Sensitive skin: review of an ascending concept (2024)

Abstract

Sensitive skin is a condition characterized by stinging, burning and itchingsensations. The diagnosis, pathophysiology and treatment of sensitive skin arestill under discussion. In the last years, studies on its epidemiology have beenperformed, showing a high prevalence and impact on quality of life. Brazilianpopulation was also considered in these studies. Cosmetics, climate changes andskin barrier impairment are the main factors that contribute for skinhyperreactivity. New studies are trying to bring new knowledge about the theme.This review will describe data on epidemiology, triggering factors,pathophysiology, diagnosis and treatment.

Keywords: Additives in cosmetics, Cosmetics, Cosmetic technology, Dermatitis, Contact Dermatitis, Hypersensitivity, Skin absorption, Skin care, Skin cream, Skin diseases

INTRODUCTION

Sensitive skin is defined as a sensory reaction triggered by contactors and/orenvironmental factors, usually without a visible clinical manifestation.^1-3

This entity was first described by Maibach in 1987 under the name of CosmeticIntolerance Syndrome (CIS). ⁴ In1990, Fisher referred to the condition as "status cosmeticus".⁵ Literature reports have shown thatthis condition can also be triggered by environmental factors (cold, heat, sun,pollution, moisture) and therefore the term has been expanded to Sensitive SkinSyndrome (SSS).^1,6 Possible synonyms for this condition arehypersensitivity, hyperreactivity, sensitivity, intolerance or skinirritation.⁷

Sensations described by patients vary largely: pruritus, burning, tingling, pungency,thickening or dryness of the skin. These symptoms may occur minutes to hours aftercontact with a cosmetic product/ environmental stimulant or even after severalepisodes of use of a topic product, triggering the conduction by cumulativeeffect.⁸

Sensitive skin syndrome can manifest itself in two forms: objective andsubjective.⁷ The objectiveform is favored by a basic dermatitis that alters the protective skin barrier suchas atopic dermatitis and acne. In these cases, clinical lesions may be visible, suchas erythema, papules and vesicles.^1,8 In the subjective form, the patientrefers only to the symptoms, without visible dermatitis, and is thus usuallyself-diagnosed.

Presence of symptoms, in the majority of exclusively subjective cases, makes thisentity a diagnostic challenge and some authors even consider a psychological originfor the picture. With the help of new technologies the presence of alterations inthe cerebral stimulus in patients with this condition was demonstrated. However, ithas not yet been possible to establish objective screening tests for the diagnosisof sensitive skin.^1-3,6 Diagnosis,pathophysiology, epidemiology and treatment are still under discussion.⁹

EPIDEMIOLOGY

Although previously considered infrequent, sensitive skin syndrome has shown highprevalence in current studies. In a survey conducted in the United Kingdom, 51.4% ofwomen and 38.2% of men considered themselves to be carriers of sensitive skin. OtherEuropean and North American studies showed similar rates.^1,3,10

In an European study, Misery et al. demonstrated a global prevalenceof 38.4% of sensitive skin in the population, which shows the magnitude of theproblem.⁹

Recently, a Brazilian population study found that 22.3% of men and 45.7% of womenconsidered their skin sensitive.¹¹Chart 1 shows the comparison between thefrequencies of sensitive skin in different countries.¹¹

Chart 1.

Comparison of frequencies of sensitive skin in different countries

Country	Sensitive skin (%)	Little or not sensitive (%)
Japan	54.47	45.53
Italy	53.80	44.80
France	51.90	48.10
USA	44.60	55.40
Russia	39.72	60.28
Germany	35.60	64.20
Brazil	34.22	65.78
Spain	31.60	68.00
Switzerland	30.80	68.00
Greece	29.80	67.80
Portugal	27.40	72.40
Belgium	25.80	69.80

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Source: Taieb C, et al, 2014.¹¹

PREDISPONENT FACTORS

Ethnicity

Racial differences in the structure of the skin may be associated with thesymptoms observed in those with sensitive skin. Higher sensitivity to capsaicinwas demonstrated in Caucasians followed by Asians and then by blacks.^3,6,9

Thin skin is more prone to flushing due to barrier damage and increased vascularreactivity. Thus, in whites, reports of erythema are more common than in blacksand Asians. However, some authors found statistically insignificant differencesbetween groups of different ethnic groups.^3,6,9

Gender

The perception of sensitive skin in women varies from 50% to 61% and, in men,from 30% to 44% according to epidemiological studies.^12,13

