They found that whether applied topically or ingested in drinking water, glycerin, or glycerol, helps calm the classic scaly, red, raised and itchy patches in their psoriasis model, Dr. Wendy Bollag, cell physiologist and skin researcher at the Medical College of Georgia and Charlie Norwood VA Medical Center and her colleagues report in the International Journal of Molecular Sciences.
The studies also provide more evidence of the different ways glycerin enables the healthy maturation of skin cells through four stages that result in a smooth, protective skin layer.
“We have experimental data now to show what these patients with psoriasis are reporting,” says Bollag, who nearly 20 years ago first reported in The Journal of Investigative Dermatology that glycerin, a natural alcohol and water attractor known to help the skin look better, also safely helped it function better by helping skin cells mature properly.
Bollag’s early report led to many anecdotal reports from individuals and their reports ultimately led to the newly published study.
Topically, glycerin is known to have a soothing, emollient effect. But another key part of its magic, which Dr. Bollag has helped delineate, is its conversion to the lipid, or fat, phosphatidylglycerol, which ultimately regulates the function of keratinocytes, our major skin cell type, and suppresses inflammation in the skin.
Glycerin gets into the skin through avenues like aquaporin-3, a channel expressed in skin cells, and the MCG scientists have shown that once inside, aquaporin 3 funnels glycerin to phospholipase-D-2, an enzyme that converts fats in the external cell membrane into cell signals, ultimately converting glycerin to phosphatidylglycerol.
In 2018, Bollag and team reported that topical application of phosphatidylglycerol reduced inflammation and the characteristic raised skin patches in a mouse model of psoriasis. This time they decided to look at the impact of its widely available precursor glycerin.
For the new studies, they used imiquimod, which is known to produce psoriasis-like plaques on humans using it for problems like genital warts and some skin cancers, to produce an animal model. The mice either drank the sweet natural alcohol or the scientists applied it topically.
Either way, glycerin helped reduce development of the characteristic skin lesions, the scientists report, a finding which helps underline that glycerin works in more than one way to improve the skin condition.
Externally, glycerin showed its action as an emollient because even in mice missing phospholipase-D-2, it was beneficial. Additionally, topically it appears to compete with hydrogen peroxide for space inside the aquaporin 3 channel.
Hydrogen peroxide is commonly known as a mild antiseptic but we produce it as well and at low levels it’s a cell signaling molecule. But at high levels, hydrogen peroxide produces destructive oxidative stress, which can actually cause psoriasis.
The scientists found that topical glycerin reduced the levels of hydrogen peroxide entering skin cells. When they added glycerin and hydrogen peroxide at the same time directly to skin cells, they found that glycerin protected against the oxidative stress from hydrogen peroxide.
“Glycerol is basically outcompeting the hydrogen peroxide in getting in there and preventing it from being able to enter and increase oxidative stress,” Bollag says.
Oil and water don’t mix, so yet another way glycerin may be helpful is by supporting the skin’s major role as a water permeability barrier so that, as an extreme, when we sit in a bathtub the bath water doesn’t pass through our skin so we blow up like a balloon, she says.
On the other hand, when glycerin was ingested by the mice missing the phospholipase- D-2, which converts fats or lipids in a cell’s membrane to signals, it simply did not work, Bollag says, which confirmed their earlier findings that internally anyway, glycerin pairs with the enzyme to produce the signal essential to skin cell maturation.
Bollag would like next steps to also include clinical trials with dermatologists and patients and is working to find a formulation scientist who can make what she thinks will be the optimal combination: glycerin and phosphatidylglycerol in the same topical cream.
The addition of phosphatidylglyerol itself, rather than just the glycerin that makes it, is essentially a backup since there is some evidence that in psoriasis the essential conversion of glycerin to phosphatidylglycerol is not optimal.
Bollag’s lab and others have shown reduced levels of aquaporin 3 in psoriasis, which likely means less phosphatidylgycerol, so making more glycerin available may help, albeit not as efficiently, raise the availability of this lipid essential to normal skin cell proliferation.
