Atopic dermatitis is a highly complex, heterogenous, chronic inflammatory skin disease. It is characterised by a pruritic, erythematous rash with an unknown immunological mechanism. Even though many paediatric cases are temporary, atopic dermatitis is commonly the first stage of the atopic march and chronic, active disease. Up to 75% of atopic dermatitis patients claim that it is first manifested in their childhood.¹

Objectives

In a study, potential signalling nodes, that contribute to disease heterogeneity and progression as well as circulating inflammatory patterns in atopic dermatitis-affected children, were characterised and identified.¹
In another study, it was investigated whether specific skin biomarkers in stratum corneum tape strips collected at 2 months of age from infants with clinically normal skin are different in children who develop atopic dermatitis compared to children who do not develop it.²

Methods

IgE: Immunoglobulin E; NMF: Natural moisturising factor; PBMC: Peripheral blood mononuclear cell; SB: Sphingoid base; SCORAD: SCORing Atopic Dermatitis.

Results

CASP-8: Caspase-8; CD4: Clusters of differentiation 4; EASI: Eczema area and severity index; IL: Interleukin; MMP-10: Matrix remodelling proteins; NMF: Natural moisturizing factor; TARC/CCL17: Thymus and activation-regulated chemokine/ CC chemokine ligand 17; AD: Atopic Dermatitis; NMF: Natural moisturizing factor; SB: Sphingoid base; SCORAD: SCORing Atopic Dermatitis.

Figure 1: Visual representation of cytokine correlations to each other (thickness of connecting line) and to SCORAD (size of circle) across all time points of the study.¹

Adapted from: Engle SM, et al. Clin Exp Immunol. 2022.

CASP-8: Caspase-8; CCL19: Chemokine ligand 19; CD5: Clusters of differentiation 5; CXCL12: C-X-C motif chemokine 12; IL: Interleukin; Eotaxin-2: CC chemokine ligand 24; TNFRSF9: Tumour necrosis factor-receptor superfamily member 9; TRAIL: Tumour necrosis factor-related apoptosis-inducing ligand; TRANCE: Tumour necrosis factor-related activation-induced cytokine; SCORAD: SCORing Atopic Dermatitis.
Purple colour denotes correlations ≥0.35. Dark blue colour denotes correlations ≤0.35.¹

Conclusions

SB: Sphingoid base; TARC/CCL17: Thymus and activation-regulated chemokine/CC chemokine ligand 17.

Acne vulgaris is a common skin condition. Acne-causing hormones such as insulin, insulin-like growth factor 1, and androgens are influenced by diet and metabolism. It has been known for many years that increased dairy consumption and foods with high glycaemic index affect the levels of hormones associated with acne aetiology.¹

Objectives

The researchers performed a systematic assessment of high-quality evidence on the association between the dietary glycaemic index and dairy intake with acne genesis.¹

Methods

• Using the 2020 Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, a thorough search of the MEDLINE database was conducted.¹
• The quality of the evidence was evaluated using the Newcastle–Ottawa Quality Evaluation Scale.¹
• After being screened for inclusion and exclusion criteria, 34 articles were included in the final data and the level of evidence (LOE) assessment.¹

Results

• Most of the included studies (82.4%) were observational, while the remaining studies were interventional controlled trials.¹
• 17.9% of the observational studies exclusively assessed the association between glycaemic index/glycaemic load and acne.¹
• 35.7% exclusively commented on the association between dairy and acne and 46.4% described the association of dairy products and glycaemic index/glycaemic load with acne.¹
• All the interventional trials included in the study examined the effect of glycaemic index/glycaemic load on acne.¹
• There were no randomized controlled trials (RCT) on the link between dairy consumption and acne, conclusions were made on observational studies.¹

Conclusions

The number of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cases has been increasing worldwide and numerous dermatologic manifestations associated with SARS-CoV-2 infection have been reported. Estimated rates of coronavirus disease 2019 (COVID-19) related cutaneous manifestations range from 4% to 20.4%.¹

Objectives

The study's objective was to review various skin manifestations brought on by SARS-CoV-2 infection.¹

Methods

• The researchers used specific key words to conduct searches on PubMed.¹
• In the narrative review, articles that were published between September 2014 and August 2021 were included.¹

