Inborn errors of metabolism are produced by an enzymatic alteration that can be fatal or leave serious neurological sequelae. Some of these conditions require specific nutritional treatment to reverse the clinical symptoms. For phenylketonuria, patients must restrict the intake of phenylalanine; for glucose transporter deficiency syndrome type 1, the treatment is a ketogenic diet; and for classic galactosemia, galactose must be eliminated from the diet. Due to nutritional restrictions, there is an increased risk of deficiency of vitamin D and calcium, which could have an effect on plasma vitamin D levels and cause alterations in bone mineral density (BMD) among children and long-term treated patients. According to scientific evidence, the risks of vitamin D deficiency among these patients are similar to those among healthy persons. While the etiology of lower BMD is not entirely clear, it is attributed to a joint effect of underlying pathology and metabolic changes generated by diet therapy. Long-term follow-up is suggested, in addition to verifying that recommendations o critical nutrients are covered. Timely evaluation of plasmatic levels of vitamin D and BMD is suggested to avoid deficiencies or excesses and to grant a better quality of life to persons with these pathologies.
Obesity is associated with lower serum levels of 25-hydroxyvitamin D (25-OH-D) and higher levels of PTH. There is an inverse relationship between these parameters in the general population, however this relationship is not well established in obesity. The 25-OH-D threshold required to completely suppress PTH has been suggested as a marker of optimal vitamin D status. We evaluated the relationship between 25-OH-D and PTH in obese patients before and after bariatric surgery, and determined the influence of obesity on the threshold for suppression of PTH by 25-OH-D. This was a retrospective study of patients followed between January 2010 and June 2017. We excluded patients with CKD (GFR < 60mL/min/1.73m²), previous history of bone fractures and abnormal levels of calcium, phosphorus and magnesium. Statistical analysis was performed with t , chi-square and linear regression tests. We evaluated 290 patients, 82.4% women, mean age 41.04 ± 10.52 years, BMI 43.57±5.66 kg/m². Before surgery, we observed a significant inverse association between 25-OH-D and PTH (β=-0.644; p<0.001), which is maintained after adjustment for gender, age, BMI and season. At 25-OH-D levels > 20 ng/mL the mean PTH was 53.24±2.68 pg/mL, increasing to 66.4±2.53 pg/mL when 25-OH-D was <10 ng/ml (p <0.001). One year after bariatric surgery, the association between the variables was weaker (β=-0.313, p=0.006), being lost in patients who kept a BMI > 30 kg/m2 (β=-0.154; p=0.434), despite the association between PTH and the presence of obesity (β=5.26, p=0.043). In patients achieving a BMI <30 kg/m², PTH increased from 41.05±1.57 pg/mL to 59.83±7.09 pg/mL for 25-OH-D levels <10 ng/mL (p=0.011) and to 96.1±14.19 pg/mL for 25-OH-D <5 ng/mL (p<0.001). In patients who maintained obesity, PTH increased from 46.66±2.81 pg/mL to 112±18.41 pg/mL from 25-OH-D <5 ng/mL (p=0.001) levels. The relationship between 25-OH-D and PTH in the obese population is modified after bariatric surgery. The PTH suppression threshold, and consequently the optimal vitamin D status, appear to be altered in obese and surgically treated patients. The 25-OH-D assay in the obese population may not be representative of the body's vitamin D reserves.
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