To the Editor: As the coronavirus disease 2019 (COVID-19) pandemic has rapidly spread around the globe, concern has been raised regarding susceptibility of patients receiving immunomodulatory therapies to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Although general guidance has been put forth, data regarding infection rate and outcomes in immunosuppressed patients are still rare.1 Recent articles, including the work by Gisondi et al,2 suggest that outcomes of patients receiving systemic immunomodulatory therapies who are infected with SARS-CoV-2 are similar to those of the general population. These findings may relate to the aberrant cytokine and inflammatory responses in severe COVID-19, which may be treated or partially blunted by cytokine-targeted therapy.3 Given the substantial outbreak of COVID-19 in our community, we tested whether, in addition to similar outcomes, patients receiving systemic immunomodulatory therapy had infection rates similar to those of the general population.
We performed a retrospective cross-sectional analysis of patients treated across all providers at Beth Israel Deaconess Department of Dermatology. Our clinical practice has 412 patients receiving systemic immunomodulatory medications, including biologics and traditional immunosuppressives, prescribed within the past year. Patients were surveyed by a clinic telephone call, by a telemedicine visit, or through an outreach wellness check-in call from March 15 to May 8, 2020, corresponding to the peak incidence of new cases of COVID-19 in Massachusetts.
Of our 412 patients, 327 were successfully contacted, with approximately 80% contacted after April 19, 2020. We were not able to identify any hospitalizations in Boston-area hospitals for the other 85 patients. Results are shown in Table I , with age distributions and conditions requiring immunomodulatory therapy displayed in Fig 1 . There were no statistical differences in age, sex, or medications between the patients who were reached and those who were not.
Table I.
Baseline characteristics of patients receiving immunosuppressive therapy
| Characteristic | All patients (n = 412) | Patients with positive and presumed-positive results (n = 5) |
|---|---|---|
| Demographics | ||
| Mean age (SD), y | 48.2 (15.9) | 48.4 |
| Men, No. (%) | 196 (48) | 2 (40) |
| Women, No. (%) | 216 (52) | 3 (60) |
| Live in Massachusetts, No. (%) | 382 (93) | 5 (100) |
| Medications, No. (%) | ||
| Biologics | ||
| TNFα inhibitor | 117 (28.4) | 2 (40) |
| IL-17 inhibitor | 29 (7) | 0 |
| IL-23 inhibitor | 30 (7.3) | 0 |
| IL-12/23 inhibitor | 54 (13.2) | 1 (20) |
| JAK inhibitor | 12 (2.9) | 0 |
| Traditional immunosuppressives No. (%) | ||
| Methotrexate | 48 (11.7) | 1 (20) |
| Cyclosporine | 5 (1.2) | 0 |
| Mycophenolate mofetil | 8 (1.9) | 0 |
| Other immunomodulatory therapies, No. (%) | ||
| IL-4Rα inhibitor | 65 (15.8) | 0 |
| Apremilast | 26 (6.3) | 1 (20) |
| Multiple medications (combination of multiple biologics, traditional immunosuppressives, and other immunomodulatory therapies) | 18 (4.4) | 0 |
| COVID-19 outcomes, No. (%) | ||
| COVID-related hospitalization | 1 (0.2) | 1 (20) |
| Any cause of death | 0 | 0 |
| Degree of contact with others, No. (%) | ||
| n = 260 | n = 5 | |
| None (patient generally not leaving home) | 158 (60.8) | 1 (33) |
| Patient with minimal degree of contact at work | 31 (11.9) | 0 |
| Patient with minimal degree of contact at home | 31 (11.9) | 1 (33) |
| Patient with minimal degree of contact both at work and home | 9 (3.5) | 0 |
| Patient with high degree of contact at work and home | 22 (8.5) | 1 (33) |
| Household member with high degree of contact at work | 9 (3.5) | 0 |
| COVID-19 symptoms/testing, No. (%) | ||
| Patients self-reporting symptoms (n = 25)∗ | Patients with positive and presumed-positive results (n = 5) | |
| Patients with symptoms and positive COVID-19 PCR test result | 2 (8) | 2 (40) |
| Patients with symptoms and negative COVID-19 PCR test result | 9 (36) | 1 (20)† |
| Patients with symptoms who were not tested for COVID-19 | 14 (56) | 2 (40)† |
IL, Interleukin; JAK, Janus kinase; PCR, polymerase chain reaction; TNF, tumor necrosis factor.