Results

Cutaneous manifestation1	Clinical presentations1	Histopathology1	Prognosis/Treatment1
Chilblain-like or pernio-like lesions	Dusky, erythematous to oedematous papules, nodules, plaques, or, less frequently, bullae formation on acral surfaces	Superficial and deep perivascular lymphocytic infiltrate of predominantly CD3+/CD4+ T cells. Negative immunofluorescence.	Chilblain-like or pernio-like lesions are self-limiting, lasting from 10–14 days and, occasionally, for a few months. It will benefit from staying out of the cold and donning warm, protective clothing, gloves, and socks. CBLL can also benefit from pharmacological treatments, such as topical corticosteroids, topical and oral vasodilators like nitric oxide paste, oral calcium channel blockers, pentoxifylline, sildenafil, or aspirin.
Maculopapular or morbilliform lesions	Erythematous macules with areas of normal-appearing skin on the trunk and extremities with pruritus	Spongiotic dermatitis with eosinophils in earlier lesions, or mixed perivascular lymphocytic infiltrate with histiocytes in later lesions	Topical corticosteroids may be used to treat mild cases of pruritus. Systemic corticosteroids may be used in severe cases.
Urticarial lesions	Migratory, pruritic, oedematous, variably-sized wheals within 24 hours, without bruising or hyperpigmentation and/or angioedema	Perivascular lymphocytic infiltrate, scattered eosinophils, and upper dermal oedema with no virally induced cytopathic changes	These lesions might be present prior to the onset of a fever or alongside pyrexia and cough. Lesions are typically a sign of a serious illness. Second-generation antihistamines are used to treat the symptoms of SARS-CoV-2-related urticaria. Short-term use of antihistamines and steroids can improve urticaria lesions.
Vesicular or varicella-like lesions	Small, scattered monomorphic vesicles on the trunk with mild or absent pruritus, pain, or a burning sensation	Vacuolar degeneration of basal layer, apoptotic keratinocytes, mild inflammatory infiltrate, and multinucleated keratinocytes	Varicella-like lesions in SARS-CoV-2–infected patients have a mixed prognosis. These lesions typically receive supportive treatment. They self-resolve without leaving any scars after a few days.
Livedoid lesions	Livedo reticularis: symmetric, lace-like dusky patches forming pale-centred rings along blood vessels. Livedo racemosa: irregular and asymmetrical dusky patches along blood vessels	Epidermal necrosis, superficial and deep dermis thrombosis vasculopathy in small and medium vessels, sweat gland necrosis, mild perivascular lymphocytic infiltrate, and complement deposition in the vessel walls	Adults with livedoid lesions commonly require support from intensive care units. In extreme circumstances, necrosis as well as skin scabbing and sloughing may be present. For milder lesions, active non-intervention is a possibility, whereas severe cases may require everything from intensive supportive care to symptomatic treatment.

CBLL: Chilblain-like lesions; CD3: Cluster of differentiation 3; CD4: Clusters of differentiation 4; SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2; T cells: T lymphocyte.

Adapted from Huynh T, et al. Am J Clin Dermatol. 2022.

Images captured from Huynh T, et al. Am J Clin Dermatol. 2022.

Conclusions

CBLL: Chilblain-like lesions; COVID-19: Coronavirus disease 2019; SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2.

• Actinic keratosis is a prevalent precancerous cutaneous neoplasm that develops on skin that has been exposed to the sun for an extended period.¹
• Although a few susceptibility loci, including interferon regulatory factor 4 (IRF4), tyrosinase gene (TYR), and melanocortin 1 receptor (MC1R), have been identified, there is a moderate genetic component to actinic keratosis susceptibility.¹

A genome-wide association study (GWAS) of actinic keratosis was conducted in non-Hispanic white participants of the Genetic Epidemiology Research on Adult Health and Aging (GERA) cohort (n=63,110, discovery cohort), with validation in the Mass-General Brigham (MGB) Biobank cohort (n=29,130).¹

Figure 1:Manhattan plot of GWAS meta-analysis of actinic keratosis combining results of GERA and MGB Biobank cohorts (n=92,240).¹

Adapted from Kim Y, et al. Commun Biol. 2022.

