The Combination of Mineral Salts and Natural Antioxidants Agents Is Highly Effective in Atopic Dermatitis

Introduction

Atopic dermatitis (AD) is a chronic inflammatory skin disease with exclusive clinical manifestations depending on age groups, race, or ethnicity. It is an important public health problem with a prevalence of 10–20% in children and 1–3% in adults.¹ The most important symptoms are intense itching and eczematous skin lesions.² In most patients with AD, a prolonged cycle of itching and scratching occurs, causing significant morbidity and discomfort. Etiologically, AD has a multifactorial origin with genetic, environmental and immunological factors that interact with each other.³ In the development of AD, as in many other dermatological diseases, a psychosomatic component may be involved.⁴ The symptoms and development of the disease can be exacerbated by psychological factors and stressful personal experiences. People with persistent AD often suffer from psychiatric illnesses. Psychosocial factors during the first years of life have been associated with more severe and persistent atopic diseases.⁵ In fact, AD may be a syndrome with different manifestations in different subpopulations of patients.⁶ In several studies, AD has been related to some non-allergic conditions, such as systemic infections,⁷ to some cardiovascular diseases⁸ and to some neuropsychiatric conditions, including depression,⁹ anxiety¹⁰ and hyperactivity disorders.^8.

Glucocorticoids have been a mainstay in the topical treatment for chronic inflammatory skin diseases for more than five decades. However, the potential for local adverse events, including skin atrophy, striae, folliculitis, telangiectasia, and purpura, limit the extent of body surface area, the duration, and the location of use of topical corticosteroids, especially medium to high potency agents.¹¹ Recently, topical steroid withdrawal has been recognized as a dermatological complication that limits conventional practice to the use of topical glucocorticoids.^12,13 New therapies with anti-IL-4, IL-13, or anti-JAK antibodies have proven effective for AD without the problems associated with corticoid use. However, they carry significant risks of infection by nonspecifically suppressing the immune system.^14.

The most commonly used nonsteroidal topical alternatives for the treatment of chronic inflammatory skin diseases include vitamin D analogs, topical calcineurin inhibitors such as pimecrolimus and tacrolimus, or topical crisaborole, which is a phosphodiesterase-4 (PDE4) inhibitor.¹⁵ However, side effects of conventional topical therapies, complicated regimens, and inadequate efficacy of some products, compromise treatment success.

Dead Sea Water (DSW) is one of the oldest treatments for skin diseases.¹⁶ The healing properties of DSW have been attributed to its mineral salts concentration, particularly magnesium.¹⁷ In a study evaluating the effects of DSW, 30 patients with AD were enrolled for six weeks. Patients were divided into two arms: those treated with a 5% solution of DSW and others used as control. A significant improvement was observed in patients treated with DSW.^18. Many efforts have been made to understand the medical benefits of Dead Sea salt baths.¹⁹ Despite numerous clinical studies, the benefits of balneotherapy in psoriasis are not conclusive. While some studies present conclusive data^20,21 others have shown that Sun exposure is the main factor producing beneficial results for psoriasis in Dead Sea spa therapy.²² The separate influence of Sun exposure and the Dead Sea salts was studied in 81 patients with psoriasis. The improvement of subjects who only bathed in Dead Sea water was 28%, while in those who only sunbathed it was 73%, and in those who did both it was 83%.^23.

These findings suggest that mineral salts including magnesium salts and other salts could be used as a treatment for AD due to their antioxidants effects. This hypothesis was based on the observation that bathing in a magnesium-rich Dead Sea salt solution improves skin barrier function and hydration, and reduces inflammation in atopic dry skin.^18. With this purpose, a prospective study was carried out to determine the effect of mineral salts and natural antioxidants agents as a treatment for AD. This would eliminate the use of corticosteroids and their unwanted side effects in AD.