Moving quickly into clinical trials should be comparatively easy since, as with glycerin, there already is experience with the use of phosphatidylglycerol in humans. For example, it’s a component of some high-end cosmetics, Bollag says.
She suspects that this sort of two-punch combination, could help keep early signs of psoriasis at bay and, with more advanced disease, use existing psoriasis treatments to get the skin condition under control then start applying glycerin to help keep it that way.
Bollag and her colleagues reported in 2018 in the Journal of Investigative Dermatology that in a mouse model of psoriasis, phosphtidylglycerol reduced inflammation and the characteristic raised skin lesions of psoriasis.
While its exact cause is unclear, psoriasis is an immune-mediated condition and patients have higher levels of inflammation, as well as too many skin cells being produced then maturing abnormally. The heightened inflammation also puts them at increased risk for problems like heart disease.
Biologics used to treat psoriasis work different ways to stem this overactive immune response but in addition to their high cost, can put the patient at risk for problems like serious infections and cancer. The only side effect she has seen in about 20 years of working with glycerin and the clinical and cosmetic use already out there, is it can leave the skin feeling slightly sticky.
Our bodies can make glycerol from the carbohydrates, proteins and fats that we eat or already have in our body.
THERAPEUTIC USE OF MOISTURIZERS
Moisturizers have a wide array of benefits for many dry skin-associated dermatoses. Skin dryness is induced by complex interactions between environmental and individual factors. Contributing factors includes low environmental temperature, low humidity, chemical exposures, microorganisms, aging, psychological stress, atopic dermatitis, and eczemas.23–25 This review emphasizes therapeutic use of moisturizers in various dematitis, such as atopic, seborrheic, contact, and nummular dermatitis.
Moisturizer for Atopic Dermatitis
Atopic dermatitis is a chronic skin inflammation, characterized with pruritus and skin barrier defect. Genetic mutations in the skin structural protein, filaggrin, lead to malfunction of the skin barrier leading to atopic dermatitis development and severity. These mutations hamper expression of filaggrin which is the structural protein responsible for maintaining epidermal barrier integrity as the skin’s vital line of defense. Filaggrin deficiency leads to skin barrier defects allowing increased trans-epidermal water loss and facilitates exposures of environmental allergen and infective organisms through the skin leading to persistent skin inflammation.26
Due to its chronic and relapsing nature, atopic dermatitis management involves treatment and prevention of flares requiring long-term skin barrier restoration through effective patient counseling and caregiver’s partnership. Moisturizers are the most important basic skin treatment for optimal atopic dermatitis recovery regardless the severity.27,28 Moisturizers can penetrate and help reorganize skin layers structure; therefore, it is recommended as a key step for atopic dermatitis treatment together with avoidance of triggers and therapeutic measures to control symptoms and inflammation. However, the choice of moisturizer ingredients should be carefully considered as atopic dermatitis patients are more prone to contact dermatitis when compared to normal population.9,26,29
Natural oils are widely used as moisturizer ingredients to treat and prevent dermatoses, such as atopic dermatitis. However, there are very limited data regarding their efficacy and safety profile. It has been suggested that oleic acid to linoleic acid ratio in natural oils determines their functions in skin hydrating and protecting effect on the skin. Positive effects are associated with high linoleic acid and low oleic acid ratios. High linoleic acid concentrations are believed to accelerate skin barrier repair and development, improving skin hydration, and ameliorate atopic dermatitis severity, making them perfect for steroid sparing.30–31
Safflower oil, sunflower seed oil, and sea buckthorn seed oil are natural oils with highest linoleic acid:oleic acid ratios.30 A recent study involving Bangladesh preterm infants reveals the excellent barrier repair and maintenance effects of sunflower seed oil, with 41 percent decreased risk for developing nosocomial infections compared to controls. However, olive oil, having relatively low linoleic acid:oleic acid ratio, can significantly deteriorate skin barrier by disrupting stratum corneum lipid structure and homeostasis.31 Further research regarding natural oils safety and efficacy for prevention and treatment of dermatoses is still required.
