Eosinofilia y síntomas sistémicos por sulfasalazina / Sulphasalazine-induced eosinophilia and systemic symptoms: a case report

RESUMEN La reacción a drogas con eosinofilia y síntomas sistémicos es una condición debida a una lista extensa de medicaciones, entre las que se encuentra la sulfasalazina. El compromiso es muy variado, desde rash cutáneo hasta afectación visceral acompañado de eosinofilia, que en ocasiones puede llevar a la muerte. El pilar del tratamiento es la suspensión del medicamento agresor y el uso de corticosteroides orales e intravenosos dependiendo de la severidad del cuadro.

ABSTRACT Drugs reactions with eosinophilia and systemic symptoms can be caused by an extensive list of medications, including sulphasalazine. The compromise is very varied, from skin rash to visceral involvement, accompanied by an eosinophilia that can sometimes lead to death. The cornerstone of the treatment is the suspension of the aggressive medication and the use of oral and intravenous corticosteroids, depending on the severity of the condition.

The Effects of Sulphasalazine on Urinary Excretion of the Hydroxypyridinium Crosslinks of Collagen in Patients with Rheumatoid Arthritis

Secondary osteoporosis is a feature of rheumatoid arthritis (RA). In recent years, several attempts have been made to develop specific markers for monitoring connective tissue metabolism in arthritic diseases. Our purpose, in this study was to assess pyridinium crosslinks (PYD and DPYD) excretion in relation to the activity of RA (changes related to sulphasalazine treatment). Fourty premenopausal female patients with active RA (mean age; 36.0 7.2 years), 20 postmenopausal women with active RA (mean age; 60.0 6.8 years), 23 postmenopausal women with OA (mean age; 56.1 6.6 years) and 17 premenopausal healthy subjects (mean age; 28.3 4.28 years) were enrolled in our study. All of the 40 premenopausal female patients with active RA were given sulphasalazine. The mean follow up period for these patients was 10.3 1.1 months. In all of these patients, urine samples were collected both in the active and in the inactive periods. Urine PYD and DPYD levels were measured by ELISA. Urine PYD levels were significantly higher in the active period (14.01 3.16 nmol/mmol cr) than in the inactive (8.25 4.23 nmol/mmol cr) period in patients with premenopausal RA (p 0.05). Urine PYD levels were significantly high in postmenopausal active RA patients (19.06 3.26 nmol/mmol cr) compared to premenopausal active and ind inactive, postmenopausal inactive RA patients, osteoarthritis and healthy controls. Urine DPYD excretion was similar in patients with premenopausal RA in the active (7.46 2.13 nmol/mmol cr) and inactive periods (5.08 0.87 nmol/mmol cr) (p 0.05). In active premenopausal RA patients, a correlation was found between PYD excretion and RAI, ESR, CRP and functional capacity (r=0.5729 p 0.01, r=0.5953 p 0.01, r=0.6125 p 0.01 and r=0.6232, p 0.01 respectively). But in the inactive period, no such correlation was was evident. In disease activity parameters did not correlate with DPYD excretion in either the active or the inactive period. As a result, urine PYD excretion was significantly high in patients with active RA. During sulphasalazine treatment, urine PYD levels decreased. This is attributed to improvement in bone destruction.