Materials and Methods

Patients

This project was designed as a prospective study conducted at Umbert Institute of Dermatology Corachan Clinic (Barcelona, Spain). All participating subjects were patients of the Umbert Institute of Dermatology (Corachan Clinic, Barcelona, Spain). Recruitment took place from January 2025 to June 2025. The patients participating in this study were those who arrived at the dermatology consultation sequentially, who met the selection criteria and who agreed to participate in the study. The inclusion criteria for this study were patients aged between 20 and 66 years of both sexes (18 females and 16 males) with confirmed AD (American Academy of Dermatology Consensus Criteria) and symptoms including eczema and itching²⁴ with moderate-to-severe disease activity and affected body surface area 10% or higher at both screening and baseline, and a documented history (within 1 year) of inadequate response to topical medications. No significant high levels of IgE were observed in any of the patients included in this study. Patients with diagnosis of dermatitis along with other dermatological conditions or other undercurrent systemic diseases were excluded from the study. The following laboratory abnormalities were used as exclusion criteria: serum creatinine concentration higher than 1.5 mg/dL; alanine aminotransferase or aspartate aminotransferase concentration 2.5 times or higher than the upper limit of normal; and neutrophil count of less than 5 × 10³ per μL; and other laboratory abnormalities that were not specified in the protocol that might affect the completion or evaluation of the study, as judged by the investigators.^25.

The studies involving human participants were reviewed on 2024/12/10 and approved by the ethics committee research with medications (CEIm), Hospital group Quiron Salud-Catalunya, Spain with protocol number 2024/48-DER-UMB. All patients gave written informed consent to participate in this study. In addition, photo consent statements had been signed by all the participants.

Clinical Evaluation

For the clinical evaluation, the following areas were photographed at each visit: scalp, forehead, eyes, ears, face, chin, neck, trunk, arms, hands, legs, genital area, and feet. The photographs were reviewed to quantitatively assess the degree of disease severity. The following clinical measures were used: Eczema Area and Severity Index (EASI), Scoring Atopic Dermatitis (SCORAD), Body Surface Area (BSA) and Validated Investigator Global Assessment for Atopic Dermatitis (vIGA-AD). The EASI assessment with a scale of 0–72, integrates body surface and the intensity of lesioned skin into one composite score.^26,27 The SCORAD Index with a scale of 0–130, calculates the following formula A/5 + 7B/2 + C. A is defined as the extent (0–100), B is defined as the intensity (0–18) and C is defined as the subjective symptoms (0–20).²⁸ Compared to several other methods, these two were considered satisfactorily validated and recommended for use in clinical assays.²⁹ BSA (0–100) is a measure of how much skin is impacted by psoriasis and can be used to track psoriasis over time.³⁰ As for vIGA-AD (0–4), this score was selected using the descriptors that best describe the overall appearance of the lesions at a given time point.³¹

Patient-reported measurements were also used: Patient-Oriented Eczema Measure (POEM), Dermatology Life Quality Index (DLQI) and the pruritus Numeric Rating Scale (NRS). POEM (0–28) is a simple validated symptom measure for atopic eczema which records seven symptoms shown to be important to patients asking about the frequency of seven symptoms valuated each from 0 to 4 (itch, sleep disturbance, dryness, flaking, weeping or oozing, bleeding and cracking) in the past seven days.³² DLQI (0–30) measures the impact of psoriasis over the previous week using 10 questions on how the disease impacts different areas of life, such as working/studying, sport/leisure activities, daily activities, interpersonal relationships and physical and emotional well-being. Questions were scored on a 4-point scale to assess severity.³³ NRS (0 to 10) is a single-item measurement used to assess skin pain severity over the past 24 hours with the question “How painful was your skin over the past 24 hours?” on a 10-point scale from 0 (not painful) to 10 (extremely painful).³⁴ In addition, the disease characteristics included age of symptom onset, duration of disease, clinical features present, sites of AD involvement, difficult locations of AD involvement, and atopic comorbidities.

