Letters to the Editor: May 2025

J Clin Aesthet Dermatol. 2025;18(5):12–15.

Feasibility of IDEOM’s Clinical Framework to Optimize Psoriatic Arthritis Care: A Cross-sectional Quality Improvement Study

Dear Editor:

Psoriatic arthritis (PsA) is a chronic inflammatory joint disease affecting up to one-third of individuals with psoriasis (PsO). Despite its high prevalence, PsA remains undiagnosed in up to 41 percent of cases and may lead to irreversible joint damage if untreated.¹ 

The International Dermatology Outcome Measures (IDEOM) group developed a clinical framework to streamline PsA recognition and symptom assessment through several studies. IDEOM initially conducted a Delphi study in which experts agreed all PsO trial participants should be screened for PsA, and symptoms should be measured using the Psoriatic Arthritis Impact of Disease (PsAID) questionnaire.^2,3 Perez-Chada et al⁴ refined this approach for clinical application, depicting a framework in which PsO patients first complete the Psoriasis Epidemiology Screening Tool (PEST).^4,5 Those with a PEST score of 3 or greater (positive PsA screen) subsequently complete the PsAID 12-item questionnaire (PsAID-12), along with those with baseline PsA to assess symptom burden. A PsAID-12 score of four or less is deemed an “acceptable” symptom state, while a score of higher than four is deemed “unacceptable” following a validated cutoff.³ Accordingly, a score higher than four prompts treatment modification or rheumatology referral.⁴ Our quality improvement (QI) initiative evaluated the feasibility of this framework in a real-world clinical setting to optimize care.

This cross-sectional study integrated the PEST and PsAID-12 into the Epic electronic medical record (EMR) at 26 Mount Sinai dermatology clinics. All English-speaking patients with a PsO or PsA diagnosis code (ICD-10 L40.0 and L40.5) were prompted to complete assessments via the electronic patient portal before each clinic visit. Questionnaire completion implied consent. Epic Best Practice Advisory (BPA) alerts, which are designed to provide clinicians with real-time warnings based on patient data, appeared when patients had a score of three or greater on the PEST or greater than four on the PsAID-12. Our BPA provided direct access to rheumatology consultations and displayed FDA-approved PsA treatments (Figure 1).  

Over 23 months, providers saw 7,424 patients with PsO, with 1,191 (16.0%) having a baseline PsA diagnosis. The mean age was 52.5±17.2 years. Figure 2 illustrates sequential outcomes of first-time response data: 36 percent (n=2246) of patients with PsO completed the PEST, with 12.6 percent (n=284) having a score of three or greater and completing the PsAID-12; 42.6 percent (n=507) of patients with PsO/PsA completed the PsAID-12. Of all PsAID-12 participants, 23.6 percent (n=187) scored greater than four, with 31.0 percent (n=58) referred to rheumatology. The demographics are detailed in Table 1.

Across all follow-up encounters, 720 (32.1%) patients had a PEST score of three or greater at least once. Among the 453 patients who completed the PsAID-12 multiple times, the mean score decreased from 2.83 initially to 2.52 at the most recent visit, over an average follow-up of 321.6 days. A paired two-tailed t-test confirmed this reduction was statistically significant (p=0.000068).

Our research demonstrates the feasibility and effectiveness of IDEOM’s clinical framework, as evidenced by the significant reduction in PsAID-12 scores suggesting PsA symptom improvement. Limitations included the low PEST response rate and the low referral rate; the latter may be explained by competing BPAs in Epic from other medical specialties. Moving forward, we aim to study PsA incidence among referred patients and track changes in patient-reported outcomes and management.

With regard, 

Gretchen D. Ball, BS; Hassan Hamade, MD; Sarah Romanelli, BS; Melissa P. Zundell, MD; Sangyoon Shin, MD; Thami Senthilkumaran, BS; Angela Lamb, MD; Saakshi Khattri, MD; Lourdes Perez-Chada, MD, MMSc; Joseph F. Merola, MD, MMSc; and Alice B. Gottlieb, MD, PhD

Keywords. Psoriasis, psoriatic arthritis, PEST, PsAID-12, quality improvement, patient-reported outcome measures

Affiliations. Msses. Ball, Romanelli, Senthilkumaran, and Drs. Hamade, Zundell, Shin, Lamb, Khattri, and Gottlieb are with the Department of Dermatology at the Icahn School of Medicine at Mount Sinai in New York, New York. Dr. Perez-Chada is with the Department of Dermatology at Harvard Medical School in Boston, Massachusetts. Dr. Merola is with the Department of Dermatology at UT Southwestern Medical Center in Dallas, Texas.

Funding. This study was funded by the International Dermatology Outcome Measure (IDEOM) nonprofit organization.

