<b><i>Background:</i></b> Epidermal growth factor receptor (EGFR) inhibitors are routinely used in advanced non-small-cell lung cancer (NSCLC) harboring EGFR mutations. However, their use is associated with gastrointestinal and cutaneous toxicities, including acneiform eruptions, pruritus, xerosis, nail and hair changes. Aside from reducing patients’ quality of life, such cutaneous reactions have a considerable impact on the oncologic treatment given that dose reduction or even drug discontinuation may be necessary, especially for the severe forms. <b><i>Objectives:</i></b> To assess the incidence, impact on treatment and management of EGFR inhibitor-related cutaneous reactions in patients with NSCLC. <b><i>Methods:</i></b> We conducted a prospective observational study on 87 consecutive patients with advanced NSCLC treated with EGFR-tyrosine kinase inhibitors from January to December 2019. Patients who developed mucocutaneous reactions were evaluated and treated by both oncologists and dermatologists, and underwent dermatologic follow-up until resolution of the cutaneous reaction. Demographic and clinical data were collected for each patient, and the severity of the cutaneous reaction was graded using the Common Terminology Criteria for Adverse Events. <b><i>Results:</i></b> Seventy-one patients (81.6%) developed cutaneous reactions. The number of cutaneous reactions per patient was 1 in 37%, 2 in 41% and 3 or more in 22%. The most common cutaneous reactions included acneiform eruptions (56.3%), xerosis ± asteatotic eczema (48.3%), nail changes (39.1%), mucositis (29.9%), pruritus (24.1%) and hair changes (12.6%). Afatinib was associated with a higher rate of nail changes and mucositis (<i>p</i> < 0.01 and <i>p</i> < 0.005, respectively) compared to other agents, while no patient-related predictive factors were identified. Dose reduction was performed in 18% of patients. Multidisciplinary management involving dermatologists allowed to resume the drug in all patients who had discontinued it due to the cutaneous reactions. <b><i>Conclusions:</i></b> A multidisciplinary approach to EGFR inhibitor-related cutaneous reactions is advantageous and can reduce the need to discontinue oncologic treatment.
Background: Red blood cell distribution width (RDW) is frequently increased in inflammatory disorders and the magnitude of its elevation correlates with disease severity. This study was hence aimed to explore RDW values in patients with psoriasis.
Methods: The study population consisted of 366 adult patients with mild to severe plaque psoriasis and 366 age- and sex-matched healthy blood donor controls. For each psoriatic patient demographic, clinical and laboratory data were regularly collected.
Results: RDW and MCV were significantly higher in psoriatic patients compared to controls (13.95 vs. 13.40% and 90.4 vs. 89 fL; both p<0.01). In order to assess whether RDW elevations were related to psoriasis severity, we divided our psoriatic patient population into two groups based on a PASI cut-off of 10. No significant differences were observed between the two groups (i.e. PASI > 10 and ≤ 10) in terms of RDW (p=0.36). Adopting different PASI cut-offs (i.e. 3, 5, 7, 12) did also not result in statistically significant differences (p= 0.93, 0.48, 0.22, 0.42, respectively). In linear regression analysis, no significant correlation was also found between RDW and PASI or CRP, nor with age, gender or the psoriasis comorbidities listed in Table I. Furthermore, no significant difference of RDW values was noted between psoriatic patients with and without PsA (p = 0.27).
Conclusions: The results of this study confirm that RDW is elevated in psoriatic patients, though the magnitude of its increase did not appear to be associated with disease severity.
Psoriatic arthritis (PsA) is a heterogeneous chronic inflammatory arthritis associated with psoriasis, which may manifest with different domains such as dactylitis, enthesitis, synovitis and spondylitis. The estimated prevalence of PsA in patients with psoriasis ranges widely between 6% and 42%. In most cases, PsA is preceded by skin involvement by an average time of 7–8 years. In the complex patho-mechanisms involved in the transition from psoriasis to PsA, the gut and skin have been proposed as the sites of immune activation triggering or contributing to the development of PsA. In such a transition, a subclinical phase has been identified, characterized by enthesopathy where soluble biomarkers and imaging findings but no clinical symptoms are detectable. Recent studies have provided some evidence that timely treated psoriasis may reduce the risk of developing PsA.
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