Background: Herein we report a rare case of acquired palmoplantar keratoderma in association with myxoedema and hypothyroidism.
Patients And Methods: A 53-year-old woman presented with palmoplantar keratoderma, dry skin, muscular weakness and cramps for 9 months. The laboratory work-up revealed autoimmune thyroiditis with hypothyroidism. Skin biopsy showed chronic eczema. Other causes of acquired palmoplantar keratoderma were ruled out. Rapid improvement was achieved within 3 weeks of institution of hormone replacement therapy.
Discussion: Although this association is very rare, hypothyroidism must be suspected in patients with acquired palmoplantar keratoderma, particularly when it occurs in association with systemic symptoms.
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http://dx.doi.org/10.1016/j.annder.2013.09.160 | DOI Listing |
Endocrinol Diabetes Metab Case Rep
January 2025
Summary: Palmoplantar keratoderma (PPK), characterised by excessive epidermal thickening of the skin on the palms and/or plantar surfaces of the feet, can be hereditary or acquired. Here, we report a case of a 53-year-old woman with a history of sub-optimally controlled diabetes mellitus presenting with fevers and decreased Glasgow Coma Scale (GCS) to a tertiary hospital. She was diagnosed with diabetic ketoacidosis (DKA), with blood glucose at 40 mmol/L and ketones at 7 mmol/L, in the setting of a methicillin-sensitive Staphylococcus aureus necrotising soft tissue back infection.
View Article and Find Full Text PDFFront Pharmacol
December 2024
Department of Pharmacy, Shaoxing People's Hospital, Shaoxing, China.
Aim: Cutaneous adverse events (CAEs) after treatment with BRAF and MEK inhibitors in patients with melanoma remain incompletely characterized. To determine the association of BRAF and MEK inhibitor treatment with CAEs in patients with melanoma compared with BRAF inhibitor alone.
Method: PubMed, Cochrane, Embase and Web of Science were systematically searched for BRAF and MEK inhibitors from database inception through 10 May 2024.
J Dermatol
January 2025
Division of Dermatology, Department of Internal Related, Kobe University Graduate School of Medicine, Kobe, Japan.
Nagashima-type palmoplantar keratosis (NPPK) has been shown to represent a form of autosomal recessive palmoplantar keratosis due to biallelic pathological variants of SERPINB7, which encodes a serine protease inhibitor expressed in the epidermis. Approximately 10 years have elapsed since NPPK was demonstrated to be an independent genetic disease, and the most prevalent palmoplantar keratoderma (PPK) in East Asian countries due to a high prevalence of founder mutations in SERPINB7. Since then, it has become evident that biallelic pathological variants of SERPINA12, which encodes a serine protease inhibitor expressed in the epidermis, can also manifest symptoms analogous to those of NPPK.
View Article and Find Full Text PDFActa Derm Venereol
January 2025
Infinity, University of Toulouse, CNRS, Inserm, UPS, Toulouse, France; CHU Toulouse, Purpan hospital, laboratory of cell biology and cytology, Federal Institute of Biology, Toulouse, France.
Front Genet
December 2024
Department of Dermatology, Peking University Shenzhen Hospital, Shenzhen, China.
Olmsted syndrome is characterized by symmetrically distributed, destructive, inflammatory palmoplantar keratoderma with periorificial keratotic plaques, most commonly due to gain-of-function mutations in the transient receptor potential vanilloid 3 (TRPV3) gene, which involves multiple pathological functions of the skin, such as hyperkeratosis, dermatitis, hair loss, itching, and pain. Recent studies suggest that mutations of located in different structural domains lead to cases of varying severity, suggesting a potential genotype-phenotype correlation resulting from TRPV3 gene mutations. This paper reviews the genetics and pathogenesis of Olmsted syndrome, as well as the potential management and treatment.
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