Clinical and Experimental Dermatology最新文献

Background: Clinician-reported outcome measures (ClinROMs) are an important part of disease assessment in daily practice and clinical trials. There is a broad disagreement on the most appropriate ClinROM for a comprehensive assessment of alopecia areata (AA) severity.

Objectives: To identify the currently available ClinROMs for AA through a systematic literature search, address their practical strengths and weaknesses, and identify the road ahead for future research.

Methods: A search was conducted of the published, peer-reviewed literature via PubMed (MEDLINE) and Embase (via Ovid) databases. Articles published in English within the past 23 years (post-2000) that objectively measured AA severity were included. We did not select scoring systems that were solely based on patient-reported outcomes.

Results: The literature search identified 1376 articles, of which 27 were chosen for full-text review. Based on our eligibility criteria, 14 articles were identified, describing 16 different ClinROMs. Five ClinROMs solely measured scalp hair loss [Severity of Alopecia Tool (SALT), SALT II, Alopecia Density and Extent (ALODEX), pediatric SALT (pSALT) and Alopecia Areata Investigator Global Assessment Scale (AA-IGA)]. Three trichoscopy-based ClinROMs assessed disease activity [Alopecia Areata Progression Index (AAPI), Alopecia Areata Predictive Score (AAPS) and the coudability hair score]. Six ClinROMs exclusively assessed nonscalp areas [Brigham Eyebrow Tool for Alopecia Areata (BETA), Brigham Eyelash Tool for Alopecia Areata (BELA), Alopecia Barbae Severity (ALBAS), ClinRO Measure for Eyebrow Hair Loss™, ClinRO Measure for Eyelash Hair Loss™ and ClinRO Measure for Nail Appearance™]. Two ClinROMs assessed both scalp and nonscalp domains [Alopecia Areata Severity Index (AASI) and Alopecia Areata Scale (AASc)]. The practical strengths and weaknesses of each assessment tool are described.

Conclusions: Various practical limitations associated with their established tools have impeded the universal implementation in routine clinical practice. There is a significant need for a composite clinical severity scoring system to capture all the key severity identifiers beyond the involvement of the scalp.

Skin cancer generally causes disproportionate morbidity and mortality in people of colour. Although skin cancers occur most frequently in White individuals overall, cutaneous T-cell lymphoma (CTCL) is an exception. CTCL is a rare skin cancer comprising several subtypes of non-Hodgkin lymphoma; each contains a unique clinical profile that varies with race. Our aim is to review and compile the differences in epidemiology, clinical presentation, treatments and outcomes of the CTCL subtypes in Black, Asian or Pacific Islander (API) and Hispanic patients. The current literature supports that there are nuances in the course of CTCL that differ with race. Across multiple studies, racial differences in incidence patterns have been reported, with the highest rates among Black patients. Cutaneous manifestations of CTCL are highly variable in people of colour, and the predilection for clinical CTCL variants often differs with race, as well as severity of cutaneous involvement (body surface area). Response to and type of treatment also differs among people of colour and may be partially attributable to the varying CTCL subtypes experienced by certain races. Prognostic factors tend to vary with race, although Black patients consistently experience poor outcomes, while API patients may have a more favourable prognosis. Currently, there is no definitive conclusion to account for differences observed in patients with skin of colour with CTCL; however, biological and socioeconomic factors have been proposed as potential drivers. As the proportion of people of colour in our population continues to grow, adequate physician awareness and knowledge of racial nuances in CTCL are necessary to begin addressing these disparities.

Lichen planus (LP) is an inflammatory disease that afflicts the skin, mucous membranes and cutaneous appendages. Moreover, LP represents a prototype of lichenoid dermatosis, being characterized by the presence of a dense dermal cell infiltrate. Although most cases of LP are idiopathic, infectious and drug-related factors must also be considered in the aetiology. In this context, the occurrence of LP and lichenoid drug eruptions following different types of vaccination is a possible event. Therefore, the aim of our review is to provide a broad perspective to clinicians by analysing the current literature of cases of LP and lichenoid eruptions following COVID-19 vaccination, and also investigating the possible pathogenetic mechanisms underlying this phenomenon. In total, 61 cases of LP and lichenoid eruption following COVID-19 vaccination have been collected. However, the number of cases of LP and lichenoid drug eruption is extremely low compared with the number of vaccines administered overall, suggesting that the risk of LP and lichenoid eruption following COVID-19 vaccination is extremely low. Certainly, further studies are desirable to identify the population most at risk and the possibility of taking preventive measures.

Background: Chronic spontaneous urticaria (CSU) is a common inflammatory disorder characterized by weals, angio-oedema, or both, for more than 6 weeks. Autoimmunity is held to be one of the most frequent causes, but little is known about the expression and relevance of autoimmunity-driving genes in CSU, such as STAT3, STAT1, IL27p28 (IL30) and IL12p35 (IL12A).

Objectives: To investigate patients with CSU and the expression of STAT3, STAT1, IL27p28 and IL12p35, and possible links to clinical features.

