This analysis was done to verify the hypothesis that psoriatic arthritis is primarily genetically predetermined and distinct from the condition of psoriasis.
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Intrinsic factors may outweigh external factors in the emergence of psoriatic arthritis (PsA) in patients with psoriasis, according to recent findings, with genetic similarities present but not identical between psoriasis and PsA.1
These conclusions represented the result of new research carried out to look into a hypothesis that PsA is essentially predetermined based on genetics and distinct from psoriasis. The investigators explored whether or not intrinsic factors had been shown to outweigh external ones in the emergence of PsA among those with psoriasis.
This research was led by An-Ping Huo, from the Institute of Medicine at Chung Shan Medical University in Taiwan. Huo and colleagues noted that conventional views suggest PsA is a progression from psoriasis, though they recognized that there is inconsistent evidence for such a view.2
“To access our hypotheses, we utilized the TriNetX database to investigate whether (a) PsO patients with type 2 DM face an elevated risk of developing PsA compared to those without type 2 DM; (b) PsO patients who smoke face a higher risk of PsA; and (c) PsO patients with type 2 DM who smoke are more likely to develop PsA than those who do not smoke,” Huo and colleagues wrote.
The investigators first noted that the genetic connection known to exist between psoriasis and metabolic conditions like type 2 diabetes mellitus led to their choosing this specific condition as an intrinsic factor. The goal was to analyze diabetes mellitus’s effect on the development of PsA among those with psoriasis.
The research team’s 2 retrospective cohort studies involved extraction of data from the TriNetX network, a research network which contains de-identified, global electronic medical records on topics such as procedures, diagnoses, medications, and genomic information.
A subset of the TriNetX database covering 56 healthcare organizations within the US was used to extract data needed by the investigators. Their analysis of this subset was done in September 2023, and a retrospective cohort study carried out by the research team was done in the period from January 2012 - December 2022.
Individuals with psoriasis were identified with the ICD-10-CM code L40 in the aforementioned timeframe and were included in the team’s first cohort, with the variable of note being type 2 diabetes. The latter condition was identified through ICD-10-CM codes E08 and E11.
The investigators made up their study cohort of individuals with psoriasis and type 2 diabetes mellitus. They formed the control group into patients with psoriasis who did not have type 2 diabetes mellitus.
Patients with diagnoses of psoriasis within the same period were assessed in the research team’s second cohort, with the team determining that smoking would be the variable of note. This cohort would be made up of patients with psoriasis and a history of smoking, with the control arm being made up of the same type of patients who were also non-smokers.
Those with psoriasis and type 2 diabetes mellitus were also grouped to compare the observable risk of PsA development with and without a cigarette-smoking history. The investigators determined that the main outcome of their research would be identification of PsA, additionally combining each outcome with mortality in a composite measure for the purposes of addressing competing risks and survivorship bias.
They considered a range of covariates within a single year prior to their index date, with the goal being to uncover possible links and impacts within the study population.
The investigators found that individuals with psoriasis alongside type 2 diabetes mellitus were overall more likely to develop PsA, noting a hazard ratio (HR) of 1.11 (95% CI 1.03–1.20). They further reported that the combined outcome for such individuals suggested an increased risk, noting an HR of 1.31 (95% CI 1.25–1.37).
In a similar vein, patients with psoriasis along with a history of cigarette-smoking were shown to be at an increased PsA risk, suggested by an HR of 1.11 (95% CI 1.06–1.17). The research team highlighted that the combined outcome showed an HR of 1.28 (95% CI 1.24–1.33).
However, the team did find that individuals with psoriasis and both type 2 diabetes mellitus and a history of smoking did not lead to greater risk of PsA development, highlighting an HR of 1.05 (95% CI 0.92–1.20). Despite this conclusion, they found that the combined result for this group suggested a slightly increased risk as well as an HR of 1.15 (95% CI 1.06).
“Considering the inconclusive findings on risk factors for (psoriasis) patients to develop PsA, except for the musculoskeletal-related symptoms, signs, and various laboratory and imaging results, we recommend that further studies may focus on genetic disparities between (psoriasis) and PsA as potential risk indicators rather than relying solely on phenotypic distinctions,” they wrote.
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