RESUMEN
BACKGROUND: Deflazacort (DFZ), an oxazoline derivative of prednisolone (PDN), has a dose equivalence of 1.2:1 (mg) to PDN. No study to date has compared adverse effects and efficacy of high doses of DFZ as against high-dose PDN in systemic lupus erythematosus (SLE). OBJECTIVES: To compare adverse effects of high dose DFZ and PDN in SLE patients, especially in terms of cushingoid features and gain in body weight, 3 and 6 months after initiation of these agents. METHODS: In both the steroid arms, the following outcome parameters were assessed at 3 and 6 months: (a) cushingoid features by Cushing's Severity Index (CSI) (b) hirsutism by modified Ferriman Gallwey score (c) weight gain by difference (Δ, delta) of weight (in kilograms). RESULTS: Patients on PDN had 1.6 kg (3.2%) and 2 kg (5.1%) higher median weight gain as compared to those on DFZ at 3 and 6 months respectively ( p = 0.012 and 0.001). PDN caused 10% and 22.2% higher increment in median hirsutism scores as compared to DFZ at 3 months and 6 months follow-up, respectively ( p = 0.004 and 0.002). PDN caused 100% higher increase in median CSI scores than DFZ at 6 months ( p = 0.03). There was no significant difference by generalized estimation equation between the groups with respect to changes in SLEDAI, renal SLEDAI, anti-dsDNA titres and C3/C4 levels. There were two serious infections (requiring hospitalization/intravenous antibiotics) in the PDN group, while none in the DFZ group. CONCLUSION: Comparable intake and tapering of high dose DFZ and PDN in active SLE revealed 2-fold less weight gain, 2.5-fold less hirsutism and 1.5-fold lower cushingoid severity index as well as lower glycaemic elevation in the DFZ group as compared to PDN group. Both had similar efficacy.
RESUMEN
Chikungunya virus (CHIKV) has been involved in epidemics in African and Asian subcontinents and, of late, has transcended to affect the Americas. Aedes aegypti and Aedes albopictus are the major vectors for CHIKV infection, which results in dissemination of virus to various vital organs. Entry of virus into these tissues causes infiltration of innate immune cells, monocytes, macrophages, neutrophils, natural killer cells, and adaptive immune cells. Macrophages bearing the replicating virus, in turn, secrete pro-inflammatory cytokines IL-1ß, TNF-α, and IL-17. Together, this pro-inflammatory milieu induces osteoclastogenesis, bone loss, and erosion. CHIKV is characterized by fever, headache, myalgia, rash, and symmetric polyarthritis, which is generally self-limiting. In a subset of cases, however, musculoskeletal symptoms may persist for up to 3-5 years. Viral culture and isolation from blood cells of infected patients are the gold standards for diagnosis of CHIKV. In routine practice, however, assays for anti-CHIKV IgM antibodies are used for diagnosis, as elevated levels in blood of infected patients are noted from 10 days following infection for up to 3-6 months. Early diagnosis of CHIKV is possible by nucleic acid detection techniques. Treatment of acute CHIKV is mainly symptomatic, with analgesics, non-steroidal anti-inflammatory agents (NSAIDs), and low-dose steroids. No vaccines or anti-viral medicines have been approved for clinical therapy in CHIKV as yet. Hydroxychloroquine and methotrexate have been used in chronic CHIKV infection with variable success.