Phosphocalcic metabolism after biliopancreatic diversion
Por:
Lozano O., García-Díaz J.D., Cancer E., Arribas I., Rubio J.L., González-García I., Galván M., Álvarez J., Martín-Duce A.
Publicada:
1 ene 2007
Resumen:
Background: Malabsorptive techniques to treat morbid obesity have been followed by alterations in phosphocalcic metabolism. Knowledge of the preoperative situation is important to assess the influence of these techniques on phosphocalcic metabolism and to consider treatments for these alterations. Methods: 61 consecutive morbidly obese patients (50 women, 11 men, age 19 to 63 years) having had biliopancreatic diversion (BPD) were studied in a prospective manner. Preoperative and postoperative levels of calcium, phosphorus, 25-hydroxyvitamin D, tartrate resistant acid phosphate, plasma parathormone (PTH), tubular absorption of phosphate, and urinary calcium and pyridinolines were analyzed, as well as the potential risk factors for their alterations. Follow-up of all patients was a minimum of 4 years. Results: Before BPD, 42.3% of patients presented an increase in PTH and 54% a decrease in the 25-OH vitamin D, but the values of calcium and plasma phosphorus maintained at normal level. 81.8% of the patients with an increase in the PTH maintained high levels after BPD, while 60% of those with a normal preoperative PTH also presented hyperparathyroidism 4 years after the intervention. A correlation between the levels of plasma PTH and body mass index was not found. Conclusion: Morbid obesity is accompanied by a high percentage of hyperparathyroidism. BPD produces malabsorption of vitamin D during the first years, favoring the persistence or appearance of hyperparathyroidism. It is important to recognize and treat the secondary hyperparathyroidism.The postoperative period could necessitate more energetic interventions to get more efficient control of the phosphocalcic metabolism. © 2007 Springer Science + Business Media B.V.
Filiaciones:
Lozano O.:
Department of Surgery, Alcalá de Henares University, Príncipe de Asturias Hospital, Madrid, Spain
García-Díaz J.D.:
Department of Internal Medicine, Alcalá de Henares University, Príncipe de Asturias Hospital, Madrid, Spain
Cancer E.:
Department of Endocrinology, Alcalá de Henares University, Príncipe de Asturias Hospital, Madrid, Spain
Arribas I.:
Department of Biochemistry, Alcalá de Henares University, Príncipe de Asturias Hospital, Madrid, Spain
Rubio J.L.:
Department of Endocrinology, Alcalá de Henares University, Príncipe de Asturias Hospital, Madrid, Spain
González-García I.:
Department of Internal Medicine, Alcalá de Henares University, Príncipe de Asturias Hospital, Madrid, Spain
Galván M.:
Department of Surgery, Alcalá de Henares University, Príncipe de Asturias Hospital, Madrid, Spain
Álvarez J.:
Department of Endocrinology, Alcalá de Henares University, Príncipe de Asturias Hospital, Madrid, Spain
Martín-Duce A.:
Department of Surgery, Alcalá de Henares University, Príncipe de Asturias Hospital, Madrid, Spain
Alcalde Luis Silvela 4, 28022 Madrid, Spain
|