What Clinical Factors Affect Length of Transition to Psoriatic Arthritis in Patients With Psoriasis?

OBJECTIVE: We aimed to identify clinical and demographic features associated with the interval between psoriasis (PsO) and psoriatic arthritis (PsA). METHODS: We identified patients with PsO and PsA diagnoses from our tertiary care psoriatic disease biorepository: a longitudinal, real-world database including clinical information and patient-reported outcomes. We used a multivariable a zero-inflated negative binomial model to evaluate several clinical and demographic features that may be associated with the time between PsO and PsA onset. RESULTS: A total of 384 patients were included, of whom 52.2% were female. The mean age of PsO onset was 31.5 years. Advanced age at PsO onset was associated with a shorter interval between PsO and PsA. Based on our model, patients with PsO onset at age 42.6 years (upper end of the interquartile range [IQR]) had a 62% shorter expected interval compared with patients with PsO onset at age 18.9 years (lower end of IQR) (P < 0.001) and were more likely to have concurrent (onset within 6 months) diagnoses (odds ratio 4.56; 95% confidence interval 2.9-7.17). Patients with a body mass index (BMI) of 34 compared with a BMI of 26 had a 10% shorter interval between PsO and PsA, which trended toward statistical significance (P = 0.053). CONCLUSION: Our study demonstrated that patients with a diagnosis of PsO at an older age have a shorter interval between PsO and PsA diagnoses and are more likely to have concurrent diagnoses compared with patients with an onset of PsO at a younger age. These results suggest that patients with a later onset of PsO may benefit from earlier PsA screening.

Diagnosis of Inflammatory Bowel Disease-Associated Peripheral Arthritis: A Systematic Review.

BACKGROUND: Inflammatory bowel disease (IBD)-associated peripheral spondyloarthritis (pSpA) decreases quality of life and remains poorly understood. Given the prevalence of this condition and its negative impact, it is surprising that evidence-based disease definitions and diagnostic strategies are lacking. This systematic review summarizes available data to facilitate development and validation of diagnostics, patient-reported outcomes, and imaging indices specific to this condition. METHODS: A literature search was conducted. Consensus or classification criteria, case series, cross-sectional studies, cohort studies, and randomized controlled trials related to diagnosis were included. RESULTS: A total of 44 studies reporting data on approximately 1500 patients with pSpA were eligible for analysis. Data quality across studies was only graded as fair to good. Due to large heterogeneity, meta-analysis was not possible. The majority of studies incorporated patient-reported outcomes and a physical examination. A total of 13 studies proposed or validated screening tools, consensus, classification, or consensus criteria. A total of 28 studies assessed the role of laboratory tests, none of which were considered sufficiently accurate for use in diagnosis. A total of 17 studies assessed the role of imaging, with the available literature insufficient to fully endorse any imaging modality as a robust diagnostic tool. CONCLUSIONS: This review highlights existing inconsistency and lack of a clear diagnostic approach for IBD-associated pSpA. Given the absence of an evidence-based approach, a combination of existing criteria and physician assessment should be utilized. To address this issue comprehensively, our future efforts will be directed toward pursuit of a multidisciplinary approach aimed at standardizing evaluation and diagnosis of IBD-associated pSpA.

This systematic review highlights the lack of an evidence-based approach to the diagnosis of inflammatory bowel disease­associated peripheral spondyloarthritis and the need to standardize evaluation and diagnosis via multidisciplinary collaboration with development of patient-reported outcomes and imaging indices.

Digital ischaemia secondary to adalimumab-induced antiphospholipid syndrome.

A 50-year-old woman with a history of Crohn's disease treated with adalimumab presented with left hand pain and duskiness. Angiogram showed non-filling of the radial and digital arteries of the hand. Antiphospholipid antibody testing was positive, leading to a diagnosis of antitumour necrosis factor-induced antiphospholipid syndrome. Adalimumab was discontinued, and she was treated with the vitamin K antagonist warfarin and low-dose aspirin. Upon resolution of the antiphospholipid antibodies, she was transitioned to aspirin alone without recurrence of thrombosis.

Obligate progression precedes lung adenocarcinoma dissemination.

UNLABELLED: Despite its clinical importance, very little is known about the natural history and molecular underpinnings of lung cancer dissemination and metastasis. Here, we used a genetically engineered mouse model of metastatic lung adenocarcinoma in which cancer cells are fluorescently marked to determine whether dissemination is an inherent ability or a major acquired phenotype during lung adenocarcinoma metastasis. We find very little evidence for dissemination from oncogenic KRAS-driven hyperplasias or most adenocarcinomas. p53 loss is insufficient to drive dissemination but rather enables rare cancer cells in a small fraction of primary adenocarcinomas to gain alterations that drive dissemination. Molecular characterization of disseminated tumor cells indicates that downregulation of the transcription factor Nkx2-1 precedes dissemination. Finally, we show that metastatic primary tumors possess a highly proliferative subpopulation of cells with characteristics matching those of disseminating cells. We propose that dissemination is a major hurdle during the natural course of lung adenocarcinoma metastasis. SIGNIFICANCE: Because of its aggressively metastatic nature, lung cancer is the top cancer killer of both men and women in the United States. We show that, unlike in other cancer types, lung cancer dissemination is a major initial barrier to metastasis. Our findings provide insight into the effect of p53 deficiency and downregulation of Nkx2-1 during lung adenocarcinoma progression.