No significant high levels of IgE were observed in any of the patients included in this study. Patients with diagnosis of dermatitis along with other dermatological conditions or other undercurrent systemic diseases were excluded from the study. In addition, patients with renal failure were excluded due to their risk of increasing high magnesium values,^35,36 as well as patients with hypertension due to their risk of increasing blood pressure.³⁷ Data presented in this study included two visits: one before treatment and one at the end of the 2-week treatment.

Study Design

Upon diagnosis, patients received a topical master formula in the form of a spray and a cream. After getting up, the patients had to spray the formula on the damaged skin for 20 minutes, and then they had to apply the cream on the damaged skin. Before going to bed, the patients had to apply the cream again on the damaged skin. This treatment had to be followed for 15 days. After medical treatment, photos of the damaged skin were taken (Figure 1). In some cases, a skin biopsy was done on days 1 and 15 and processed for morphology and histochemistry.

Figure 1 Schematic diagram of study schedule.

The master formula corresponding to the spray and cream are under European patent number 4335431 and patent applications (numbers EP4335431A1, WO2025022033, US18/997843, INP202517015652). The composition of the spray is as follows: magnesium sulfate 0.31 (wt %), sodium chloride 0.17, sodium fluoride 0.006, potassium chloride 0.06, Rosemary dry extract 0.009, fermented papaya extracts 0.006, green tea extracts 0.0006, ferulic acid 0.0006, nicotinamide 0.03, zinc gluconate 0.009, melatonin 0.0000006, resveratrol 0.0000009, chamomile glycolic extract 0.0000006, water Q.S. The composition for the cream is as follows: NaCl 0.336 (wt %), ferulic acid 0.012, NaF 0.012, nicotinamide 0.06, MgSO4 0.6216, papaya dry extract 0.012, Zn gluconate 0.018, Rosemary dry extract 0.018, green tea dry extract 0.0012, chamomile glycolic extract 0.006, Melatonin 0.004, water-alcohol solution 0.186, vitamin C 1, vitamin E-acetate 1, Aqua preservatives 20, Oil-in-water emulsion Q. S. Both the spray and the cream are for topical use. In some cases, patients may be allergic to one of the components and thus, depending on the component, both the spray and the cream were reformulated specifically for such patients, eliminating the component producing the allergy.

Histological Studies

Punch biopsies of the patients’ damaged skin were obtained from 10 patients before and after treatment. Sections of 3μm formalin-fixed and paraffin-embedded tissue of each sample were stained using Hematoxylin and Eosin for histopathological evaluation. Two independent evaluators (I.U. and J.G.) simultaneously analyzed each sample and recorded the following histopathological features: epidermal spongiosis (absent, mild, moderate, severe), epidermal parakeratosis (present, absent), epidermal hyperplasia (absent, mild, moderate, severe), dermal edema (present, absent), dermal fibrosis (present, absent), perivascular inflammation (none, mild, moderate, severe), neutrophils in dermis (present, absent), eosinophils in dermis (present, absent), and finally dermal vascular congestion (present, absent). Other morphological abnormalities were also noted such as intraepidermal blister formation, acantholysis, and other findings.^38,39 To compare the histological differences before and after treatment we summarized the different parameters obtaining the total histology assessment. Independently the epidermis thickness was measured. The epidermal thickness was evaluated as the average in five fields per section. Quantitative analysis was done using ImageJ software.⁴⁰

In addition, immunohistochemistry tests were conducted in 7 patients. All immunohistochemical stainings were performed in 3-μm thick sections containing the full samples. They were performed using a BenchMark immunostainer (Ventana, Tucson, Arizona). The following antibodies were used in the present study: CD20 (clone L26; Ventana, Tucson, Arizona), CD3 (clone 2GV6; Ventana, Tucson, Arizona), CD4 (clone SP35; Ventana, Tucson, Arizona), CD8 (clone SP239; Ventana, Tucson, Arizona), CD117 (clone EP10; Ventana, Tucson, Arizona). All immune-stained slides were simultaneously reviewed by 2 authors (I.U. and J.G.) in a blind manner. The number of positive cells was counted using light microscopes.

