Since the discovery of glucocorticoids (GCs), their important anti-inflammatory effect, rapid mechanism of action, low cost, and accessibility have made them one of the mainstays of treatment for Systemic lupus erythematosus (SLE). Although their use has allowed controlling the disease and reducing acute mortality in severe conditions, the implementation of a scheme based on high doses for long periods has inevitably been accompanied by an increase in adverse effects and infections, including long-term damage. The objective of this review is to answer some important questions that may arise from its use in daily clinical practice, and to propose a paradigm based on the use of methylprednisolone pulses followed by medium-low doses and a rapid decrease of prednisone.
ObjectivesTo determine the prevalence of renal relapse (RR) and remission in patients with Systemic Lupus Erythematosus (SLE), to identify the risk factors and evaluate the influence of the use of Methylprednisolone pulses in induction therapy.MethodsRetrospective study. Medical charts of 243 patients diagnosed with SLE (ACR 1982) between January 2.000th and December 2.012th, were reviewed at the Rheumatology Department of Angel C. Padilla Hospital in Tucuman. We included patients with Lupus Nephritis (LN) that completed induction therapy. The variables were: demographic, socioeconomic, laboratory, SLEDAI, SLICC/SDI, WHO class, induction and maintenance therapy, Glucocorticoid use (methylprednisolone pulses and cumulative dose). Response to treatment was defined as complete remission (CR), partial remission (PR) and non-responders (NR). Renal relapse (RR) was evaluated in patients who achieved remission after induction therapy. Progression to chronic kidney disease (CKD), end stage renal disease (ESRD), death and cause of death.Statistical analysis: Chi square test, Fisher's exact test, Unpaired t-test, Mann-Whitney U test and Kruskal-Wallis test were used for comparison, as appropiate. To determinate risk factors, we used logistic regression analysis.ResultsOut of 122 patients with renal involvement, 53 who completed the induction therapy were enrolled in the study (44 achieved remission and 9 were NR), 89% were women, the mean age was 32 years ±10.9, and 61% amerindians. The mean time from diagnosis of SLE to NL was 1.4 years ±2.4, the mean SLEDAI was 14.9±6.2, SLICC/SDI was 2±0.6, proteinuria 5.6g/24 hours ±1.5, the mean creatinine 2.4mg/lt. ±1.3, active sediment 67%, low complement levels 89%, positive anti-DNA in 75%. A renal biopsy (RB) was performed to 29 patients (21 class IV, 4 class V and 2 class II, 1 class III and 1 class VI). The induction treatments were: cyclophosphamide (CPM) in a monthly basis (27), mycophenolate mofetil (11) CPM 500 mg-EUROLUPUS (3) and other schemes (12). During the induction therapy 22% received Methylprednisolone pulses. The mean maximum dose of meprednisone was 42.2mg ±8.2. The patients who received Methylprednisolone pulses (12) had significantly higher levels of basal proteinuria than those who did not receive them (4g/24 hours versus 2.7g/24 hours, p=0.024). Completed maintenance therapy 79% patient. Out of 44 patients who achieved renal remission (24 CR and 20 PR), 24 renal relapsed (54.4%, IC 95% 38-69.6).Patients with positive anti-DNA, low complement and high levels of basal proteinuria who received Methylprednisolone pulses in induction therapy had a higher frequency of RR (OR 5.8, IC 95% 1.06-32.1; p=0.04). Ten patients progress to CKD, 8 to ESRD, and 6 died.ConclusionsMethylprednisolone use was associated with a higher prevalence of full remission, however, in the presence of low complement, positive anti-DNA and elevated proteinuria, RR was more frecuent. There was a higher prevalence of renal relapse (54%).Disclosure of InterestNone declared
IPAF groups individuals with ILD and other clinical, serologic, or pulmonary manifestations with an underlying systemic autoimmune condition, but do not meet current rheumatologic criteria for a CTD. ILD is a frequent clinical manifestation of CTDs; may appear in the context of a well known CTD but is often the first and only manifestation of an unknown CTD. Identifying an underlying CTD in patients presenting with initial interstitial involvement can be challenging; such evaluations can be optimized using a multidisciplinary approach. We present the case of three patients, of different presentation, evolution and treatment, all characterized to date as IPAF.
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