Humectants, such as 10% urea, have been shown to reduce trans-epidermal water loss in atopic patients.2 Urea also reduce skin irritation from sodium lauryl sulfate exposure in both atopic and normal skin. In mouse models of atopic dermatitis, application of glycerin-based moisturizer demonstrated a rapid hydration effect compared to untreated skin.32 Alphahydroxy acids are also effective treatment for dry skin. While lactic acid, particularly the L-isomer of lactic acid, stimulates ceramide synthesis, resulting in a higher production of stratum corneum ceramide and promoting a superior skin lipid barrier and dry skin resistance.9
Ceramides restore skin water permeability and barrier function. Recent studies suggested that low skin ceramide levels is a major etiologic factor in skin diseases, such as in atopic dermatitis.33 Stratum corneum consist of a significantly high ceramide composition (50% from total lipids). Many evidences showed that epidermal lipid barrier recapitulation with ceramides is effective as adjunctive treatment for eczematous processes.
According to Chamlin et al,34 topical mixtures of three key stratum corneum lipids consisting of ceramide, cholesterol, and free fatty acids in optimal proportions (3:1:1 molar ratio) can accelerate barrier repair following various external, acute, or sustained skin barrier disruption. Unlike non-physiologic lipid mixtures such as petrolatum, physiologic lipids (ceramides, cholesterol, and free fatty acids) can traverse both intact and disrupted stratum corneum.34
Therefore, natural or synthetic ceramides containing moisturizers are mostly recommended for atopic dermatitis. Lipophilic compounds like cholesterol and ceramides had been used in atopic dermatitis creams as they easily incorporate into liposomes, softening and smoothing skin texture. Nanoencapsulated triceramides are also being used to improve skin hydration.35
Nowadays, anti-inflammatory agents are incorporated with emollients or humectants; providing additional barrier repair and control dry skin. They are claimed as suitable for relieving mild-to-moderate atopic dermatitis, may reduce or substitute topical corticosteroids use, thus minimize side effects.36,37 Some anti-inflammatory agents added in moisturizers for atopic dermatitis are reviewed here. The use of these agents are to be carefully considered and selected for each patient, as some of them may be unsuitable for certain individuals who are allergic to these compounds.
Aloe vera has anti-inflammatory, anti-pruritic, analgesic and wound healing properties.38 It contains substances such as salicylic acid, magnesium lactate and gel polysaccharides.39 Previous study demonstrate that application of 0.1%, 0.25% and 0.5% of aloe vera extract for two weeks increase skin hydration, without any significant effect on trans-epidermal water loss.40
Bisabolol, extracted from chamomile (Matricaria recutita) plant, contains anti-inflammatory and anti-spasmodic substances such as sesquiterpene alcohol, chamazulene and flavinoids. The anti-inflammatory effect is attributed to cyclooxygenase and lipoxygenase inhibition. Bisabolol was also thought to play role in promoting granulation tissues for wound healing acceleration.41
A randomized, double blind clinical trial among 278 atopic dermatitis patients demonstrated that heparin and levomenol (α-bisabolol) formulation, applied twice daily for eight weeks significantly improve pruritus and disease symptoms. Bisabolol alone can ameliorate itching and inflammation; however, combination of these two agents showed higher efficacy.42
Shea butter is a fat derivation of Butyrospermum parkii kernels composed of five major fatty acids, including palmitic, stearic, oleic, linoleic, and arachidic acids. Stearic and oleic acids account for 85–90% of this fatty acids.43 It also contains triterpene acetate and cinnamate esters, demonstrating anti-inflammatory and anti-tumor promoting effects.44
Glycyrrhetinic acid, a triterpenoid compound extracted from licorice root, has anti-inflammatory, antiviral and antitumor effects. Evidence demonstrated that glycyrrhetinic acid suppress surface markers and inflammatory mediators expression of lipopolysaccharide-stimulated mature dendritic cells, thereby reduce skin inflammation.45 Other extracted compound from licorice root is Glycyrrhiza inflata.
