Deficiency Following Antiretroviral Regime Change: Results from the MONET trial. AIDS Research and Human Retroviruses 2011;27(1):29-34 Pearce S, Cheetham T. Diagnosis and management of vitamin D deficiency. BMJ 2010;340:b5664 ICHT Family Clinic 2011. Guideline for the management of vitamin d deficiency in HIV positive treatment: screening, treatment and prevention