It compared their ability to reduce Disease Activity Score-28 with CRP (DAS-28 CRP), a measure of rheumatoid arthritis disease severity that includes number of tender and swollen joints, C-reactive protein level (a marker of inflammation), and overall health reported on a standardized scale. The trial found that after 12 weeks of treatment, people treated with upadacitinib had lower DAS-28 CRP scores and a higher rate of remission. There was also a higher rate of serious and opportunistic infections, elevated liver enzymes, and thromboembolism in the upadacitinib group. History
Upadacitinib was approved for medical use in the United States in August 2019.The US Food and Drug Administration (FDA) approved upadacitinib based on evidence from five clinical trials (Trial 1/NCT02706873, Trial 2/NCT02706951, Trial 3/NCT02675426, Trial 4/NCT02629159, Trial 5/NCT02706847) of 3,141 participants with active rheumatoid arthritis (RA). The trials were conducted in Australia, New Zealand, Israel, South Africa, Asia, North/Central/South America, and Europe.Five trials established the benefits and side effects of upadacitinib. Trials enrolled participants with moderate to severe active RA in whom disease-modifying antirheumatic drugs (DMARDS) did not work well or could not be tolerated. All participants had at least six tender and six swollen joints, and increased levels of high sensitivity C-reactive protein (hsCRP). hsCRP is a substance produced by the body to protect itself from illness. Trials lasted up to 5 years.Trial 1 enrolled participants who had never been treated with MTX. Participants were randomly assigned to receive one of two doses of upadacitinib or MTX daily for 24 weeks.
Rhinitis medicamentosa (or RM) is a condition of rebound nasal congestion suspected to be brought on by extended use of topical decongestants (e.g., oxymetazoline, phenylephrine, xylometazoline, and naphazoline nasal sprays) and certain oral medications (e.g., sympathomimetic amines and various 2-imidazolines) that constrict blood vessels in the lining of the nose, although evidence has been contradictory. Presentation
The characteristic presentation of RM involves nasal congestion without rhinorrhea, postnasal drip, or sneezing following several days of decongestant use. This condition typically occurs after 5–7 days of use of topical decongestants. Patients often try increasing both the dose and the frequency of nasal sprays upon the onset of RM, worsening the condition. The swelling of the nasal passages caused by rebound congestion may eventually result in permanent turbinate hypertrophy, which may block nasal breathing until surgically removed. Causes
Common issues that lead to overuse of topical decongestants:
Deviated septum
Upper respiratory tract infection
Vasomotor rhinitis
Cocaine use and other stimulant abuse
Pregnancy (these products are not considered safe for pregnancy)
Chronic rhinosinusitis
Hypertrophy of the inferior turbinates

Pathophysiology
The pathophysiology of RM is unclear, although several mechanisms involving norepinephrine signaling have been proposed.