AIMTo identify the predictors of vitamin D deficiency in patients with and without inflammatory bowel disease (IBD).METHODSPatients with ulcerative colitis (UC) or Crohn’s disease (CD) related diagnostic codes who received medical care at University of Mississippi Medical Center between July 2012 and 2015 were identified. After thorough chart review, we identified patients with biopsy proven IBD who had also been tested for serum 25-hydroxyvitamin D [25(OH)D] concentration. We compared these patients to a previously studied cohort of healthy controls who also had vitamin D concentration checked. Logistic regression analysis was performed to determine the association between vitamin d deficiency and UC, CD, race, age, gender and body mass index (BMI).RESULTSWe identified 237 patients with confirmed IBD. Of these, only 211 had a serum 25(OH)D concentrations available in the medical record. The group of healthy controls consisted of 98 individuals with available serum 25(OH)D concentration. 43% of IBD patients were African American (AA). Patients with CD were more likely to have vitamin D concentration checked. Bivariate analysis showed that AA (51% vs 21%, P = 0.00001), subjects with BMI >30 kg/m2 (39% vs 23% P = 0.01) and CD (40% vs 26%, P = 0.04) were more likely to be vitamin D deficient than vitamin D sufficient. Those with Age > 65 were more likely to be vitamin D sufficient (46% vs 15%, P = 0.04). Multiple regression showed that only BMI > 30 kg/m2 and AA race are associated with vitamin D deficiency.CONCLUSIONBMI > 30 kg/m2 and AA race are predictive of vitamin D deficiency. Gender, age and diagnosis of IBD are not predictive of vitamin D deficiency.

Renal tubular acidosis (RTA) is a disorder with variable presentations and oftentimes a nebulous underlying primary diagnosis. We describe a rare cause of RTA as an unusual complication of proton pump inhibitor (PPI) therapy. We report a case of a 33-year-old male with history of hypertension, acid reflux, allergic rhinitis, and low testosterone admitted with complaints of fatigue, weight loss, and unexplained acidosis for ~ 2 months. His medications prior to admission included losartan, omeprazole, potassium chloride, sildenafil, and testosterone propionate injections. His physical exam was unremarkable with a blood pressure of 120/80 mmHg. Initial lab work showed a nonanion gap metabolic acidosis with serum bicarbonate level of 16 mM/L and potassium 3 mM/L. Urine studies showed urine pH of 6.5 and a positive urine anion gap. The serum creatinine was within normal range(1.13 mg/dL). He required massive doses of bicarbonate and potassium supplementation with minimal improvement of serum chemistries achieved. The cause of apparent distal RTA remained elusive despite extensive blood, urine, and imaging testing. Ultimately a renal biopsy was obtained showing mild to moderate tubule-interstitial inflammation with 5% fibrosis. PPI therapy (omeprazole) was stopped, and he was started on prednisone 60 mg per day. Two weeks later, his RTA findings resolved, and he no longer required bicarbonate and potassium supplementation. Our case highlights the importance of recognizing a unique complication of RTA following PPI therapy. It also underscores the possible need for considering a kidney biopsy in the setting of nondiagnostic laboratory work up to uncover the underlying etiology of RTA and suspected allergic interstitial nephritis (AIN).

check and action the test results, following dose reductions, following guidance. Chemotherapy is prescribed prior receiving the genetic report in 10 CPT. 6 hospitals would delay administration when result is missing. Conclusion and RelevanceThere is a rich multidisciplinary involvement in checking the results of the test, including making the correct dose adjustments. The use of DPYD tests to prevent chemotherapy toxicity follows a safe and robust pathway within our region. REFERENCES AND/OR ACKNOWLEDGEMENTS[i] UK Chemotherapy Board, 'Personalised Medicine Approach For Fluoropyrimidinebased Therapies,' 2020. [Online]. Available: https://www.theacp.org.uk/userfiles/file/ resources/dpd-testing-ukcb-july-2020-updated.pdf [ii] EMA recommendations on DPD testing prior to treatment with fluorouracil, capecitabine, tegafur and flucytosine | European Medicines Agency (europa.eu) [iii] 5-fluorouracil (intravenous), capecitabine, tegafur: DPD testing recommended before initiation to identify patients at increased risk of severe and fatal toxicity -GOV.UK (www.gov.uk) [iv] Nijjar R, Shaunak N, Mahmoud S, Thwaites B, Desai M, Ajediti C, Brown A, Yeoh I, Patel T, Masento S. 'A collaborative audit on DPYD testing of all patients initiated on fluoropyrimidines (5-fluorouracil, capecitabine and oral prodrug tegafur) across 5 London teaching hospitals

BackgroundGenetic-polymorphisms in thiopurine-methyltransferase (TPMT) and Nudix-hydrolase15 (NUDT15) have been related to higher risk of toxicity associated with administration of 6-mercaptopurine(6-MP).PurposeTo describe the implementation of polymorphisms determination in TPMT and NUDT15 in paediatric patients by a simple and economic method.Material and methodsA multi-centre, prospective, observational study with a expected duration of 32 months was carried out. Participants were patients younger than 18 years who received treatment with 6-MP. Single nucleotide polymorphisms (SNPs) analysed were: TPMT (rs1800462;rs1800462; rs1800460;rs1142345 and rs1800584) and NUDT15 (rs116855232;rs147390019;rs554405994 and rs186364861).DNAg extraction was carried out using the Ramos et al. method and genotyping was done using PCR and subsequent DNA sequencing. The study was approved by the hospital’s Ethical Committee (CEIC).Legal guardians were requested to sign an informed consent form prior to inclusion.ResultsDuring the first 8 months, nine patients were included, with an average age of 3.5 (1–18)and 62.5% of them were females. Six of the included patients (66.6%) were diagnosed with acute lymphoblastic leukaemia, two with non-Hodgkin’s lymphoma (22.2%) and one with acute myeloid leukaemia.Eighty-one genetic-determinations were carried out. None of the patients presented a high-risk genotype for the TPMT gene. One of the children showed a medium-risk genotype *1/*3B,*1/*3C, but after 3 months of treatment with 6-MP he has not shown toxicity. This patient also showed a wild-type genotype for the NUDT15 gene which could explain the absence of toxicity during the treatment. Another patient has shown a heterozygous genotype for the rs116855232 and rs554405994 (NUDT15 gene). This patient has not already received treatment with 6-MP so we cannot evaluate the mutation influence yet.ConclusionAlthought we have not found patients with high-risk polymorphisms in TPMT yet, we support the implementation of this screening because the presence of this genotypes is related to severe toxicity and even death-risk in these patients.We also have completed the procedure with the determination of mutations in the NUDT15 gene, increasing the probability of identifying patients with low tolerance to 6-MP.To our knowledge, the present study is the first to evaluate the effect of polymorphisms in both TPMT and NUDT15 in the treatment with 6-MP, so definitive results could cidentify how those polymorphisms affect the toxicity related to 6-MP.References and/or Acknowledgements1. Ramos-Díaz. 2015May;75(5):1095–8.2. Kotur, et al. 2015;16(15):1701–12.No conflict of interest