Symptoms include any patient-reported symptom of cough, fever, diarrhea, body aches, loss of smell, or dyspnea. These patients would meet COVID-19 testing criteria at our institution while receiving immunosuppression.
Patient was evaluated by a primary care physician who believed that the patient had COVID-19.
Fig 1.
A, Age distributions of all patients receiving immunomodulatory therapy. B, Underlying diagnoses being treated. ∗Other diagnoses included bullous pemphigoid (6), pyoderma gangrenosum (4), alopecia areata (2), lichen planopilaris (2), unspecified pruritus (2), vasculitis (2), acne keloidalis nuchae (1), discoid lupus erythematosus (1), granuloma annulare (1), lichen planus (1), lichen simplex chronicus (1), morphea (1), pemphigus vulgaris (1), pityriasis lichenoides (1), pityriasis rubra pilaris (1), and systemic lupus erythematosus (1).
As one of the hot spots of viral spread in the United States, Boston and the surrounding areas are ideal locations for studying effects of viral transmission. At data collection, slightly greater than 1% of Massachusetts residents had received a diagnosis of COVID-19, and slightly fewer than 10% of these patients required hospitalization.4 These numbers were similar in our patient population, with only 5 infections and 1 hospitalization, suggesting that the risk of both COVID-19 and poor outcomes is minimally affected by dermatologic immunomodulatory medications. However, many patients were successfully isolating to a large degree, and the low infectious rates appear to be due, at least in part, to enhanced social distancing efforts. As has been proposed previously,5 our findings suggest that when combined with patient education and encouragement to minimize exposure risks, systemic immunomodulatory therapies for dermatologic indications can be safely continued during the COVID-19 pandemic.
Limitations include the unknown number of asymptomatic infections, lack of available confirmatory COVID-19 testing in some cases, and the effect of social distancing as a confounding factor on infection rates. Also, our practice consists of only adult patients. Despite these limitations, we did not observe evidence of increased infectious risk, and we hope that these data will inform treatment decisions for patients who need these medications despite the ongoing COVID-19 pandemic.
Footnotes
Funding sources: None.
Conflicts of interest: Dr Rosales Santillan has received fellowship funding from AbbVie and Janssen that went directly to her institution. Dr Her's spouse works for AbbVie. Dr Kimball is a consultant and investigator for AbbVie, Bristol Meyers Squibb, Janssen, Eli Lilly, Novartis, Pfizer, and UCB; a consultant for Kymera and AmirallInvestigator ChemoCentryx; receives fellowship funding from Janssen and AbbVie; served on the board of directors and served as president of the International Psoriasis Council; and served on the board of directors of the HS Foundation. Dr Porter is a consultant and investigator for UCB, Pfizer, Eli Lilly, and Novartis and an investigator for AbbVie, Janssen, and Bristol Meyers Squibb. Dr Holcomb and Authors Morss-Walton, Salian, and Giannotti have no conflicts of interest to declare.
Reprints not available from the authors.
References
- 1.Lebwohl M., Rivera-Oyola R., Murrell D.F. Should biologics for psoriasis be interrupted in the era of COVID-19? J Am Acad Dermatol. 2020;82(5):1217–1218. doi: 10.1016/j.jaad.2020.03.031. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Gisondi P., Zaza G., Del Giglio M., Rossi M., Iacono V., Girolomoni G. Risk of hospitalization and death from COVID-19 infection in patients with chronic plaque psoriasis receiving a biological treatment and renal transplanted recipients in maintenance immunosuppressive treatment. J Am Acad Dermatol. 2020;83(1):285–287. doi: 10.1016/j.jaad.2020.04.085. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Shi Y., Wang Y., Shao C. COVID-19 infection: the perspectives on immune responses. Cell Death Differ. 2020;27(5):1451–1454. doi: 10.1038/s41418-020-0530-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Massachusetts Department of Public Health Information on the outbreak of coronavirus disease 2019 (COVID-19) 2020. https://www.mass.gov/resource/information-on-the-outbreak-of-coronavirus-disease-2019-covid-19
- 5.Schett G., Sticherling M., Neurath M.F. COVID-19: risk for cytokine targeting in chronic inflammatory diseases? Nat Rev Immunol. 2020;20(5):271–272. doi: 10.1038/s41577-020-0312-7. [DOI] [PMC free article] [PubMed] [Google Scholar]