Disclosures. Misses Ball, Romanelli, Senthilkumaran, and Drs. Hamade, Zundell, and Shin have no conflicts of interest to disclose. Dr. Lamb declares a conflict of interest with Pfizer. Dr. Khattri is a member of the speaker bureau and/or advisory board for UCB, BMS, Regeneron, Sanofi, Abbvie, Lilly, Pfizer, and Janssen. She has received research support from Abbvie, BMS, Takeda, and Incyte. Dr. Perez-Chada receives grant funding from the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA). Dr. Merola is a consultant and/or investigator for Amgen, Astra-Zeneca, Boehringer Ingelheim, Bristol-Myers Squibb, Abbvie, Dermavant, Eli Lilly, Incyte, Moonlake, Novartis, Janssen, UCB, Sanofi-Regeneron, Sun Pharma, Biogen, Pfizer and Leo Pharma. Dr. Gottlieb receives research/educational grants from Highlights Therapeutics, Bristol-Myers Squibb, Janssen, and UCB Pharma, (all paid to Mount Sinai School of Medicine). Dr. Gottlieb has received honoraria as an advisory board member and consultant for Amgen, AnaptypsBio, Avotres Therapeutics, Boehringer Ingelheim, Bristol-Myers Squibb, Dice Therapeutics, Eli Lilly, Highlights Therapeutics, Janssen, Novartis, Sanofi, Teva, UCB, and Xbiotech (stock options for a rheumatoid arthritis project).

References

1. Mease PJ, Gladman DD, Papp KA, et al. Prevalence of rheumatologist-diagnosed psoriatic arthritis in patients with psoriasis in European/North American dermatology clinics. J Am Acad Dermatol. 2013;69(5):729–735. 
2. Perez-Chada LM, Gottlieb AB, Cohen J, et al. Measuring psoriatic arthritis symptoms: A core domain in psoriasis clinical trials. J Am Acad Dermatol. 2020;82(1):54–61. 
3. Gossec L, de Wit M, Kiltz U, et al. A patient-derived and patient-reported outcome measure for assessing psoriatic arthritis: elaboration and preliminary validation of the Psoriatic Arthritis Impact of Disease (PsAID) questionnaire, a 13-country EULAR initiative. Ann Rheum Dis. 2014;73(6):1012–1019.
4. Perez-Chada LM, Kohn A, Gottlieb AB, et al. Report of the Skin Research Working Groups From the GRAPPA 2020 Annual Meeting. J Rheumatol Suppl. 2021;97:10-16. 
5. Ibrahim GH, Buch MH, Lawson C, et al. Evaluation of an existing screening tool for psoriatic arthritis in people with psoriasis and the development of a new instrument: the Psoriasis Epidemiology Screening Tool (PEST) questionnaire. Clin Exp Rheumatol. 2009;27(3):469–474. 

Condyloma HPV Typing: A Clinical Necessity?

Dear Editor:

Condyloma acuminata (CA), caused by human papillomavirus (HPV), is the most prevalent sexually transmitted infection (STI) globally with most cases occurring in late adolescence or early adulthood.¹ HPV is a double-stranded DNA virus that transmits by sexual contact, with over 100 identified strains.¹ HPV-6 and 11 account for 90 percent of CA cases and are considered low-risk, as they are rarely found in invasive squamous cell carcinoma (SCC).² However, a single CA lesion may contain multiple HPV genotypes, including high-risk types such as 16, 18, 31, 33, 35, 39, 45, 51, 56, and 59. These subtypes are associated with an increased risk of carcinogenesis.³ Untreated high-risk HPV infections cause various cutaneous SCC’s.⁴ In the United States (US), high-risk HPV strains are linked to 3 percent of all cancers in women and 2 percent in men.⁴ 

Several preventative strategies for HPV infection have been discussed in the literature, including sexual abstinence, condom use, vaccination, smoking cessation, and male circumcision.^5,6 Currently, the Gardasil 9-valent HPV vaccine covers genotypes 6 and 11 (the most common causes of CA), as well as high-risk types 16, 18, 31, 33, 45, 52, and 58. It is recommended for both male and female patients aged 9 to 45.⁷

Biopsies are sometimes performed to differentiate CA from conditions like bowenoid papulosis and Buschke–Löwenstein tumor. Spontaneous regression occurs in 90 percent of CA cases due to the host immune response.⁸ However, infected cells can remain dormant for months to years, with a 70 percent chance of transmission to sexual partners during this period.⁸ 

Early detection of cancer and precancerous lesions is critical, as it reduces healthcare burdens and improves survival rates. For example, Papanicolaou (Pap) smears led to a 70-percent decrease in cervical cancer mortality in the United States from 1955 to 1992.⁹ Despite its impact, CA is not a reportable disease, possibly due to vaccine availability and its low risk of progression to malignancy. However, patients with high-risk HPV subtypes should be identified, and appropriate preventative measures should be initiated. For instance, patients should be encouraged to inform their sexual partners of their HPV status. The US Preventive Services Task Force has included high-risk HPV screening in its guidelines for cervical cancer prevention, and a similar approach could be beneficial for skin cancer prevention.¹⁰ 

