ABSTRACT
Upadacitinib, an oral Janus kinase (JAK) inhibitor, is used to manage rheumatoid arthritis. The objective was to generate statistical evidence from the existing data for upadacitinib efficacy and safety in various treatment regimens with different dosages in active rheumatoid arthritis patients. We searched PubMed, Cochrane, and ClinicalTrials.gov using PRISMA guidelines, providing data on the efficacy and safety of upadacitinib versus placebo in rheumatoid arthritis. 20% improvement in the American College of Rheumatology (ACR20) score response at 12 weeks was the primary outcome measure. Safety in adverse events, infections, or hepatic dysfunction was considered. The Mantel-Haenszel formula with random effect was used for the pooled odds ratio (OR) at a 95% confidence interval (CI) for dichotomous data. Meta-analysis was performed using RevMan version 5.4. Statistical heterogeneity was reported using I2 statistics; I2 > 75% was considered significant heterogeneity. A P value of less than 0.05 was considered significant. Data from 3233 patients were included in the analysis. The use of upadacitinib was associated with increased rates of achieving an ACR20 response compared with placebo (pooled OR 3.71; 95% CI 3.26-4.23; p-value <0.00001). Compared to a placebo, a 12 mg twice daily dose had the greatest effect, followed by a 15 mg once daily dose. Compared to the placebo, the incidence of any adverse event (pooled OR 1.66; 95% CI 1.36-2.02; p-value 0.0001) and infection (pooled OR 1.46; 95% CI 1.23-1.74; p-value 0.001) was found to be significantly higher in upadacitinib. Other adverse events, such as hepatic disorders and herpes zoster infections, were not statistically significant (p-value> 0.05). Maximum adverse events were seen at 12 mg twice daily. Upadacitinib, 15 mg once daily in combination with Methotrexate, was the most efficacious treatment regimen and was not associated with a significant risk for treatment-related adverse events in rheumatoid arthritis patients.
ABSTRACT
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung condition marked by lung scarring that progresses over time and with usual interstitial pneumonia histology (UIP). It is linked to a worsening cough, dyspnea, and a worse quality of life. Around 3 million persons worldwide suffer from IPF, and the prevalence rises sharply with advancing age. The detection of the UIP pattern, generally using high-resolution CT; lung biopsy may be necessary in certain individuals; the diagnostic approach also includes the elimination of other interstitial lung illnesses or overlapping problems. The UIP pattern is mostly bilateral, peripheral, and basal, with clusters of subpleural cystic airspaces and reticular alterations linked to traction bronchiectasis. Although there are still many uncertainties about how to define susceptibility, it is believed that the molecular mechanisms causing IPF reflect an abnormal reparative response to repeated alveolar epithelial damage in an aging genetically sensitive individual. With the availability of two pharmacotherapeutic drugs, pirfenidone and nintedanib, that slow physiological advancement and potentially increase progression-free survival, significant progress has been made in our knowledge of the clinical treatment of IPF. The goal of current research is to develop early biomarkers for IPF that may include circulating variables, demographic information, and imaging data.