Data Analysis

To compare the parametric variables, paired t tests were done for individual values before and after treatment. In addition, non-parametric linear Gaussian test was performed to find correlations between the levels of variables. All statistics analyses were accomplished using GraphPad Prism, version 10 (GraphPad Software, San Diego, California, USA).

Results

The Treatment with Mineral Salts and Natural Anti Inflammatory Agents Drastically Reduced Disease Severity

Using the visual scorings, a strong difference was observed before and after two weeks of treatment. The difference of EASI, SCORAD, vIGA-AD and BSA scores in all patients was strongly significant (Figure 2A–D). Moreover, the improvement of the injuries before and after treatment in the SCORAD score correlated with the improvement in the EASI score (r= 0.50, p<0.001; Figure 2E). Concerning the patient-reported measures for itching, the three systems used, DLQI, POEM and NRS, showed that, subjectively, itching was reduced in all patients and disappeared in many (Figures 2F–H).

Figure 2 Effect of treatment on the clinical evaluation parameters (n= 34). (A) EASI score. (B) SCORAD Score. (C) viAG-AD score. (D) BSA score. (E) Correlation between SCORAD and EASI. (F) DlQI score. (G) POEM score. (H) NRS score. Data were analyzed using the paired t test and non-parametric Gaussian test was performed for correlation.

The photos of the damaged areas before and after treatment showed the disappearance of skin lesions (Figures 3 and 4 and Supplementary Figures S1–S8). The efficacy of the treatment was independent of the location of the lesions: anus (Figure 3A and Supplementary Figure S1A–S1B), arms (Supplementary Figures S1C, S1D, S2A–S2D), back (Supplementary Figure S3A and S3B), face (Figure 3B and 3C, and Supplementary Figure S3C and S3D), feet (Supplementary Figure S4A), hands (Figure 4A and Supplementary Figures S4B-S4D and S5A), legs (Figure 4B, and Supplementary Figures S5B, S5C, S5D, S6A, S6B and S6C), neck (Figure 3A, and Supplementary Figure S6D), penis (Supplementary Figure S7A), testicles (Supplementary Figure S7B), trunk posterior (Supplementary Figure S7C) and vulval area (Supplementary Figures S8A and S8B).

Figure 3 Effect of treatment on patient 1 (A), patient 2 (B) and patient 3 (C).

Figure 4 Effect of treatment on patient 4 (A) and patient 5 (B).

The beneficial effect of mineral salts and natural antioxidants agents was also independent of the patient’s age, symptoms at the onset, duration of disease, clinical features present, sites of AD involvement, difficult locations of AD involvement, and atopic comorbidities. This topic treatment was very well tolerated, with no adverse events reported.

Histological Studies on the Effect of Treatment with Mineral Salts and Natural Antioxidants Agents

In 10 patients a biopsy before and after the treatment with mineral salts and natural antioxidants agents was performed. The histopathological evaluation was double-blinded and quantitated following the criteria described under Material and methods. Summarizing all the criteria before and after treatment, a significant difference was observed (p<0.01, Figure 5A). The effect of the treatment on the thickness of epidermis, a marker of AD,⁴¹ was also determined. There was a strong difference before and after treatment (p<0.001, Figure 5B and Supplementary Figures S9 and S10). Another important parameter was the lymphocytic infiltration, which also showed a significant difference before and after treatment (p<0.01; Figure 5C).

Figure 5 Histological studies of biopsies stained with H&E (n=10). (A) Total histological assessment (Summatory of histopathological features. (B) Lymphocytic infiltration. Data were analyzed using the paired t test.

Immunohistochemistry tests were evaluated in 7 biopsies. A barely significant (p<0.05) difference was found with the mineral salts and natural antioxidants reagents treatment in all cases: for T lymphocytes (CD3, CD4 and CD8, Figure 6A–C respectively), B lymphocytes (CD20, Figure 7A) and mastocytes (CD117, Figure 7B).