Licochalcone A, its main component demonstrated inhibition of T cell proliferation and inflammatory cytokines production.46 Other components of Glycyrrhiza inflata includes licochalcone B and D which demonstrated anti-inflammatory effects.47 Previous study involving mildmoderate atopic dermatitis children revealed that licochalcone containing formula application twice daily improve atopic dermatitis symptoms comparable to hydrocortisone lotion.
Furthermore, licochalcone application site showed less relapse compared to other site, though this difference was insignificant.48 Interestingly, a randomized half-head study among scalp inflammation patients revealed that a leave-on tonic containing urea, lactate, polidocanol, and licochalcone A could ameliorate dryness, pruritus and inflammation.49
Niacinamide improve skin barrier functions by increasing epidermal ceramide and other intercellular lipid levels as well as promoting serine palmitoyltransferase upregulation.50 Furthermore, twice daily application of niacinamide formulation may reduce inflammation, decrease transepidermal water loss and increase stratum corneum thickness.51
Niacinamide also decrease trans-epidermal water loss in atopic dry skin significantly better, compared to white petrolatum.52 In randomized, controlled, comparative studies on stratum corneum integrity, niacinamide containing moisturizers application resulted in more rapid and sustained skin dryness and stratum corneum barrier improvement compared to conventional moisturizers.53
Palmitoylethanolamide is an endogenous lipid from fatty-acid N-acylethanolamine family. It resembles stratum corneum components and functions as peroxisome proliferators-activated receptor α agonist.54 Thereby, palmitoylethanolamide possesses both anti-inflammatory and analgesic properties.55 A large multinational, multicenter study involving 2,456 mild to moderate severity atopic dermatitis patients demonstrated that palmitoylethanolamide containing moisturizers could improve pruritus, dryness and eczema lesion. Moreover, 56% of patients can discontinue topical corticosteroid usage.56
Zinc gluconate, is an effective treatment for many skin inflammations. Recent evidence shows that its anti-inflammatory effects may target at peroxisome proliferator-activated receptors-α (PPARs-α), human β-defensin-2, and psoriasin.57,58
Several examples of nonsteroidal, noncalcineurin inhibitor agents are now available.59 MAS063DP was the first approved by the U.S. Food and Drug Administration to alleviate atopic dermatitis and allergic contact dermatitis symptoms. It is a nonsteroidal barrier repair cream, integrating glycyrrhetinic acid, Vitis vinifera extract and telmesteine in combination with shea butter (emollient) and hyaluronic acid (humectant). Some randomized, vehicle-controlled studies supported that this an effective monotherapy for pediatric and adult cases of mild to moderate atopic dermatitis.59,60
Selection of moisturizer composition for atopic dermatitis plays a crucial role for treatment outcome as it determines whether it will strengthen or deteriorate skin barrier function. Atopic dermatitis patients are particularly vulnerable to adverse skin reactions due to impaired barrier function, with thinner stratum corneum cell layers and larger follicular pores. In the worst scenario, application of the wrong moisturizer could increase dermatitis and asthma risk.6
There is still lack of knowledge as to the necessary moisturizer ingredients to overcome the specific epidermal defect.13 Therefore, moisturizers selection in clinical practice is mainly influenced by safety, efficacy, absence of sensitizing agents and individual preference.61
United Kingdom clinical experts developed a guidance regarding moisturizer selection for specific dry skin types in atopic dermatitis patients. For mild to moderate atopic dermatitis, occlusive emollient creams were recommended, while considering barrier thickness, lipid content variability, atopic dermatitis severity and body site. For more severe atopic dermatitis, occlusive emollient ointment was recommended; with the concern that this may reduce its acceptability. For very severe atopic dermatitis, occlusive ointment with zero water content is considered. Lastly, for pruritus, emollients with antipruritic substances were recommended.28
Recent Asian-Pacific region consensus guidelines recommend regular moisturizer application for atopic dermatitis maintenance and adjunctive therapy. It emphasized considerations of environmental humidity, climate, skin type and degree of dryness for moisturizer selection. Furthermore, atopic dermatitis duration, severity, patient age, treatment compliance, and financial resources should all also be taken into account. Other considerations include adjuvant properties, cosmetic acceptability, and product availability.29
Moisturizers for Seborrheic Dermatitis
Seborrheic dermatitis is a chronic-recurrent skin inflammatory disorder that commonly affects male adults. Onset may occur during puberty, due to cutaneous lipids abundance from increasing androgen-driven sebaceous gland development and sebum secretion.62
Seborrheic dermatitis commonly affects the scalp, face, and periauricular region. In some cases, the central chest, axillae and genital region are also involved. Pruritus is often present but not always found. Lesions most often appear as ill-defined erythematous patches with pityriasiform scaling involving predilection sites.62,63 In some cases, a thicker, more confluent area, sometimes with oval, discoid plaques (medallion lesions), may appear.