BNC2: Basonuclin 2; DEF8: Differentially expressed in FDCP 8 Homolog; FOXP: Forkhead Box P; HERC2: Homologous to the E6-AP carboxyl terminus And RLD Domain Containing E3 Ubiquitin Protein Ligase 2; HLA-DQA1: Human leukocyte antigen -major histocompatibility complex, class II DQ alpha 1; RALY: RNA binding protein; MMP24: Matrix metalloproteinase-24; SLC45A: Solute carrier family 45 members 2; TYR: Tyrosinase gene; TRPS1: Trichorhinophalangeal syndrome type I.

The Y-axis represents log-scale p-values, and loci with the smallest p obtained from the logistic regression are labelled with the nearest or corresponding gene’s name. Known loci are in dark blue triangles and newly identified loci in discovery analysis are in purple triangles and newly identified loci in meta-analysis are in light blue triangles.¹

Atopic dermatitis (AD) is one of the most frequently encountered chronic inflammatory skin condition in the UK.^1,2 It affects both, children and adults; however, the paediatric population is predominantly affected.^3,4 The overall prevalence of diagnosed AD in European paediatric population was found to be the lowest in Germany (8.4%), while the highest prevalence was observed in the Southern European countries of Spain (18.6%) and Italy (17.6%). Figure 1 depicts the prevalence of AD in children, across different regions of the globe.⁵ The Global Burden of Disease 2017 data highlights that this chronic condition is highly prevalent in Asian countries, particularly in the high-income territories.⁶

The burden of this disease is substantially high⁷ and the quality of life of AD patients may be significantly reduced.^7,8 Several studies have highlighted the need for psychological support for patients with AD as well as their caregivers to help them cope with the disturbed sleep, disruption of daily life activities, depression, anxiety, and difficulty in maintaining social life.^7,8 Also, AD patients are always prone to infections owing to the defective skin barrier, dysregulated immune system, and altered skin microbiome, which may cause complications in these patients.^9-11 Health care utilization is significantly increased in AD patients, which also results in significant financial burden.¹² Recent developments have promulgated the role of keratinocytes, as a component of the innate and adaptive immune system, in regulating the release of several key molecules triggering inflammatory reactions and immune responses in AD. A better understanding of the pathogenesis would help formulate appropriate treatments to improve the quality of life in these patients and to prevent allergic disorders associated with AD.¹³

AD has been found to be genetically inheritable.^14,15 AD patients express distinct immune and barrier signs, as detected by RNA-sequencing tape strip profiling, which is a minimally invasive technique. Recent studies propose the use of this technique as an alternative to the regular biopsies for detection of AD (both lesional and non-lesional) biomarkers, although further studies are warranted to establish this fact.^16,17 With the development of more targeted therapies, AD biomarkers are valuable sources to understand patient-specific molecular dysregulations differing between the several AD subtypes,¹⁷ contributing to more tailored treatment and may help to predict which patients are most likely to benefit from the specific targeted therapies.¹⁸

A short time ago, treatment for AD mainly targeted emollients, topical steroids, and topical calcineurin inhibitors. Patients who were severely affected by the disease were encouraged to take systemic immunosuppressants. Novel therapeutic strategies, including biologics, aiming at different molecular events involved in the development of AD, have been developed recently.^19,20 These options mainly target the type 2 immune pathway and have been found to control the disease effectively and are well-tolerated.^1,2,21 The emerging systemic therapies include monoclonal antibodies targeting IL-4,²² IL-¹³,23 IL-31,²⁴ IL-33, thymic stromal lymphopoietin,^9,25 and OX40.²⁶ Latest advances on some probiotic preparations have been shown to be beneficial in decreasing allergic symptoms of AD in children; yet further studies with larger sample sizes are warranted to elude the robustness of this evidence.²⁷ Treatment of a pregnant patient for AD, using systemic drugs, may pose a challenge as it can affect the unborn child. Recent studies advocate that treatment with topical agents should be considered in pregnancy.^28,29 The European task force on atopic dermatitis recommends the use of UV radiations in addition to topical corticosteroids. It also adds that moderate sun exposure may be used in such patients.²⁹ Although there have been many promising treatment options for AD, which particularly affects the high-income countries of Asia, further planned prospective studies involving the long-term follow-up of AD patients and cost-effective analyses are warranted to aid clinical decisions in the application of these novel drugs for its treatment.