Figure 6 Immunohistochemistry studies of biopsies stained with the indicated antibodies (n=7). (A) CD3, (B) CD4, (C) CD8. Data were analyzed using the paired t test.

Figure 7 Immunohistochemistry studies of biopsies stained with the indicated antibodies (n=7). (A) CD20. (B) CD117. Data were analyzed using the paired t test.

These studies are consistent with the reduced inflammation observed in skin treated with mineral salts and antioxidants compounds. This topic treatment was very well tolerated, with no adverse events.

Discussion

Intrinsic AD is associated with chronic itching that produces a damaging clinical condition. The heterogeneity of this disease results in a major dispute regarding clinical treatment. Genetic studies and single-cell sequencing data delivered neuro-immunologic links that explain the induction of itching through different mechanisms. Therefore, there is no effective therapy for all cases. This study showed that the combination of topical mineral salts and other salts and natural antioxidants components was a highly effective treatment for AD regardless of its anatomical location. The efficacy of this treatment was demonstrated through clinical parameters, patient satisfaction, photographs and histology of the lesions, as well as counting inflammatory cells with immunohistochemistry tests. This formula was based on the observation of the effectiveness of balneo-therapy with Dead Sea bath salt in psoriatic patients where manganese and lithium seem to play a significant role.⁴² Other mineral salts such as sodium fluoride at low concentrations have been shown to be effective as anti-inflammatory compounds and in wound healing.⁴³ The combination of potassium chloride and sodium chloride seems to be useful in the treatment of AD.^44.

There is emerging evidence indicating that infections may be a trigger for psoriasis.⁴⁵ Virus-recognizing receptors are critical for these processes. Nucleotide-binding leucine-rich domains (NLRs; NOD-like receptors) play essential roles in virus detection and are characterized by their pro-inflammatory biological function. Specifically, these receptors involve the formation of multi-protein complexes defined as inflammasomes that regulate the production of cytokines such as IL-1β, IL-18, and pyroptosis, or the induction of NF-ΚB.⁴⁶ In addition, inflammasomes cleave pro-IL-1 and pro-IL-18, converting them from inactive to active pro-inflammatory forms⁴⁷ This may contribute to the origin or aggravation of psoriasis. Topical and oral antioxidants modulate the immune response to NLR.⁴⁸ This research with magnesium salts and other salts, antioxidants, and plant extracts confirms previously published results.⁴⁹ For these reasons, a set of natural antioxidants compounds whose effect we have previously demonstrated were added.⁵⁰

Dermatitis leads to a significant increase in epidermis (hyperplasia), and therefore any treatment aims at inducing a significant decrease in physiological levels. However, non-lesional AD skin is clearly distinct from normal skin in terms of terminal differentiation and some immune abnormalities showing a cutaneous expansion of T cells.⁵¹ Although patients do not exhibit clinical symptoms, superficial plexus depth in relation to healthy individuals cannot be ruled out.⁵² For this reason, patients were used as internal controls both before and after treatment in the present study.

The results of histopathology and immunohistochemistry tests presented here are supported by previous observations. Danby et al⁴¹ showed that treatment with a non‐steroidal anti‐inflammatory agent (crisaborole ointment) decreased pathologic epidermal thinning in patients with AD. More interestingly, histological evaluations showed that lesions were significantly reduced when compared to treatment with topical glucocorticoids.

Recently, the beneficial effects of magnesium oil have been recognized due to its anti-inflammatory properties. In humans, transdermal administration of magnesium oil improves the quality of life of patients with fibromyalgia and helps reduce chronic pain, fatigue, depression, and sleep disorders, along with pain and fatigue associated with arthritis.⁵³ Magnesium nanoparticles induce wound healing due to their antioxidants and antibacterial effects.^54.