The entity was initially described in women and justified by its lower cutaneousthickness when compared with men, in addition to hormonal factors interfering incutaneous hydration.^13,14 However, a study conducted in2010 ¹¹ showed a prevalence ofsensitive skin in 68% of the interviewees, with no differences between thesexes. With the increased use of cosmetics by men, this condition has also beendescribed in men.^12,13

Age

Sensitive skin is described in patients aged >18 years, probably due to thefact that research with epidemiological data has been performed onadults.^1,3,6,11,15

Studies have shown that young patients are more likely to have sensitive skin. Onthe one hand, elderly people have changes in the integrity of the skin tissue,which would favor sensitive skin. On the other hand, tactile sensitivitydecreases with age, and irritability tests have diminished response.^1,3

Location

The main location is the face, mainly the nasolabial fold.⁷ Factors that contribute to thisare probably the greater use of cosmetics in this area, the presence of thinnerskin barrier and the existence of a greater number of nerve endings on theface.³

Other regions related to sensitive skin already described are: volar surface offorearms, hands, genital region and scalp.^1,7

Presence of other dermatoses

Atopic dermatitis and other dermatites, such as acne, rosacea, seborrheicdermatitis, contact dermatitis, psoriasis, and physical urticaria(dermographism) favor the picture described by altered skin barrier or thepresence of inflammation. In these patients, sensitive skin is considered as anobjective form, since the dermatitis can present with visible clinical lesions,erythema, cutaneous xerosis and eczema.^1,3,7,16

When there is erythema, the diagnosis of sensitive skin may be confused withseveral dermatitis. However, the presence of abnormal sensations, triggeringfactors and transient nature suggest the diagnosis of sensitive skin. ^9,17

Environmental factors

Low temperature, humidity, wind, heat and sun exposure favor the manifestation ofsensitive skin.^1,3 Pollution, common in theindustrialized world, has been one of the factors responsible for thisentity.

Cosmetic products

Cosmetics are the main triggering factors of sensitive skin, especially in women,due to overuse and sometimes inappropriate use. Presence of potentiallyirritating substances in its composition (alpha-hydroxy acids, propylene glycol,alcohol, fragrances, etc.) increases the possibility of symptoms.³

Maintenance of cutaneous pH (5.5 on the surface) keeps the whole barrier andadequate hydration of the skin.¹ When the barrier is compromised, the penetration ofsubstances leads to the inflammatory reaction with release of a series ofcytokines. Thus, products that alter cutaneous pH favor sensitive skin.

The same way the irritants alter the function of the epidermal barrier, favoringsensitive skin, so the sensitizing substances, when phagocytized by Langerhanscells, lead keratinocytes and T lymphocytes to produce mediators ofinflammation.¹

Sociocultural factors

Differences in the prevalence of sensitive skin could be attributed to varietiesof habits (diet and body hygiene practices) and diversity in the perception ofthe symptomatology.^1,3

PATHOPHYSIOLOGY

Pathophysiology of sensitive skin is not completely elucidated; however it isrecognized that this condition has no immunological or allergic origin.¹¹

Changing of the stratum corneum

The main hypothesis attributed to the occurrence of sensitive skin is theincrease in the permeability of the stratum corneum, leading to greaterpenetration of substances and also to water loss. There is an inverse relationbetween corneal layer thickness and skin permeability.^1,6

The decrease in the thickness of the corneal layer facilitates the penetration ofsubstances capable of inducing the release of cytokines, leukotrienes andprostaglandins. These mediators induce the formation of neurotransmitters which,in turn, stimulate the nerve endings.¹²

Measurement of transepidermal water loss (TEWL) has been used to aid in thediagnosis of sensitive skin. Individuals with increased TEWL are predisposed tointolerance to products in contact with the skin. Thus, adequate hydration ofthe skin improves the symptomatology of patients with sensitive skin.¹ Studies performed withmenopausal women showed improvement of sensitive skin with the use ofmoisturizers and emollients.¹⁵

In addition, in the sensitive skin, a decrease in ceramide levels and decrease incapacitance were also detected. ⁶

Dermatitis that lead to the alteration of the epidermis barrier, such as atopicdermatitis, seborrheic dermatitis and rosacea, act as factors predisposing tosensitive skin.²

Sensorineural change

Other evidence reported in the literature was dysfunction of the sensorineuralactivity of the cutaneous nerves. Current studies have demonstrated a thermalreceptor of transient potential V1 (TRPV1) that would act as a facilitator ofneurogenic inflammation.^3,7

Transient receptor potential (TRP) channels are expressed throughout the organismin various tissues and with diverse functions. Both the transient receptorpotential melastatin 8 (TRPM8) and the transient receptor potential ankyrin 1(TRPA1) are stimulated by cold and by certain substances, such as menthol.Transient receptor potential vanilloid 1 (TRPV1) is stimulated by chemicals,heat, cold, mechanical changes in the lipid layer and capsaicin; it acts as acellular sensor, having an important role in pain and inflammation.

