LAUSR

Aquagenic syringeal acrokeratoderma (ASA) is a rare, acquired disease affecting predominantly young women. It is characterised by the development of hypopigmented, translucent, flat-topped, oedematous papules and plaques that form hyperwrinkling or keratoderma.1 It occurs after 3-5 minutes of contact with water and resolves when the hand dries.1 Although its aetiology is not known exactly, it has been suggested that the disease may develop due to genetic predisposition or diseases such as cystic fibrosis, focal hyperhidrosis and Raynaud's phenomenon.2,3 However, increased personal hygiene measures such as wearing personal protective equipment, excessive hand washing and disinfection in the COVID19 epidemic may play a role in the aetiology of ASA.5 Here we present ten cases with a very short history of ASA where lesions were first seen after the COVID-19 outbreak. The ages of the patients varied between 5 and 24 years (6 female, 4 male). The duration of disease was between 20 days and 2 months. Lesions of all patients were occurred by continuous water contact for 5 minutes. Cystic fibrosis transmembrane conductance regulator (CFTR) gene test could not be performed due to technical difficulties. The disease was diagnosed clinically. Two patients had atopic dermatitis and one patient had a history of hyperhidrosis. Parents of 60% of the patients were working in the health sector. Case 7 and 8 were siblings, although they lived in separate cities, the lesions occurred at approximately the same time. Also, the case 9 and 10 were siblings and lesions occurred at the same time. All lesions were localised in the palmar regions of the hands (Figure 1). Seventy percentage of the patients was washing their hands frequently for hygiene. The patients had no previous history of ASA and the first lesions of all patients appeared during the COVID-19 pandemic. The lesions of 70 percent of the patients were left untreated, and the lesions largely disappeared with the reduction of water contact. One patient was cured with a mixture of glycerin, petrolatum, salicylic acid, mometasone furoate, vitamin E and Centella asiatica. One patient was unresponsive to aluminium chloride therapy. The clinical and demographic data of the patients are shown in Table 1. In the pathogenesis of aquagenic syringeal acrokeratoderma, the increase in the water-binding capacity of epidermal keratinocytes due to the increase in epidermal sodium concentration has been accused.2 The aetiology of the disease is not fully known. However, in the COVID-19 pandemic, hygiene practices are carried out excessively. According to a recently published case reports, it was evaluated that ASA was formed as a result of excessive and prolonged water contact during the COVID-19 pandemic.4,5 Due to the COVID-19 epidemic, 70 percent of our patients was washing their hands frequently and were in frequent contact with the disinfectant. In addition, it was thought that the fact that at least one of the parents of 70% of the cases was a healthcare worker, strict hygiene measures were followed and this could lead to the development of ASA. Most cases are sporadic and acquired, but familial cases with significant female dominance have also been reported..6 The fact that there are three siblings (6 patients in total) among our cases shows that ASA also has a genetic tendency. Treatment options include topical aluminium chloride, glycerol, salicylic acid, urea and ammonium lactate creams, iontophoresis and botulinum toxin.4 The vast majority of our cases were left untreated, and their lesions largely regressed with the reduction in water contact. As a result, although there are discussions on the pathophysiology of ASA, we think that the implementation of long-term and strict hygiene rules in the COVID-19 epidemic contributes to the emergence of ASA. In addition, the fact that 60% of the cases are siblings suggests that the disease has a genetic predisposition.