One important question is understanding how magnesium works in the treatment of AD. However, there are some evidence that helps understanding its role as a cutaneous antioxidant agent. Skin lesions in AD occur when the patient scratches due to itching. This causes a tear exposing the dermis to the outside environment. In addition, there is an increase in the permeability of the outermost layer of the skin, the stratum corneum. This is due to the terminal differentiation of epidermal keratinocytes, which transform into protein-rich cornets surrounded by extracellular layers of epidermal lipids, which confer a permeability barrier function.⁵⁵ Increased skin permeability leads to environmental stresses that cause inflammation.^55,56

As in any type of inflammation, the first thing that occurs is the expression of E-selectin by the vascular endothelium. This allows neutrophils to access the inflammatory focus from the blood by binding to this molecule.⁵⁷ This results in the production of a vicious cycle that further deteriorates the structure of the stratum corneum. Neutrophils infiltrating the epidermis secrete IL-17A, which acts on keratinocytes disrupted by neutrophil infiltration to produce IL-23. In this way, the framework for the IL-23/Th17 axis is created, which in turn maintains or exacerbates psoriasis.⁵⁸ Furthermore, neutrophils can have local and systemic effects on cells of innate and adaptive immunity, as well as on resident cells in the skin, including keratinocytes. The aberrant formation/clearance of neutrophil extracellular traps (NETs) in systemic autoimmunity and chronic inflammatory diseases has been associated with the externalization of modified self-antigens into the peripheral blood and tissues. NETs can affect the function of many cells, including macrophages, lymphocytes, dendritic cells, fibroblasts, and keratinocytes. Evidence has shown that neutrophils play a key role in the pathogenesis of psoriasis and other chronic inflammatory conditions.⁵⁹ NETs play a key role in the induction of type 17 T helper cell responses.⁶⁰ The function of neutrophils is to destroy microorganisms, despite causing their own death or apoptosis. After 24–48 hours, the endothelium stops expressing E-selectin and instead expresses ICAM-1 (intercellular adhesion molecules), which allows the extravasation of Ly6C^high monocytes. These monocytes then turn into macrophages in the dermis, destroying the remaining bacteria (pro-inflammatory phase or M1) and phagocytizing apoptotic bodies. After this, macrophages express an anti-inflammatory or M2 phenotype and tissue reconstruction or healing begins.^61,62 Topical treatment with magnesium salts prior to ultraviolet irradiation not only reduces the number of Langerhans cells in the epidermis, but also reduces their activity as antigen-presenting cells in the skin.^63.

Magnesium acts at different levels in the inflammatory processes. In vitro and in vivo studies have shown that the effects of magnesium are due to its immunosuppressive capacity. One of the mechanisms for destroying infectious agents, in both neutrophils and macrophages, is the production of reactive oxygen species (ROS). Under experimental conditions, it has been demonstrated that magnesium acts on the skin as a ROS scavenger, increasing the number of fibroblasts and blood vessels, as well as the amount of collagen.⁶⁴ It has been demonstrated that magnesium induces an innate immune response in the polarization of macrophages causing them to switch from a pro-inflammatory (M1) to an anti-inflammatory (M2) phenotype.^65,66

It is well known that skin atrophy is caused by the inhibition of cell proliferation in the dermal and epidermal layers. The reduced growth of fibroblasts in the dermis is related to a diminished collagen synthesis. Therefore, a major objective in the treatment of AD should be to accelerate skin barrier recovery. Magnesium salts accelerate skin barrier recovery.⁶⁷ By increasing the permeability of the skin, environmental aggressions occur that result in inflammation.⁵⁶ As inflammation develops, neutrophils enter the capillaries and secrete IL-17A, which acts on keratinocytes disrupted by neutrophil infiltration to produce IL-23. This creates the framework for the IL-23/Th17 axis, which acts to maintain or exacerbate psoriasis.⁵⁸ In addition, hypertonic saline solution enhances intracellular bacterial killing while attenuating receptor-mediated activation of pro-inflammatory cascades.⁶⁸ In the biopsies of the patients in this study, treatment with mineral salts and natural antioxidants compounds has shown to repair the epidermis and the dermis, thus eliminating the problems caused by increased membrane permeability.