Methods: We enrolled 26 patients with CSU and 19 healthy controls (HCs) and determined their expression levels of STAT3, STAT1, IL27p28 and IL12p35 by quantitative real-time polymerase chain reaction. Patients were assessed for total IgE and IgG-anti-thyroid peroxidase (TPO), markers of autoimmune CSU.

Results: Patients with CSU showed significantly higher expression of STAT3 but not STAT1: 17 (65%) and 10 (38%) of the 26 had elevated STAT3 expression and STAT3/STAT1 ratios, respectively, as compared with only 1 (5%) of the 19 HCs. High STAT3 expression and STAT3/STAT1 ratios were linked to low IgE and elevated IgG-anti-TPO. As compared with HCs, patients with CSU had markedly lower and correlated IL27p28 and IL12p35 mRNA expression levels. Low IL27p28 and IL12p35 expression levels were linked to higher STAT3/STAT1 ratios and low IgE.

Conclusions: STAT3 upregulation and higher STAT3/STAT1 ratios, along with IL27p28 and IL12p35 downregulation, clusters with features of autoimmune CSU. The role of STAT3 as a potential pathogenic driver of autoimmune CSU and target of treatment should be explored further.

Background: Hidradenitis suppurativa (HS) is associated with increased cardiovascular disease (CVD) risk. Systemic immune inflammation index (SII), neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR) and monocyte/lymphocyte ratio (MLR) are biomarkers of systemic inflammation and CVD. One small study identified a lower NLR and PLR in patients treated with adalimumab (ADA).

Objectives: To assess changes in SII, NLR, PLR and MLR in a larger cohort and to evaluate their association with disease severity and treatment response.

Methods: This was a post hoc analysis of PIONEER I (ClinicalTrials.gov ID: NCT01468207) and PIONEER II (ClinicalTrials.gov ID: NCT01468233), two phase III randomized placebo-controlled clinical trials of ADA for HS. SII, NLR, PLR and MLR were log10-transformed and a linear mixed model was used to estimate the treatment effect.

Results: SII, NLR, PLR and MLR decreased from baseline levels with ADA treatment by week 12, when the primary response endpoint was assessed. Significant changes first appeared at week 4 and were maintained to week 36. In contrast, no significant changes were observed in placebo-treated patients. In patients re-randomized at week 12 from placebo to ADA, SII, NLR, PLR and MLR also reduced within 4 weeks. In patients re-randomized from ADA to placebo, these biomarkers returned to baseline by week 36. In addition, SII, NLR and PLR correlated with draining fistula count (r = 0.26-0.43, P < 0.001). ADA nonresponders in PIONEER I had a higher SII, NLR and PLR at baseline and week 12, but this change did not achieve statistical significance when draining fistulae were adjusted for.

Conclusions: Treatment of patients with HS with ADA resulted in rapid sustained reduction in systemic inflammation, measured by the biomarkers SII, NLR, PLR and MLR, which correlate with CVD risk. SII, NLR and PLR may predict ADA response, although this may be dependent on their interaction with the number of draining fistulae.

Background: Biologics are effective for the treatment of psoriasis, but little is known regarding patients treated with one biologic for an 'ultra-long' duration.

Objectives: To explore the prevalence, patient and treatment characteristics, and treatment outcomes of ultra-long users of biologics for psoriasis.

Methods: Data for patients with psoriasis who had received continuous treatment with the same biologic for ≥ 10 years were collected from the prospective, multicentre BioCAPTURE cohort. Baseline characteristics of these ultra-long users were determined and compared with the total BioCAPTURE population. The proportion of patients using concomitant systemic treatment and receiving dose adjustments, the trajectory of Psoriasis Area and Severity Index scores and drug survival rates beyond 10 years were also analysed.

Results: Among the BioCAPTURE cohort, 30.5% of patients with the potential to achieve a treatment episode of ≥ 10 years reached this treatment duration. These patients were treated with ustekinumab, etanercept, adalimumab and infliximab. The proportion of ultra-long users was highest for ustekinumab (37.1%). The ultra-long user cohort had a slightly longer disease duration at registry entry, and a higher proportion of men and patients diagnosed with psoriatic arthritis (PsA) than the total BioCAPTURE population. Among the cohort, 69.5% of patients had at least one comorbidity and 66.1% used no additional systemic antipsoriatic treatment. Dose adjustments were often applied, varying from dose escalation (29.7%), dose reduction (40.7%) or both (13.6%); only 16.1% of patients consistently used the standard dose throughout their treatment. The median PASI score for ultra-long users from month 6 onwards was consistently < 3, with only a small proportion achieving complete clearance of their psoriasis (3.9-13.7% at the various timepoints). Drug survival analysis beyond 10 years showed that 62.3% of patients were still being treated with the same biologic after 15 years.

Conclusions: Ultra-long use of the same biologic in patients with psoriasis was common in real-world practice but varied between biologics. The median PASI score was around 2.5 throughout the 10-year treatment course; complete clearance was often not achieved. Remarkably, ultra-long use was also recorded in patients with multiple comorbidities (including PsA). Dose adjustments of the biologic were applied in the majority of patients. These results provide clinicians with important evidence on ultra-long treatment with biologics, thereby improving psoriasis care and the management of treatment expectations.