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Pyridoxine Deficiency After Solid Organ Transplant

S. Van Arsdale,1 S. Yost,2 M. Meer,1 S. Schoentag,1 P. Kadambi,3 S. Habib.3

1Department of Nutrition Services, University of Arizona Medical Center, Tucson, AZ
2Department of Pharmacy, University of Arizona Medical Center, Tucson, AZ
3Department of Medicine, University of Arizona College of Medicine, Tucson, AZ.

Meeting: 2015 American Transplant Congress

Abstract number: D39

Keywords: Cadaveric organs, Immunosuppression, Outcome, Post-operative complications

Session Information

Session Name: Poster Session D: Diabetes/Metabolic/Bone/Malignancy/Pregnancy

Session Type: Poster Session

Date: Tuesday, May 5, 2015

Session Time: 5:30pm-6:30pm

 Presentation Time: 5:30pm-6:30pm

Location: Exhibit Hall E

Background

Micronutrient deficiencies have been discussed in the literature regarding post-transplant recipients. A proposed theory is that immunosuppressive medications or altered immune system cause pyridoxine deficiency post-transplant. The purpose of this study is to identify solid organ transplant recipients with pyridoxine deficiency to assess the clinical significance, improve the patients overall long-term outcomes, and improve standard of care

Methods

This is a retrospective study with data collected from 48 solid organ transplant recipients, who were admitted to UAMC who had a pyridoxine level checked post transplantation and nutritional evaluation.

Results

48 recipients were identified to have pyridoxine level checked after transplant and have a formal dietary consultation. Of the 48 patients, 30 (63%) of the study cohort were diagnosed with pyridoxine deficiency. General characteristics of the cohort: mean age of 46 (SD +/-16) years, male 63%, white race 50%, kidney recipients 33%, heart 31%, kidney with other organ 21%, liver 11%, lung and pancreas 2% each. Mean time interval between transplant and level checked was 910 days (SD +/-456). Mean weight at the time of consultation was 80 kg (SD+/-20.7). Groups with normal and low pyridoxine were compared for all study variables as described above. All liver (5/5), lung (1/1) and pancreas (1/1) transplant recipients were found to be deficient. 9/10 (90%) kidney with other organ, 8/16 (50%) kidney alone, and 6/15 (40%) of heart recipients were deficient in pyridoxine (p=0.03). More subjects in the deficient group were on fluconazole (90% vs. 67%: p=.05) , received induction with thymoglobulin (77% vs. 24%: p=.028), received thymoglobulin for rejection (56% vs. 0%: p=.006), were malnourished (54% vs.17%: p=0.06), and were normal weight (12/15) or underweight (3/3). Mean length of stay in hospital at the time of transplantation was longer in deficient group (25 vs. 12 days, p=.09). Neurological comorbidities were not different between the two groups.

Conclusions

Pyridoxine deficiency seems to be relatively common post-transplant, especially those who are malnourished, underweight or normal weight, and who received thymoglobulin induction. Prospective studies are needed to confirm and evaluate the significance of deficiency.

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To cite this abstract in AMA style:

Arsdale SVan, Yost S, Meer M, Schoentag S, Kadambi P, Habib S. Pyridoxine Deficiency After Solid Organ Transplant [abstract]. Am J Transplant. 2015; 15 (suppl 3). https://atcmeetingabstracts.com/abstract/pyridoxine-deficiency-after-solid-organ-transplant/. Accessed May 19, 2025.

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