The exact seborrheic dermatitis etiology remain unknown, several factors such as sebaceous activity, Malassezia colonization and individual susceptibility appears to contribute to seborrheic dermatitis pathogenesis. Epidermal barrier integrity; host immune response, neurogenic factors, emotional stress, and nutritional factors are several factors influencing individual susceptibility.63
Recent evidence shows strong correlation between epidermal barrier integrity and seborrheic dermatitis severity. In seborrheic dermatitis, alterations of corneodesmosomal hydrolysis and impaired lipid organization were observed that caused disruption of the desquamation process leading to aberrant barrier function.64 Electron microscopy findings detected epidermal barrier structural abnormalities in scalp dandruff, including corneocyte shape and corneodesmosomes alterations, disrupted lipid lamellar structure and intercellular Malassezia yeasts.64,65
Furthermore, dandruff patients are more reactive to scalp applications of histamine or oleic acid with higher itch perception or flaking.66 These findings indicate that disrupted epidermal barrier function plays a role in dandruff aggravation. Recent genetic studies suggest that disrupted barrier function may even directly cause seborrheic dermatitis-like conditions.66,67
Biochemical analysis further showed that scalp dandruff demonstrate alteration of SC protein, ceramides and free fatty acids profiles in the absence of apparent inflammation.67 These evidences emphasized the crucial role of barrier restoration and maintenance in the management of seborrheic dermatitis.
The main goals of seborrheic dermatitis therapy are to alleviate visible signs and associated symptoms of seborrheic dermatitis, particularly pruritus. Available treatment options include topical corticosteroids, topical antifungal agents, topical calcineurin inhibitors, and most recently, a nonsteroidal “device” cream.68,69
Nonsteroidal topical device cream is a water-based, fragrance-free cream approved by U.S. Food and Drug Administration as medical device to manage and relieve seborrheic dermatitis symptoms, such as itching, erythema, scaling, and pain. Nonsteroidal topical device cream is suggested to be applied on affected areas two to three times daily. The formulation won’t be able to claim any individual active ingredient(s).
However, ingredients which may contribute to symptoms improvement include the biocide piroctone olamine, multiple antioxidants (eg, telmesteine, tocopheryl acetate, ascorbyl tetraiso-palmitate), multiple skin conditioning agents (eg, ethylhexyl palmitate, bisabolol, shea butter, Vitis vinifera), and alglycera, composed of allantoin and glycyrrhetinic acid, the latter demonstrated anti-inflammatory quality.69
Two studies had evaluated nonsteroidal topical device cream antifungal activity. In a guinea pig model, once-daily topical application of both nonsteroidal topical device cream and ciclopirox cream for three days decreased M. furfur counts below quantification limit. In humans, tape stripping evaluation of Malassezia spp colony-forming units following twice-daily nonsteroidal topical device cream application for seven days to one side of the chest was compared to untreated healthy volunteers (N=10).
