A “Cracked Porcelain” Appearance on a Woman’s Shins

Authors:
Alexander K. C. Leung, MD; Benjamin Barankin, MD; and Amy A. M. Leung, MD

Citation:
Leung AKC, Barankin B, Leung AAM. A “cracked porcelain” appearance on a woman’s shins. Consultant. 2019;59(1):3-5,12.

A 65-year-old woman presented with a 6-month history of pruritic areas of dry scaly skin with fissures affecting her lower legs. The lesions had grown slowly larger and had become increasingly pruritic with time.

She enjoyed taking hot baths. She denied using aggressive cleansers or scrubs. According to the patient, the skin condition worsened during the winter months. Findings of a review of systems were unremarkable; there was no functional impairment and no recent weight loss. Her past heath was unremarkable, and she was not on any medications.

Physical examination revealed large polygonal scales delineated by superficial erythematous cracks on the shins, simulating a “cracked porcelain” appearance (Figure 1). Generalized xerosis was also present. The rest of the physical examination findings were essentially normal. In particular, there were no signs of edema or venous insufficiency.

Answer: Asteatotic Eczema

Asteatotic eczema, also called eczema craquelé or xerotic eczema, is characterized by pruritic, dry, rough, cracked, and polygonally fissured skin with irregular scaling.¹ The French term eczéma craquelé was coined by Brocq in 1907 to describe the cracked appearance of the lesion.²

Epidemiology

Asteatotic eczema typically affects individuals aged 65 years or older, although it can also occur in younger people.^3,4 The male to female ratio is 1.3 to 1.⁴ The exact prevalence in the general population is not known. In a prospective study of 240 geriatric patients aged 65 years or older attending a dermatology outpatient clinic in Turkey, 21.7% had eczematous dermatitis.⁵ Of those individuals with eczematous dermatitis, 26.9% had asteatotic eczema. Given that the studied population is highly selected, the results are not generalizable.

Etiopathogenesis

Increased transepidermal water loss secondary to breakdown of the skin barrier plays a major role in the pathogenesis.^6-8 It has been shown that the transepidermal water loss in lesional skin is 75-fold higher than in normal skin.⁹ The skin has two barrier structures, namely, the stratum corneum and tight junctions. In patients with asteatotic eczema, the stratum corneum can be dysfunctional as a result of a deficiency in ceramide, a major lipid present in this layer.¹⁰ Tight junctions reside immediately below the stratum corneum and regulate the selective permeability of the paracellular pathway. Some authors have speculated that tight junctions might regulate the lipid components found in the stratum corneum and suggest that the transepidermal water loss in asteatotic eczema results from a dysfunction of keratinocyte tight junctions. The keratinocytes shrink as a result of increased transepidermal water loss, thereby impairing the elasticity of the skin and leading to fissure formation. Decreased sebaceous and sweat gland activity as a result of aging contribute to the development of asteatotic eczema.^7,10-12 Analysis of sebum-derived lipids present in the stratum corneum shows that there is a significant decline in free fatty acids and triglycerides in asteatotic eczema compared with healthy age-matched controls.^11,13 In the acute edema/cutaneous distension syndrome, which may result from hypoproteinemia, edema and distension in the dermis lead to additional stretch on the overlying epidermis with aggravation of the cracks and fissures.^14,15

Predisposing factors for asteatotic eczema include low environmental humidity; dry, cold climates; prolonged and/or frequent bathing in hot water; overuse of soaps and detergents; overcleaning of the skin; infrequent use of emollients; and xerosis.^1,16

In most cases, asteatotic eczema is idiopathic and is an isolated finding. Occasionally, asteatotic eczema may occur in association with other conditions such as medications (eg, diuretics, retinoids [isotretinoin, acitretin], cimetidine, interferon, chemotherapeutic agents [nab-paclitaxel, pemetrexed, erlotinib]),^8,9,11,17,18 hypoalbuminemia,¹⁵ malnutrition,¹⁶ zinc deficiency,^19,20 myxedema,²¹ diabetes mellitus,¹⁶ amebiasis,²² rheumatoid arthritis,²³ leprosy,²⁴ traumatic denervation,¹⁰ and graft-versus-host disease.²⁵ Asteatotic eczema, especially when recalcitrant, widespread, and/or associated with deep red and inflammatory fissures or purpura,^26,27 may be a sign of internal malignancy (eg, lymphoma, angioimmunoblastic lymphadenopathy, adenocarcinoma of the gastrointestinal tract, lung cancer, breast cancer, pancreatic cancer, glucagonoma).^27-33 It is postulated that secretion of cytokines by malignant tumor cells disrupting the epidermal lipid barrier might be responsible.²⁷

