Early Experience With Interleukin-6 Receptor Antagonists in Patients With COVID-19 Admitted to a Community Hospital.

Background/objective: The efficacy of interleukin-6 (IL-6) inhibitors in hospitalized patients with severe coronavirus disease 2019 (COVID-19) pneumonitis is unclear. Method: This retrospective, observational cohort study included patients hospitalized at a community hospital with COVID-19 pneumonia from March 2020 to May 2020. All patients were treated with standard of care (SOC), and a nonrandomly selected subset of patients also received an IL-6 inhibitor. The primary outcome was clinical response, defined as an improvement of at least 2 categories relative to baseline on a 7-category ordinal scale up to hospital discharge or 30 days. In adjusted analyses, logistic and linear regression models were conducted, controlling for covariates of hospital length of stay (LOS), intensive care unit (ICU) care, ICU LOS, gender, age, race, and Charlson Comorbidity Index. Results: A total of 133 patients met inclusion criteria. In all, 30 patients received an IL-6 inhibitor plus SOC. There was no statistical difference in clinical outcome between groups as 76.7% in the SOC alone group and 70.0% in the IL-6 inhibitor group met the defined endpoints for clinical response (P = 0.477). In the adjusted analysis, patients treated with IL-6 inhibitors were approximately 4 times more likely to meet the primary endpoint compared with patients with SOC alone (adj. odds ratio = 4.325; P = 0.038, 95% confidence interval = [1.09-17.18]). Conclusions: Compared with SOC alone, IL-6 inhibitors were not associated with a significant clinical response. However, after adjusting for covariates, this study suggests that the initiation of IL-6 inhibitors in patients with early COVID-19 pneumonitis before progression to the ICU may be associated with improved clinical status.

IgG4-related disease with multiorgan involvement: a case-based review.

IgG4-related disease (IgG4-RD) is an immune-mediated multi-organ inflammatory disorder caused by tissue infiltration of lymphocytes with IgG4-secreting plasma cells. Herein, we discuss a case of a patient with IgG4-RD who had involvement of multiple organs: the kidneys, lymph nodes, bone marrow (biopsy performed), lungs, liver, and small intestine (imaging abnormalities). Although several case reports and series of IgG4-RD involving different organ involvement are in the literature, our patient has extensive simultaneous multi-organ involvement. We utilized the four domains (serologic, pathologic, radiologic, and pathologic) as discussed in the new 2019 ACR/EULAR classification criteria to provide a useful framework in considering an alternative tool for IgG4-RD in multi-organ involvement, where biopsy is more invasive and not always accessible. We highlight the findings of each organ involved that increase the likelihood that the patient has IgG4-RD. In our patient, the IgG4-RD classification criteria was fulfilled with total points adding up to 48. Our case meets the classification criteria for IgG4-RD, since at least one organ is involved to meet entry criteria (biopsy proven), no exclusion criteria are present, and the total points are ≥ 20. When such extensive involvement of IgG4-RD occurs, early diagnosis and treatment are recommended to avoid irreversible organ damage and better outcomes.

Trauma-induced concomitant psoriatic arthritis and complex regional pain syndrome.

To report the simultaneous occurrence of psoriatic arthritis (PsA) and chronic regional pain syndrome type I (CRPS I) both triggered by intense walking in a male golfer with a history of scalp psoriasis. Sequential existence of these two conditions have been reported in the literature; however, to our knowledge, this is the first report of a simultaneous occurrence of PsA and CRPS I. This case illustrates the complex interplay between genetic predisposition and environmental risk factors with the central nervous and immune systems. As the pathogenesis of PsA has been better understood in recent years, we propose a mechanism that explains how the release of pro-inflammatory cytokines and neuropeptides following a traumatic event elicits a vicious cycle that is a common ground for the development of both PsA and CRPS I. Even unperceived trauma, such as intense walking, when directed to the synovio-entheseal complex, can precipitate the development of PsA and CRPS I in predisposed individuals.