Source:
1. Plant A, Ardern-Jones MR. Clin Med (Lond). 2021;21(3):177-81. 2. Cork MJ, et al. Journal of Dermatological Treatment. 2020;31(8):801-9. 3. NHS.Available from: https://www.nhs.uk/conditions/atopic-eczema/. 4. Kowalska-Olędzka E, etal. Journal of Drug Assessment. 2019;8(1):126-8. 5. Silverberg JI, et al. Ann Allergy Asthma Immunol. 2021;126(4):417-28.e2. 6. Urban K, et al. JAAD International. 2021;2:40-50. 7. Ražnatović Ðurović M, et al. Ital J Dermatol Venerol. 2021;156(1):29-35. 8. Capozza K, et al. Dermatitis. 2020;31(3):223-7. 9. Wang V, et al. Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology. 2021;126(1):3-12. 10. Ong PY,Leung DY. Clin Rev Allergy Immunol. 2016;51(3):329-37. 11. Cai SC, et al. Br J Dermatol. 2012;166(1):200-3. 12. Sandhu JK, et al. Pediatr Dermatol. 2019;36(3):303-10. 13. Chieosilapatham P, et al. Clin Exp Immunol. 2021;204(3):296-309. 14. Brown SJ. J InvestDermatol. 2021;141(1):19-22. 15. Mucha S, et al. Journal of Allergy and Clinical Immunology. 2020;145(4):1208-18. 16. He H, et al. J Allergy Clin Immunol. 2021;147(1):199-212. 17. Renert-Yuval Y, Thyssen, J. P., Bissonnette,R., Bieber, T., Kabashima, K., Hijnen, D., & Guttman-Yassky, E. Journal of Allergy and Clinical Immunology. 2021;147(4):1174–90.e1. 18. Bakker DS, et al. J Allergy Clin Immunol. 2021;147(1):189-98. 19. Ramamoorthy R. Journal of Skin and Sexually Transmitted Diseases.0. 20. Katoh N. J Dermatol. 2021;48(2):152-7. 21. Puar N, et al. Ann Allergy Asthma Immunol. 2021;126(1):21-31. 22. Hajar T, et al. An Bras Dermatol. 2018;93(1):104-7. 23. Furue K, et al. Immunology. 2019;158(4):281-6. 24. Ruzicka T, et al. N Engl J Med. 2017;376(9):826-35. 25. Newsom M, et al. Drugs. 2020;80(11):1041-52. 26. Guttman-Yassky E, et al. J Allergy Clin Immunol. 2019;144(2):482-93.e7. 27. Tan-Lim CSC, et al. Pediatr Allergy Immunol. 2021;32(1):124-36. 28. Napolitano M, et al. Dermatol Ther. 2021;34(1):e14475. 29. Vestergaard C, et al. Journal of the European Academy of Dermatology and Venereology. 2019;33(9):1644-59.

NON-2022-9857-N

Here are a few highlights on the relation between physical activity and incidence of psoriasis based on three aspects:

· The Effect of Sports on Psoriasis

· The Impact of Psoriasis on Sport Activities

· The Importance of Sports in Psoriasis

Sports may improve the quality of life of patients with psoriasis. Sport activities seem to be a notable, non-pharmacological source for promoting a healthier lifestyle in psoriasis patients. Yet, the impact of different types of sport activities on psoriasis needs further research.