At the end of the study, percentage reduction in Malassezia spp colony forming units was 94% on the treated side versus 49% on the untreated side (P=0.03). These studies suggest that nonsteroidal topical device cream may be effective for seborrheic dermatitis, at least partially due to reduction in Malassezia spp, with the antifungal effect likely related to the presence of piroctone olamine.70,71
A randomized, investigator-blinded, parallel-group, multicenter, pilot study comparing safety and efficacy of nonsteroidal topical device cream (n=38) versus desonide cream 0.05% (n=39) twice daily for mild-moderate facial seborrheic dermatitis in adults demonstrated significant signs and symptoms improvement following 14 and 28 days of treatment. Subjects percentage achieving “clear” or “almost clear” according to Investigator Global Assessment was 92% in the desonide group and 85% in the nonsteroidal topical device cream group.
Even when number of patients rated as “clear” at day 14 was greater in desonide (39%) than nonsteroidal topical device cream group (20%), in nonsteroidal topical device cream arm 71.4% of subjects who were clear at day 14 remained clear at day 28 as compared to 14.3% in the desonide arm (P=0.0173).72
Despite the limited sample, this study demonstrated that response onset may be faster with topical corticosteroids in the first two weeks, but with prolonged application, both therapies have comparable efficacy. Furthermore, following lesion clearing, relapses were sooner and more frequently occurred with the topical corticosteroid treatment. Larger studies with longer follow up duration are required to further explore timing and seborrheic dermatitis relapse rate with different therapeutic agents.
For treating mild to moderate seborrheic dermatitis, a variety of nonsteroidal treatment options, including ketoconazole 2%, ciclopirox 1%, pimecrolimus 1%, or nonsteroidal topical device cream are applied twice-daily. Many patients favorably respond to such application. For mild symptoms, many patients achieve seborrheic dermatitis relief within 1 to 4 weeks.
Except pimecrolimus 1% cream, these agents may be continued long term to prevent relapse without concerning any adverse effects. All four of these agents can be used intermittently to control milder flares with favorable speed. However, in more prominent cases with moderate-to-severe involvement, and/or symptoms, a short course of topical corticosteroids, once or twice daily for 1 to 2 weeks (depending on potency), in combination with a nonsteroidal agent, is a rational therapeutic choice.
Once the symptoms are controlled to a milder state or lesion clearance, usually within the first few to several days, topical corticosteroids can be ceased at once or tapered off over 1 to 2 weeks. Nonsteroidal agent should be continued for at least a few more weeks to prevent relapse. There is no single way to approach seborrheic dermatitis. Clinicians should individually modulate approaches to manage seborrheic dermatitis cases based on disease severity, response to treatment, and tendency for relapse.69
Moisturizers for Contact Dermatitis
Contact dermatitis is a common skin inflammation characterized by pruritic and erythematous skin lesions induced by contact with foreign substances. It is divided into two major groups: irritant and allergic.73
Clinical manifestation of contact dermatitis varies according to the causative allergen or irritant and the skin’s affected area. Contact dermatitis usually appears as erythema and scaling with relatively well-demarcated, visible borders. The hands, face, and neck are usually involved, although it may occur in any area. Some contact dermatitis manifestations can be both allergic and irritant.
Patients may complain of itching and discomfort, but some seek medical care due to the appearance of a rash. Acute cases may involve a dramatic flare with erythema, vesicles, and bullae; chronic cases may involve lichen with cracks and fissures. Patient history is crucial for diagnosis, and causative substance must be identified and avoided to resolve contact dermatitis and prevent further aggravation.73,74
Localized acute allergic contact dermatitis lesions are successfully treated with mid- or high-potency topical corticosteroids. On thinner skin areas, lower-potency topical corticosteroids are helpful to minimize the side effects.74 There are insufficient data to support the use of topical corticosteroids for irritant contact dermatitis. However, because it is difficult to distinguish clinically between allergic and irritant contact dermatitis, these agents are often used successfully for irritant contact dermatitis.