Physiological itch results from the introduction in the skin of a pruritogen that activates some receptors of unmyelinated neural C fibers with cell bodies in the dorsal root ganglion. From there, the signals travel to the spinothalamic tract and the parabrachial nucleus until they reach the somatosensory thalamus where they are transmitted to the cortex provoking the itch feeling.⁶⁹ The receptor of unmyelinated C fibers is G protein–coupled receptors (GPCRs) that induce the opening of ion channels to produce action potentials, and thus nervous activation begins. The receptors are transient receptor potential vanilloid 1 [TRPV1] and transient receptor potential ankyrin 1 [TRPA1], and voltage-gated sodium channels [NaV s].⁷⁰ There are two itch-sensitive neurons subtypes, histaminergic (acute itch) and non-histaminergic (chronic itch). The itch signals ascend through the spinal cord using separate tracts, and brain activation is different. Histamine is released mainly by mast cells and other immune cells and through H1 and H4 receptors on histaminergic nerves; then, phospholipase is released thereby activating TRPV1.⁷⁰ In addition, histaminergic neurons discharge neuropeptides such as calcitonin gene–related protein (CGRP) and substance P (SP) which cause “neurogenic inflammation”, producing local vasodilation, plasma extravasation, and mast cell degranulation. The non-histaminergic pathway is activated by proteases, cytokines/chemokines, and amines that produce phospholipases in non-histaminogenic nerves, activating the TRPV1 or TRPA1 receptors that in turn activate Na V 1.7, and NaV 1.7 controls action potentials in neurons.⁷⁰ Studies using animal models showed that magnesium sulfate can block the receptors TRPV1 and TRPA1 inhibiting pain.⁷¹ In another study, magnesium ions released from implants have shown to enhance the synthesis of CGRP in the dorsal root ganglion and the release of its sensory nerve endings.⁷² These data suggest that magnesium may control neuro-inflammation.

One of the biggest problems with AD is that once symptoms disappear, the disease recurs. Attempts have been made to control it with atopic corticosteroids to reduce inflammation and emollients to improve the integrity of the barrier.⁷³ However, three-quarters of patients are not satisfied with current treatments.⁷⁴ Recently, an excellent correlation has been found between the severity of AD and the intensity of spinal biomechanical alterations.⁵⁰ In these patients, treatment with antioxidants creams reduced the EASI score, but after three months, dermatitis symptoms flared again and the EASI scores returned to baseline values. In contrast, in patients treated with chiropraxis, the EASI levels remained low three months later. This study shows the importance of spinal biomechanical alterations in the etiology of AD and that alternatives such as chiropractic treatment should be sought.⁵⁰ These studies also indicate that treatments should continue to ensure that subclinical inflammation is resolved. These strategies have been shown to increase the remission period between flares.⁷⁵ The strategy for developing long-term treatments for dermatitis must take into account safety and efficacy as the two fundamental pillars. The treatment described herein meets these requirements and can be used as a preventative treatment, demonstrating its high efficacy and lack of side effects.

Conclusions

The results of a new treatment consisting of a combination of mineral salts magnesium and other salts and natural antioxidants compounds demonstrates its high efficacy in AD. This cream is moisturizing, antioxidant, and antipruritic. It works by stabilizing the epidermal barrier and controlling bacterial, fungal, and viral flora, thus preventing the development of autoimmune processes. This treatment is very well tolerated and has no side effects. The lack of adverse events means that this treatment can be used for long periods of time to ensure that sub‐clinical inflammation is inhibited.⁵¹ This treatment can be used preventatively to alleviate the increasingly frequent problems of itching due to neurogenic inflammation caused by spinal biomechanical alterations.