EpistemisHaxthausen Keratoderma
Specialty: Skin.
Why it occurs
- Abrupt and severe decrease in systemic estrogen levels associated with physiological or surgical menopause that alters the metabolism of epidermal lipids and keratinization of palms and soles
- Individual genetic predisposition to hormonal reactive hyperkeratosis
- Coexisting exogenous obesity that increases mechanical friction and constant pressure on the heels and soles
- Concomitant nutritional deficiencies of essential fatty acids
- Inappropriate use of open flat footwear that promotes cracking of hyperkeratotic skin.
Initial workup
Eminently clinical diagnosis based on the patient's profile (postmenopausal woman with asymmetric fissured hyperkeratoderma on the heels and palms that spares the plantar arch). Direct scraping with KOH of the edges of the fissures to rule out concomitant tinea pedis. Analytical measurement of serum estradiol levels, thyroid profile and lipid profile.
red flags
Presence of very painful deep hyperkeratotic fissures with recurrent active bleeding, obvious signs of ascending infectious cellulitis in the legs, or absolute inability to stand or walk normally due to exquisite localized pain.
Standard management
- 10% salicylic acid ointment combined with 30% urea in occlusive base — applied at night under plastic film occlusion to peel and soften hard keratin
- Conjugated estrogens in locally applied topical cream or systemic hormone replacement therapy — under strict gynecological indication and ruling out oncological contraindications
- Calcipotriol 0.005% in ointment — applied daily to regularize keratinization
- Barrier cream with zinc oxide and panthenol to promote rapid healing of painful open fissures.
Educational guidance for study. It is NOT a prescription recommendation. The actual choice depends on the cause, the patient, and current guidelines.
- Area
- Skin
- Listed causes
- 5
- Treatment options
- 4