Primary prevention of irritant and allergic contact dermatitis involves avoidance of exposure to irritants and allergens. It may be accomplished by several means including substance elimination, substitution, training, and job task rotation. The use of personal protective equipment such as gloves, goggles face shields, and/or other skin protective equipment is important.74 Cotton liners under gloves can be used to enhance comfort and sweat absorption. Skin should be kept clean, dry, and as well moisturized as possible.
Patients with contact dermatitis should wash their skin using lukewarm water with mild soap and dry it gently. Soap should be removed carefully from finger web spaces as it is a surface-active agent, providing alkaline environment which is not gentle for the skin. Jewelry, including rings, could trap allergens and retain local moisture.74,75
Emollients are a good secondary prevention measure to avoid continuous exposure.74 After-work creams should be procured in workplaces and workers should be instructed to use them regularly. Barrier creams are often recommended to prevent occupational contact dermatitis, this may also involve the use of specialized creams such as barrier creams containing quaternium-18 bentonite (organoclay) to prevent rhus dermatitis or creams containing chelators such as penta-acetic acid to prevent nickel, chrome, or copper dermatitis.76 However, Cochrane systematically reviewed that barrier creams may not have a long-term protective effect. Another reason why it shouldn’t be promoted is that it may prevent workers from using more effective preventative measures.74
Frequent moisturizer application provides protection and strengthens skin barrier function. Lipid-rich moisturizers are particularly recommended to be routinely used in all contact dermatitis patients. When frequent moisturizer application is impractical to do, overnight application of a proper emollient may be recommended.76
Ointments are preferred over creams, as creams may have sensitizing preservatives and mildly irritating emulsifiers.77 Simple petroleum-based emollients are nearly as effective as emollients containing skin-related lipids, although several studies suggest that topical mixtures of key stratum corneum lipids, including ceramides, may accelerate barrier repair.34,78
Regardless of contact dermatitis type, restoration of damaged epidermal barrier and adequate skin hydration is extremely important for prevention of chronic contact dermatitis, even when all symptoms have resolved. Gutman et al79 advocate the “soak and smear” approach with mid- to high-potency topical corticosteroid ointments or emmolients application over a dampened skin following thorough skin hydration to “lock in” moisture.
Keratolytic agents such as salicylic acid or urea are helpful in hyperkeratotic dermatitis. In double-blind studies, moisturizers with urea have demonstrated reduced trans-epidermal water loss in atopic and ichthyotic patients. Urea also makes normal and atopic skin less susceptible against irritation to sodium lauryl sulphate.2 Treatments improving skin barrier function may decrease the possibility of further aggravation of contact dermatitis.
A sterol-enriched fraction from canola oil has demonstrated to ameliorate clinical signs of sodium lauryl sulphate-induced irritation, while other lipids (eg, fish oil, petrolatum, shea butter, and sunflower seed oil) had no effect on the degree of irritation.9 Loden and Andersson80 suggested that canola oil supplies the damaged skin barrier with adequate lipids for healing. Essential fatty acids (ie, linoleic and alpha-linoleic acids) influence skin physiology and pathology via their effects on skin barrier functions, eicosanoid production, membrane fluidity, and cell signaling.80
Squalene is the most commonly produced sebum component. It is a single oxygen quencher, protecting skin from lipid peroxidation due to ultraviolet and other ionizing radiation exposure. Although it is naturally produced by human body, production drastically slows after age thirty; causing skin dryness.81
Squalane is a saturated form of squalene, where hydrogenation has eliminated the double bonds making it oxidation resistant and good as moisturizers. An added quality of squalane is that even though it is technically oil, it is less greasy, odorless, non-comedogenic, antibacterial, and safe for sensitive skin. Moreover, it is also effective for treating skin disorders such as contact, seborrheic, or atopic dermatitis.82
Moisturizers for Nummular Dermatitis
Nummular dermatitis (also known as nummular eczema) is an eczematous disorder with pruritic coin-shaped patches on the skin that are often mistaken for ringworm or psoriasis. Men usually get nummular dermatitis later in their life while women get it sooner. The etiology is unknown, but most patients have very dry skin, which allow epidermal breach and permeation of allergens.83,84 Local trauma, such as arthropod bites, chemicals contact, or abrasions, may precede an outbreak.