Histopathology

Histopathology shows a mild subacute spongiosis and mild parakeratosis with a varying amount of inflammatory dermal infiltrate.¹⁸

NEXT: Clinical Manifestations

Clinical Manifestations

Asteatotic eczema typically presents with polygonal superficial, erythematous, linear cracks/fissures intersecting plates of dry scaly skin.^10,15 The appearance simulates that of “crazy paving,” “cracked porcelain,” “dry river bed,” or a “stained-glass window.”^10,15,34 The skin surface is typically xerotic, brittle, and eczematous (Figure 2).^30,35 The most commonly affected site is the shins.^7,11,35,36 Occasionally, it can also occur elsewhere such as on the trunk, thighs, and upper extremities.^7,11,35,36 Patients may experience an itching and/or stinging sensation.³⁷ In general, the severity of itch increases with age and disease duration.³⁸

Asteatotic eczema is usually localized but at times may be generalized.³⁰ Generalized asteatotic eczema may be associated with use of medications or underlying diseases (malignancy or systemic disease).¹

Other variants have also been reported, including those with hemorrhagic linear cracks,^30,39 purpura,²⁶ halo,⁴⁰ and deep red and inflammatory fissures.²⁷

Diagnosis

The diagnosis is mainly clinical. Skin biopsy is not indicated. Tests are not necessary in most cases. Laboratory tests, if necessary, should be directed by history and clinical findings. For example, thyroid function tests should be considered if there are features of hypothyroidism (eg, fatigability, lethargy, cold intolerance, constipation, weight gain, dry skin, coarse hair, bradycardia). Investigations for internal malignancy or systematic disease should be considered for patients with generalized asteatotic eczema of recent onset, especially if accompanied by weight loss, malaise, fever, night sweating, or excessive scaling.

Differential Diagnosis

Differential diagnosis includes lamellar ichthyosis, nummular eczema, stasis dermatitis, allergic contact dermatitis, and irritant contact dermatitis.²⁷

Complications

Asteatotic eczema can be disfiguring and socially embarrassing for those who prefer to wear short pants or skirts. The associated soreness and pruritus may adversely affect sleep and quality of life.

NEXT: Prognosis and Management

Prognosis and Management

Asteatotic eczema responds well to treatment, provided the underlying cause is properly treated. The course can be chronic; relapses are frequent during times of low humidity and during winter months.

Successful treatment requires a systemic multipronged approach that consists of avoidance of triggering factors, optimal skin care, and pharmacotherapy. Triggering factors such as irritants (eg, harsh soaps, wool clothing) and prolonged exposure to hot water should be avoided. Offending medications should be discontinued.

Hydration of the skin helps to improve the dryness and restore the disturbed skin’s barrier function and is of paramount importance. Hydration of the skin can be achieved by limiting baths to no more than once daily in lukewarm (not hot) water for no more than 10 minutes, followed by patting (not rubbing) the body dry with a towel.^36,41,42 A thicker moisturizer such as a balm or ointment should be applied within 3 minutes to prevent evaporation of water and keep the skin soft and flexible. This “soak and seal” method helps to improve the integrity of the skin barrier.^41,42 Frequent applications of moisturizers throughout the day help to maintain a high level of hydration in the stratum corneum. Moisturizers containing phospholipids like N-palmitoylethanolamine and N-acylethanolamine, ceramides, urea, α-hydroxy acids, or hyaluronic acids have been shown to improve the integrity of the stratum corneum.^12,43-45

Pharmacotherapy usually consists of topical application of corticosteroids or calcineurin inhibitors.^12,46 In general, the least-potent corticosteroid that can control the symptom should be used.^41,42 Topical corticosteroids should not be applied more than twice a day, because frequent use does not improve efficacy and may increase the risk of adverse effects such as atrophy of the skin that might aggravate the problem.^12,41,42 Topical immunomodulators (pimecrolimus and tacrolimus) are beneficial and safe and represent a major alternative to chronic corticosteroid use.^12,41,42,47

Alexander K. C. Leung, MD, is a clinical professor of pediatrics at the University of Calgary and a pediatric consultant at the Alberta Children’s Hospital in Calgary, Alberta, Canada.

Benjamin Barankin, MD, is a dermatologist and the medical director and founder of the Toronto Dermatology Centre in Toronto, Ontario, Canada.

Amy A. M. Leung, MD, is a resident in the Department of Family Medicine at the University of Alberta, in Edmonton, Alberta, Canada.

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