Source:
1. Custurone P, Macca L, Bertino L, Di Mauro D, Trimarchi F, Vaccaro M, et al. Mutual Influence of Psoriasis and Sport. Medicina (Kaunas). 2021;57(2):161. 2. Do YK, Lakhani N, Malhotra R, Halstater B, Theng C, Østbye T. Association between psoriasis and leisuretime physical activity: findings from the National Health and Nutrition Examination Survey. J Dermatol. 2015;42(2):148-53. 3. Schwarz PEH, Pinter A, Melzer N, Barteczek P, Reinhardt M. ERAPSO: Revealing the High Burden of Obesity in German Psoriasis Patients. Dermatol Ther (Heidelb). 2019;9(3):579-87. 4. Frankel HC, Han J, Li T, Qureshi AA. The association between physical activity and the risk of incident psoriasis. Arch Dermatol. 2012;148(8):918-24. 5. Balato N, Megna M, Palmisano F, Patruno C, Napolitano M, Scalvenzi M, et al. Psoriasis and sport: a new ally? J Eur Acad Dermatol Venereol. 2015;29(3):515-20. 6. Torres T, Alexandre JM, Mendonça D, Vasconcelos C, Silva BM, Selores M. Levels of physical activity in patients with severe psoriasis: a cross-sectional questionnaire study. Am J Clin Dermatol. 2014;15(2):129-35. 7. Nyunt WW, Low WY, Ismail R, Sockalingam S, Min AK. Determinants of health-related quality of life in psoriasis patients in Malaysia. Asia PacJ Public Health. 2015;27(2):15. 8. Leino M, Mustonen A, Mattila K, Koulu L, Tuominen R. Perceived impact of psoriasis on leisure-time activities. Eur J Dermatol. 2014;24(2):224-8. 9. Jenner N, Campbell J, Plunkett A, Marks R. Cost of psoriasis: a study on the morbidity and financial effects of having psoriasis in Australia. Australas J Dermatol. 2002;43(4):255-61. 10. Wilson PB. Cardiorespiratory Fitness Among Individuals With Psoriasis in the General Population. J Phys Act Health. 2016;13(7):771- 5. 11. Gyldenløve M, Storgaard H, Holst JJ, Vilsbøll T, Knop FK, Skov L. Patients with psoriasis are insulin resistant. J Am Acad Dermatol. 2015;72(4):599-605. 12. Kim HN, Han K, Park YG, Lee JH. Metabolic syndrome is associated with an increased risk of psoriasis: A nationwide population-based study. Metabolism. 2019;99:19-24. 13. Wilson PB. Prevalence of weight loss attempts and behaviors used by individuals with psoriasis in the United States population. J Dermatolog Treat. 2017;28(6):515-9.

NON-2022-9859-N

Ketogenic Diet	Ketogenic diet can aid as effective adjuvant therapy for a variety of inflammatory, autoimmune, and oncologic cutaneous pathologies caused due to the overexpression of IL-1β and abnormal activation of nuclear factor–κB.1 Ketogenic diet may help resolve certain cutaneous conditions such as chronic plaque psoriasis in overweight individuals.2
Low FODMAP (Fermentable oligosaccharides, disaccharides, monosaccharides,and polyols) Diet	Low FODMAP diet can play a key role in treatment of rosacea and psoriasis, which are, linked to small intestinal bacterial overgrowth, irritable bowel syndrome, and some patients with inflammatory bowel disease.1,3
Gluten-free Diet	Gluten-free diet may improve skin health in psoriasis patients and may benefit several other dermatological conditions.4-6
Low Histamine Diet	This diet has been reported to improve urticaria and atopic eczema.7,8
Mediterranean Diet	Close adherence to this diet has been reportedly proven to reduce the occurrence and severity of psoriasis, thus improving the quality of life of these patients.9 Mediterranean diet also has been inversely correlated to hidradenitis suppurativa10 and the severity of acne vulgaris.11 The diet may have a chemo-preventive effect and inhibit and/or reverse UV radiation-induced DNA damage caused to the cutaneous tissues.1
Whole-food, Plant-based Diet	Whole-food, plant-based diet can slow down the process of aging of skin, thus improving skin hydration and elasticity, and decreasing skin permeability. It has also been found to decrease angiogenesis, weaken immune function, and reduce the synthesis of vitamin D.1
Paleolithic Diet	This diet is theoretically proven to be beneficial as an adjunctive therapy for treating cutaneous conditions associated with metabolic disorders and obesity.1

Further, randomised controlled trials are warranted to assess the efficacy of these dietary modifications in patients with various skin ailments.