Contact dermatitis due to nickel, cobalt, or chromates may play a role in some nummular dermatitis cases. Venous insufficiency, stasis dermatitis, and edema may be related to involvement of lower extremities.85,86 Autoeczematization may account for the presence of multiple plaques. Severe, generalized nummular dermatitis has been associated with interferon and ribavirin therapy for hepatitis C and tumor necrosis factor inhibitors.87,88
Patients may complain of pruritic, burning or stinging eruption that usually starts on the legs within days to months. Symptoms wax and wane with winter; cold or dry climates, are exacerbated by temperature swings and may improve with sunlight, humidity exposure or moisturizer use. Lesion recurrence in previous lesion locations is frequent. Patient may reveal past history of eczema, atopic dermatitis, or dry and sensitive skin.85
Diagnosis is made by observing the characteristic round to oval erythematous plaques, particularly on the legs; however, they may occur anywhere on the trunk, hands, or feet. Lesions may start as erythematous-to-violaceous papules or vesicles, coalescing to form confluent plaques. Lesions often distributed symmetrically and size several centimeters. It may have overlying erosions from excoriation. Aggressively scratched old lesions may develop lichen simplex chronicus, often on lower legs, neck, scalp, or scrotum. Nummular dermatitis never affects the face and scalp.85
Treatments aimed at skin rehydration, epidermal lipid barrier repair, and inflammation/infection control. Modification of cleansing habits should be advised where soap is applied only to the axilla and groin. Soapless, lukewarm or cool showers, followed by moisturizers or medicated topical preparations application on damp skin may alleviate itching and rehydrate skin. Medicine application to dampened skin results in more effective penetration and faster healing.
The “soak-and-smear” therapeutic regimen consists of 20-minute plain water soak followed by topical corticosteroid ointment or petrolatum application on wet skin. One study showed over 90% improvement in 27 of 28 patients with refractory chronic puritic eruptions when the regimen was properly followed.79
Wet wrap treatments are often effective, involving skin dampening with lukewarm water for 10 minutes followed by petrolatum or topical corticosteroid ointment application and 1-hour occlusion. Plastic wrap can be used for occlusion of small areas. Petrolatum application can be repeated five to six times a day while topical corticosteroid use should be carefully monitored to avoid adverse effect upon over usage.
When eruption has resolved, ongoing aggressive hydration may decrease the flares frequency, especially in dry environments. Ointments are more effective than creams due to more occlusion of skin barrier to the environment and more effective water retention in the skin. Heavy moisturizers or petrolatum applied to dampened skin are often effective. Emollients consist of bath oils, soap substitutes and moisturizing creams should be applied as often as required to alleviate itching, scaling and dryness.
Emollients should also be applied on unaffected skin to overcome dryness. It may be necessary to try several different products to a find suitable one. Many people find one or more of these emollients to be effective: sorbolene, glycerine and cetomacrogol cream, white soft paraffin/liquid paraffin mix, fatty cream, as well as wool fat lotions.
As nummular dermatitis often starts from minor skin injuries, skin should be carefully protected. If the hands are affected, use gloves and protective tools to ensure the skin is avoided from friction, detergents, solvents, other chemicals or excessive water exposure.
reference link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5849435/
More information: Vivek Choudhary et al, Glycerol Improves Skin Lesion Development in the Imiquimod Mouse Model of Psoriasis: Experimental Confirmation of Anecdotal Reports from Patients with Psoriasis, International Journal of Molecular Sciences (2021). DOI: 10.3390/ijms22168749