Various HPV testing methods are commercially available, including PCR/nucleic acid amplification tests (NAATs), immunoperoxidase staining, and immunohistochemical staining (IHC). Author CJC’s experience with immunoperoxidase screening for HPV subtypes 6, 11, 16, and 18 in lesions suspicious for malignancy showed a low positive yield, even when histopathology suggested malignancy. PCR is a highly sensitive and specific method for detecting the HPV genome, capable of identifying a single HPV molecule in 105 cells.¹¹ A previous study assessing the sensitivity of PCR screening for cervical precancerous lesions, using biopsy as the gold standard, found a minimal false-negative rate but a specificity of 61.8 percent.¹² PCR’s limitations include being time-consuming, costly, and often not covered by insurance.¹² 

The authors recommend reserving PCR for cases of suspected carcinoma based on histological and clinical examinations when immunoperoxidase results are negative. Even with negative results from both tests, patients should still be counseled on the potential exposure to high-risk HPV subtypes and the risk of transmission. HPV testing in CA lesions could be a valuable tool for anogenital cancer screening and prevention, though there are limitations. Further rigorous studies are needed to validate the sensitivity, specificity, positive predictive value, negative predictive value, and cost-effectiveness of this approach. Current supporting evidence is based on HPV DNA screening for cervical cancer, and it is assumed that these findings can be extrapolated to stratify CA-positive patients for anogenital cancer. Additionally, it is controversial whether HPV screening should focus solely on the most common high-risk subtypes (16, 18, 33, and 35) or include all high-risk types.

With regard, 

Haowei Han, DO; Faraz Yousefian, DO; Ciaran Smyte, DO; Clay J. Cockerell, MD, JD, MBA; and Mark Nestor MD, PhD

Keywords. Condyloma acuminata, Human papillomavirus (HPV), High-risk HPV subtypes, cancer screening, HPV testing methods, PCR diagnostics, anogenital cancer prevention

Affiliations. Dr. Han is with St. John’s Episcopal Hospital in Far Rockaway, New York. Dr. Yousefian is with the Department of Dermatology and Mohs Surgery at the Philadelphia College of Osteopathic Medicine in Roswell, Georgia. Drs. Smythe and Cockerell are with Lake Granbury Medical Center in Granbury, Texas. Dr. Cockerell is also with Cockerell Dermatopathology in Dallas, Texas. Dr. Nestor is with the Center for Clinical and Cosmetic Research in Aventura, Florida and the University of Miami Miller School of Medicine in Miami, Florida.

Funding. No funding was provided for this article.

Disclosures. Drs. Han, Yousefian, Smythe, and Nestor have no conflicts of interest to disclose. 

References

1. Pennycook KB, McCready TA. Condyloma Acuminata. 2023 Jun 21. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2025 Jan–.
2. Clanner-Engelshofen BM, Marsela E, Engelsberger N, et al. Condylomata acuminata: A retrospective analysis on clinical characteristics and treatment options. Heliyon. 2020;6(3):e03547.
3. Pisani T, Cenci M. Prevalence of multiple high risk human papilloma virus (HR-HPV) infections in cervical cancer screening in Lazio region, Italy. Cancer Diagn Progn. 2024;4(1):42–45.
4. VCU Massey Comprehensive Cancer Center. HPV and Cancer. Accessed 1 Nov 2024. Updated 4 Apr 2023. https://www.masseycancercenter.org/cancer-types-and-treatments/cancer-types/anal-cancer/hpv-and-cancer/.
5. Larke N, Thomas SL, Dos Santos Silva I, et al. Male circumcision and human papillomavirus infection in men: A systematic review and meta-analysis. J Infect Dis. 2011;204(9):1375–1390.
6. Minkoff H, Feldman JG, Strickler HD, et al. Relationship between smoking and human papillomavirus infections in HIV-infected and -uninfected women. J Infect Dis. 2004;189(10):1821–1828.
7. Centers for Disease Control and Prevention. Human papillomavirus (HPV) vaccine safety. Updated 31 Jul 2024. Accessed 1 Nov 2024. https://www.cdc.gov/vaccine-safety/vaccines/hpv.html.
8. Diţescu D, Istrate-Ofiţeru AM, Roşu GC, et al. Clinical and pathological aspects of condyloma acuminatum – review of literature and case presentation. Rom J Morphol Embryol. 2021;62(2):369–383.
9. McGraw SL, Ferrante JM. Update on prevention and screening of cervical cancer. World J Clin Oncol. 2014;5(4):744–752.
10. U.S. Preventive Services Task Force. Cervical cancer: Screening. Updated 21 Aug 2018. Accessed 22 Sept 2022. https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/cervical-cancer-screening.
11. Young LS, Bevan IS, Johnson MA, et al. The polymerase chain reaction: a new epidemiological tool for investigating cervical human papillomavirus infection. BMJ. 1989;298(6665):14–18.
12. Zazove P, Reed BD, Gregoire L, et al. Low false-negative rate of PCR analysis for detecting human papillomavirus-related cervical lesions. J Clin Microbiol. 1998;36(9):2708–2713.