Tratamiento con adalimumab en la amiloidosis secundaria a artritis reumatoide: a propósito de dos casos / Treatment with adalimumab in amyloidosis secondary to rheumatoid arthritis: two case reports

Las patologías reumatológicas, y en primer lugar la artritis reumatoidea (AR), siguen siendo unas de las principales causas de amiloidosis secundaria. La aparición de agentes biológicos como el adalimumab en el tratamiento precoz de la AR puede ser una alternativa eficaz para frenar el desarrollo y la progresión de la amiloidosis secundaria. No todos los pacientes responderán igual al tratamiento; debemos considerar la comorbilidad asociada, los factores de mal pronóstico para predecir la repuesta terapéutica y los posibles efectos adversos. Dentro de los efectos adversos de las terapias biológicas, hay que destacar el aumento de la tasa de infecciones letales y cuadros de insuficiencia cardíaca. Presentamos dos casos clínicos con amiloidosis renal secundaria a AR que han seguido un curso clínico diferente: nuestro primer caso tuvo una buena repuesta al adalimumab, mientras que el segundo caso evolucionó desfavorablemente después del inicio del tratamiento, falleciendo por complicaciones cardiovasculares (AU)

Rheumatological diseases and, firstly, rheumatoid arthritis (RA) remain a major cause of secondary amyloidosis. The emergence of biological agents such as adalimumab in the early treatment of RA can be an effective alternative to stop the development and progression of secondary amyloidosis. Not all patients will respond the same way to treatment; we must consider associated comorbidity, the poor prognosis factors for predicting therapeutic response and possible adverse effects. In the adverse effects of biological therapies, there has been an increase in the rate of lethal infections and congestive heart failure. We present two cases with renal amyloidosis secondary to RA who had a different clinical course: our 1st case had a good response to Adalimumab while the 2nd case evolved unfavourably after treatment, and died from cardiovascular complications (AU)

Lanthanum carbonate reduces FGF23 in chronic kidney disease Stage 3 patients.

BACKGROUND: In chronic kidney disease (CKD) patients, the ability to excrete a phosphate load is impaired. Compensatory increase in parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) promote phosphaturia. Serum FGF23 concentration is considered an early biomarker of excess phosphate load and high levels of FGF23 have been associated with increased mortality. In the present study, we have evaluated the changes in plasma FGF23 after treatment with the phosphate binder lanthanum carbonate in patients with CKD-3 and a normal serum phosphate concentration. METHODS: Eighteen Caucasian CKD Stage 3a/3b patients with serum phosphate <4.5 mg/dL were recruited in a prospective longitudinal open-label study. Patients received a 4-week period of standardized phosphorus-restricted diet containing 0.8 g/Kg/day protein. Thereafter, the same diet was maintained and patients received lanthanum carbonate (750 mg with the three main meals) for 4 weeks. RESULTS: No significant changes were observed in serum phosphate, however, lanthanum carbonate significantly decreased urinary excretion of phosphate and fractional excretion of phosphate (P < 0.004). This was accompanied by a significant decrease in carboxyterminal FGF23 (median percent change from baseline -21.8% (interquartile range -4.5, -30%), P = 0.025). No changes were observed in PTH. CONCLUSIONS: In conclusion, lanthanum carbonate reduced phosphate load, as assessed by urinary phosphate excretion, and also reduced plasma FGF23 in CKD-3 patients. This occurs in the presence of unchanged normal serum phosphate levels.