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There is a lack of validated tools to measure fatigue in patients with inflammatory skin, neuropsychiatric, and medical disorders. The use of nonvalidated tools may compromise the quality of data. The purpose of this meta-review was to evaluate existing fatigue scales commonly used to assess fatigue in other inflammatory conditions and to identify if there are scales that have been validated in dermatologic conditions. The PubMed/MEDLINE and SCOPUS databases were systematically searched from inception through March 10, 2020, in accordance with the PRISMA statement. Validated tools were identified and assessed according to their main measurement properties. The literature search identified 403 references, and eight studies were eligible and assessed in this review. The unidimensional fatigue scales included were the Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-F), Brief Fatigue Inventory, Fatigue Severity Scale, Numerical Rating Scale - Fatigue, and Visual Analog Scale - Fatigue. The multidimensional fatigue scales found were the Checklist Individual Strength, Chalder Fatigue Scale, Multidimensional Assessment of Fatigue, Multidimensional Fatigue Inventory Scale, and Piper Fatigue Scale. To measure fatigue, a brief scale with the ability to detect change is needed as there is a growing interest in evaluating this dimension of treatment response. In addition, a good content validity is also needed. From this systematic review, none of the selected scales have had content validation, even though the FACIT was validated in patients with psoriatic arthritis. Validation studies in specific disorders are urgently warranted.

Preterm infants are at high risk for developing bronchopulmonary dysplasia and pulmonary hypertension from inflammatory lung injury. In adult models, adiponectin (APN)—an adipocyte‐derived hormone—protects the lung from inflammatory injury and pulmonary vascular remodeling. Cord blood APN levels in premature infants born, Extremely low birth weight infants are at increased risk of developing acute and chronic lung disease from inflammation; they have low fat stores at birth and thus low circulating levels of the adipokine, adiponectin. Adiponectin is a potent anti‐inflammatory and anti‐oxidant adipokine. Here we show that recombinant adiponectin (rAPN) given to newborn rats in the saccular stage of lung development decreases LPS‐induced expression of proinflammatory cytokines and chemokines in lung homogenates and histopathological changes in the lung as shown in this graphical abstract. LPS was given intrapharyngeally and rAPN was given intraperitoneally. rAPN was effective in decreasing lung inflammation whether it was given as prevention or rescue therapy. Safe strategies that elevate endogenous APN may be benefical to extremely premature infants at risk of lung disease.