Source:
1. Svoboda SA, Christopher M, Shields BE. Reexamining the Role of Diet in Dermatology. Cutis. 2021;107(6):308-14. 2. Castaldo G, Rastrelli L, Galdo G, Molettieri P, Rotondi Aufiero F, Cereda E. Aggressive weight-loss program with a ketogenic induction phase for the treatment of chronic plaque psoriasis: A proof-of-concept, single-arm, open-label clinical trial. Nutrition. 2020;74:110757. 3. Drago F, De Col E, Agnoletti AF, Schiavetti I, Savarino V, Rebora A, et al. The role of small intestinal bacterial overgrowth in rosacea: A 3-year follow-up. J Am Acad Dermatol. 2016;75(3):e113-e5. 4. Afifi L, Danesh MJ, Lee KM, Beroukhim K, Farahnik B, Ahn RS, et al. Dietary Behaviors in Psoriasis: Patient-Reported Outcomes from a U.S. National Survey. Dermatol Ther (Heidelb). 2017;7(2):227-42. 5. Song MS, Farber D, Bitton A, Jass J, Singer M, Karpati G. Dermatomyositis associated with celiac disease: response to a gluten-free diet. Can J Gastroenterol. 2006;20(6):433-5. 6. Egan CA, Smith EP, Taylor TB, Meyer LJ,Samowitz WS, Zone JJ. Linear IgA bullous dermatosis responsive to a gluten-free diet. Am J Gastroenterol. 2001;96(6):1927-9. 7. Son JH, Chung BY, Kim HO, Park CW. A Histamine-Free Diet Is Helpful for Treatment of Adult Patients with Chronic Spontaneous Urticaria. Ann Dermatol. 2018;30(2):164-72. 8. Maintz L, Benfadal S, Allam JP, Hagemann T, Fimmers R, Novak N. Evidence for a reduced histamine degradation capacity in a subgroup of patients with atopic eczema. J Allergy Clin Immunol. 2006;117(5):1106-12. 9. Korovesi A, Dalamaga M, Kotopouli M, Papadavid E. Adherence to the Mediterranean diet is independently associated with psoriasis risk, severity, and quality of life: a cross-sectional observational study. Int J Dermatol. 2019;58(9):e164-e5. 10. Barrea L, Fabbrocini G, Annunziata G, Muscogiuri G, Donnarumma M, Marasca C, et al. Role of Nutrition and Adherence to the Mediterranean Diet in the Multidisciplinary Approach of Hidradenitis Suppurativa: Evaluation of Nutritional Status and Its Association with Severity of Disease. Nutrients. 2018;11(1). 11. Skroza N, Tolino E, Semyonov L, Proietti I, Bernardini N, Nicolucci F, et al. Mediterranean diet and familial dysmetabolism as factors influencing the development of acne. Scand J Public Health. 2012;40(5):466-74.

NON-2022-9863-N

With increasing awareness about the role of dietary modifications in skin care treatment, dermatologists play an imperative role in recommending modified diets to their patients.¹ Gluten-free (GF) diet is becoming immensly popular worldwide. Besides celiac disease and wheat allergic patients, GF diets are frequently adapted by other patients as well, including those with non-celiac gluten sensitivity (NCGS).^2-4

Patients with NCGS

Although these patients do not have celiac disease or wheat allergy, they show intestinal as well as extra-intestinal manifestation on ingestion of gluten. GF diet may prove beneficial for some NCGS patients.¹

GF diets may prove to be beneficial beneficial for patients suffering from various skin ailments, yet, more high-quality studies are warranted to elucidate these benefits in patients without celiac disease and wheat allergy.

Source:
1. Bell KA, Pourang A, Mesinkovska NA, Cardis MA. The effect of gluten on skin and hair: a systematic review. Dermatol Online J. 2021;27(4). 2. Hietikko M, Hervonen K, Salmi T, Ilus T, Zone JJ, Kaukinen K, et al. Disappearance of epidermal transglutaminase and IgA deposits from the papillary dermis of patients with dermatitis herpetiformis after a long-term gluten-free diet. Br J Dermatol. 2018;178(3):e198-e201. 3. Graziano M, Rossi M. An update on the cutaneous manifestations of coeliac disease and non-coeliac gluten sensitivity. Int Rev Immunol. 2018;37(6):291-300. 4. Sapone A, Bai JC, Ciacci C, Dolinsek J, Green PHR, Hadjivassiliou M, et al. Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC Med. 2012;10:13-.

NON-2022-9861-N