In patients with sensitive skin, the increase in sensorineural impulse isinterpreted as unpleasant sensations. Neurotransmitters and their receptors thatregulate the neuroendocrine system of the skin, present in keratinocytes,recognize the stimuli and lead to the release of neurotransmitters as substanceP and calcitonin gene-related peptide (CGRP).^18-20These neurotransmitters induce vasodilation and degranulation of mast cells,which also act on sensory perception through endothelin A and B (ETA and ETB)receptors.

Several published articles have demonstrated the participation of TRPV1 inrosacea and sensitive skin. ^21-22

DIAGNOSIS

Clinical diagnosis

Symptoms (burning, pruritus, tingling, etc.) may or may not be accompanied bysigns such as mild erythema, telangiectasias, xerosis, desquamation, orurticaria. However, in most cases, there are only subjective symptoms.^1,3,6

Patients with cosmetic intolerance usually have multiple subjective symptoms andtherefore, the recording and evaluation of the history arefundamental.²³

Anamnesis and physical examination

It is essential to question the patient about personal, family and occupationalhistory, as well as habits and use of cosmetic products. Complete physicalexamination should exclude signs of inflammation and the presence of otherdermatitis, such as contact and atopic dermatitis.³

Due to the frequent absence of objective physical signs, self-assessmentquestionnaires are valid tools for identifying individuals with sensitiveskin.¹⁰

A possible proposed questionnaire is shown in chart 2. Patients who meet one of the following criteria areconsidered compatible with sensitive skin: ²⁰

Chart 2.

Sensitive Skin Questionnaire

1. Do you consider having sensitivefacial skin?

2. Do you think you have sensitivefacial skin that is prone to irritation?

3. Do you think you have reactivefacial skin (which has a pungency, burning or itching, with orwithout redness)?

4. Do you avoid some cosmetics, whichyou think may cause reactive facial skin (which presentspungency, burning or itching, with or without redness)?

5. Do you consider your facial skin tobe reactive (exhibiting pungency, burning or itching, with orwithout redness) as soon as you contact with cosmetics andtoiletries?

6. Does any cosmetic or toiletry makeyour facial skin appear pungent, burning or itching?

7. Have you ever had any adversereactions on the face due to the use of cosmetics ortoiletries?

8. Does the expression "does nottolerate cold weather or cold environment" apply to your facialskin?

9. Does the expression "does nottolerate warm weather or warm environment" apply to your facialskin?

10. Does the expression "does nottolerate sudden changes in temperature" (e.g. leaving from awarm, indoor environment to a cold, outdoor environment) applyto your facial skin?

11. When coming into contact with thewind, does your facial skin show pungency, burning oritching?

12. When coming into contact with thesun, does your facial skin show pungency, burning oritching?

13. Is your facial skin reactive (pungency, burningor itching, with or without redness) to air pollution?

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Source: Jourdain R, et al, 2005.20

Complementary tests

Although research is being conducted, still no success have been achieved inthe attempts to develop diagnostic tests for objective identification of theentire sensitive skin profile, probably due to the heterogeneity of thesymptoms, the subjectivity of the discomfort reactions and the absence ofvisible signs.

Studies to identify active substances in sensitive skin focus on inflammatorymechanisms, such as vasodilation, edema, mast cell degranulation and releaseof TNF-alpha.

Some models use nerve cell cultures to assess the inhibition ofcapsaicin-induced CGRP peptide release by neurons. Clinical studies use thestinging test and TEWL to evaluate the epidermal barrier.

Because it is still a difficult condition to assess, several trials have beendeveloped to improve the diagnosis of sensitive skin. ²⁴

