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This article discusses a case of occupational protein contact dermatitis in a fitness studio employee. The 45-year-old woman experienced inflammatory changes to her hands during her work, which involved increased hand washing and sanitization. She also had reactions to accidental contact with protein powder. Allergological testing revealed elevated specific Immunoglobulin E (IgE) levels to milk protein, whey protein, and chicken egg white. The diagnosis was occupational protein contact dermatitis due to whey protein. The article emphasizes the need for increased awareness and accurate diagnosis of this condition. [Extracted from the article]

Aim Methods Results Conclusion Increasing the dietary intake of K+ in the setting of a high salt intake promotes renal Na+ excretion even though K+ concurrently enhances the secretion of aldosterone, the most effective stimulus for renal Na+ reabsorption. Here, we questioned whether in the high salt state a mechanism exists, which attenuates the aldosterone response to prevent renal Na+ reabsorption after high K+ intake.Mice were fed diets containing varying amounts of Na+ combined with KCl or KCitrate. Murine cortical connecting duct (mCCDcl1) cells were cultured in media containing normal or high [Cl−]. The response to aldosterone was analyzed by high‐resolution imaging and by biochemical approaches.The canonical cellular response to aldosterone, encompassing translocation of the mineralocorticoid receptor (MR) and activation of the epithelial Na+ channel ENaC was repressed in Na+‐replete mice fed a high KCl diet, even though plasma aldosterone concentrations were increased. The response to aldosterone was restored in Na+‐replete mice when the extracellular [Cl−] increase was prevented by feeding a high KCitrate diet. In mCCDcl1 cells, an elevated extracellular [Cl−] was sufficient to disrupt the aldosterone‐induced MR translocation.These findings indicate a pivotal role for extracellular [Cl−] in modulating renal aldosterone signaling to adapt MR activation by a high K+ intake to the NaCl balance. An impairment of [Cl−]‐mediated aldosterone resistance may contribute to excessive MR activation by aldosterone in the presence of a high salt intake characteristic of the Western diet, resulting in an inappropriate salt reabsorption and its downstream detrimental effects. [ABSTRACT FROM AUTHOR]