Sensory reactivity test
This is the cutaneous sensorineural evaluation of the applicationof chemical substances or physical stimuli. The stinging testconsists of the application of 10% lactic acid in a nasolabialsulcus and saline solution in the other (control), evaluatingthe intensity of symptoms reported by the patient according tovisual analog scale. Other substances can be used, such ascapsaicin, ethanol, sorbic acid, among others.^{3,16,19,20,24,25} A patient-reported discomfort scale may beused: ¹⁹
- 0: no discomfort or very mild discomfort
- 1: mild discomfort
- 2: moderate discomfort
- 3: severe discomfort
Such tests are quick and easy to perform, although they aresubjective, lacking predictive value.^3,15
Magnetic Resonance
New studies aimed to evaluate brain activation during provocativetests of cutaneous sensory reactivity through nuclear magneticresonance imaging, both in individuals with normal skin and inthose with sensitive skin, by verifying differences between thetwo groups.²⁶
Irritation tests
These tests measure the signs of skin irritation afterapplication of substances known as irritants (such as sodiumlauryl sulfate), by means of colorimetry or electricalcapacitance measurement, for example. They are noninvasive andobjective exams. However, they require specificdevices.³
Epidermal function tests
Epidermal function tests seek to measure structural orphysiological changes in the skin after application ofirritants. The most used parameters are: measure oftransepidermal water loss, cutaneous pH, epidermalthickness.³
Dermoscopy
Recently, some authors have reported the presence of structuralalterations in the sensitive skin visualized through dermoscopy(demonstrating capillary dilations) and confocal microscopy(showing epidermis with thinner than normalthickness).²⁷
Contact tests
Contact tests and contact phototests should always be consideredin the investigation of the patient with sensitive skin, seekingto exclude allergic and photoallergic contact dermatitis. Inaddition to the standard and complementary batteries (accordingto the medical history), it is essential to test the patient'sown cosmetic products.³
Unlike patients with allergic contact dermatitis, most of thosewith sensitive skin respond negatively to contacttests.²³
Other methodologies
One way to accentuate local conditions by increasing theirritative component of product use would be the behind-the-kneeprotocol in which the substance to be tested is applied in thepopliteal fossa of the individual, Thus, a mechanical frictioncomponent to the traditional test.^1,24
In addition, evidence for type I hypersensitivity, such as pricktests, can be performed when considering the diagnosis ofcontact urticaria.

TREATMENT

The treatment of sensitive skin comprises several steps. In cases where there is apredisposing dermatitis to the symptomatology, the control of the diseasecontributes to the improvement of the condition.

In the acute phase, some active ingredients may be used to relieve symptoms such as:low and medium potency topical corticosteroids (to be used for a short period ofthree to four days) and topical immunomodulators such as pimecrolimus or tacrolimus(they can be indicated for a longer period).

In addition, the use of all cosmetics should be discontinued for a period of twoweeks. After this period, the products are reintroduced one at a time.³ Next, the patient should bereassessed and perform complementary tests.^3,6,8 Prior to the reintroduction of each patient'sproduct, the open test should be performed for each patient.

Proper skin hydration helps to recover and maintain the skin protection barrier.Moisturizers with few components, without perfume and without substances that canirritate the skin (like urea), are indicated.

Photoprotectors should also be used in patients with sensitive skin, since, asalready mentioned, ultraviolet radiation can trigger the symptomatology.

Regarding the formulation of products for sensitive skin, the type of vehicle and itscomponents must be taken into consideration. In addition to the established tests toassess irritability and sensitivity of the products, it is necessary:

To evaluate the stability of components;
To eliminate unnecessary ingredients;
To leave few active principles (minimum or unique for each product);
To eliminate allergens and common irritants from the formulation. Whenthis is not possible, to reduce the concentration of thesesubstances;
To avoid substances that increase the penetration of other substancesinto the skin, such as ethanol or propylene glycol; ⁷
To prefer powder cosmetics to those in cream or lotion;
To use cosmetics easily removable with water;
Not use fragrance products.

The study of the functions of TRPs, especially TRPV1, has led scientists to open upnew perspectives for the treatment of pain. TRPV1 plays an important role in thesymptoms of sensitive skin. Trans-4-tert-butylcyclohexanol was identified as aselective inhibitor of TRPV1, antagonizing its capsaicin-inducedactivation.³ Some protocolsare already using antagonists of this receptor as a new line of treatment ofsensitive skin symptoms.^3,28-30 Another drug described as a TRPV1 inhibitor isfurocoumarin, with properties of decreasing pain related to this receptor.³¹ However, there are stillexperimental studies without clinical trials in which these drugs were used astherapy for sensitive skin.

Demonstration of sensorineural changes through magnetic resonance imaging in previousstudies with patients presenting with sensitive skin suggests that this is not onlya subjective disease, but a dermatitis with a varied symptomatology and few clinicalmanifestations. The evolution of studies of this dermatitis will contribute in thefuture to new therapies and guidelines for patients with sensitive skin.

Footnotes

Conflict of interest: none.

Study conducted at Dermatology Clinic of Santa Casa de Misericórdia deSão Paulo - São Paulo (SP), Brazil.

Financial support: none.

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