Definition:

Anaphylaxis is an acute, potentially lethal, multi system syndrome resulting from the sudden release of mast cell- and basophil-derived mediators into the circulation. It most often results from immunologic reactions to foods, medications, and insect stings, although it can also be induced through non immunologic mechanisms by any agent capable of producing a sudden, systemic degranulation of mast cells or basophils.

Pathophysiology:

The World Allergy Organization (WAO), an international umbrella organization representing a large number of regional and national professional societies dedicated to allergy and clinical immunology, has proposed discarding this nomenclature. The WAO categorizes anaphylaxis as either immunologic or nonimmunologic.

1- Immunological Anaphylaxis: 

The classical mechanism associated with human allergic disease is initiated by an antigen (allergen) interacting with allergen-specific IgE bound to the receptor on mast cells and/or basophils.

B cells are driven to differentiate into IgE-producing cells via the activity of the type 2 subset of CD4-bearing helper T cells (Th2 cells). This process largely takes place in the peripheral lymphoid tissues. The cytokines interleukin (IL) 4 and and IL-13 contribute to IgE responses in humans.

Once produced, allergen-specific IgE diffuses through the tissues and vasculature and constitutively occupies high-affinity IgE receptors (Fc-epsilon-RI) on mast cells and basophils.

When allergen diffuses into the proximity of a mast cell or basophil, it interacts with any surface-bound IgE that is specific for that allergen. If signaling is sufficiently robust, the mast cell (or basophil) becomes activated and degranulates, releasing preformed mediators, enzymes, and cytokines (such as histamine, tryptase, and tumor necrosis factor [TNF], respectively) and initiating additional mediator, cytokine, and enzyme production.

2- Non Immunological Anaphylaxis:

Anaphylactic reactions to various drugs have revealed potential mechanisms by which mast cells and basophils could be activated without evidence of involvement of IgE, other antibodies, or immune complexes.

Clinical features:

Skin and mucosal involvement:

• Generalized hives
• Itching
• Flushing
• Swollen lips, tongue or uvula
• Periorbital edema

Respiratory:

• Nasal congestion
• Sneezing
• Throat itching
• Sensation of throat closure or choking
• Wheezing
• Shortness of breath

Gastrointestinal:

• Nausea and vomiting
• Crampy abdominal pain
• Diarrhea

Cardiovascular:

• Syncope 
• Dizziness
• Hypotension
• Tachycardia

Diagnosis:

Because acute anaphylaxis can be immediately life-threatening, the diagnosis must be made quickly and efficiently, often while administering initial medication. Diagnosis is essentially made based on:

• Sudden onset of typical symptoms and signs, involving at least two organ systems (hypotension, airway swelling, wheeze, urticaria)
• Development of specific symptoms after exposure to a known or likely allergen
• Exclusion of other diseases that may have similar signs and symptoms.

Management:

Acute anaphylaxis must be treated as a medical emergency with stabilisation of airway, breathing and circulation. Intramuscular epinephrine 0.3–0.5 mg (0.3–0.5 mL of 1:1000 using an autoinjector or syringe) must be given immediately to adult patients with signs of shock, airway swelling, or definite difficulty in breathing. The epinephrine is repeated after 5 minutes if there has been no improvement in hypotension, airway swelling, or wheeze.

Agents that may be given as adjunctive therapies to epinephrine in the treatment of anaphylaxis include H1 antihistamines, H2 antihistamines, bronchodilators, and glucocorticoids. None of these medications should be used as initial treatment or as sole treatment, because they do not relieve upper or lower respiratory tract obstruction, hypotension, or shock and are not lifesaving.

To reduce the risk of recurrence, patients who have been successfully treated for anaphylaxis subsequently require confirmation of the anaphylaxis cause as well as anaphylaxis education. All those at risk of anaphylaxis should wear a Medic alert/emergency bracelet with full details of allergies and contact details of their doctor. In some cases, a patient or caregiver should always carry an emergency kit containing self-injectable Epinephrine and antihistamine tablets.

Written by: 

Bandar Alharbi, Medical Intern

Revised by: 

 Naif Alshehri, Medical Intern

Resources:

UpToDate

Dermnet

Ministry of health

Mayo clinic

What is Psoriasis?

Psoriasis is a chronic dermatological condition characterized by pruritic erythematous patches and silvery scales, with symptom severity varying from mild to severe.

In normal skin, the cells are normally replaced every three to four weeks; however, in individuals with psoriasis, this process is accelerated, occurring within approximately three to seven days. Consequently, this rapid proliferation of skin cells leads to a buildup of skin layers and the manifestation of various symptoms associated with psoriasis.

Risk factors of Psoriasis

Risk factors for developing psoriasis include:

• Family History
• Infections: Viral infections (like HIV) and bacterial infections (such as strep throat) can trigger psoriasis
• Psychological Stress
• Obesity
• Smoking

Causes of Psoriasis

The etiology of psoriasis is not yet fully understood but involves a combination of genetic, immune, and environmental factors Key triggers can include:

• Skin trauma
• Psychological stress
• Infections, notably streptococcal throat infections
• Smoking 
• Certain medications

Clinical features of Psoriasis

The disease typically follows a relapsing course characterized by intervals of symptom-free periods. It is characterized by well-defined erythematous plaques and/or papules with silver-white scaling. Initial presentations often consist of solitary lesions, which may subsequently merge to form larger confluent areas. These lesions predominantly occur on the scalp, trunk, elbows, and knees—typically the extensor surfaces—though any area of the skin may be involved. Pruritus is reported in approximately 80% of cases, generally mild but occasionally severe.

Characteristic features include:

Auspitz sign, which refers to pinpoint bleeding that occurs upon the removal of scales, revealing dermal papillae.

Additionally, the Koebner phenomenon describes the occurrence of psoriatic lesions on previously unaffected skin in response to physical stimuli or skin injury, such as trauma, scratching, or the friction of irritating clothing, reflecting an isomorphic response. Nail involvement occurs in approximately 50% of cases.

Common manifestations include:

• Nail pitting: characterized by small, round depressions on the nail surface.
• Brittle nails: which exhibit dystrophy and crumbling.
• Onycholysis: defined as partial separation of the nail plate, predominantly at the distal edge.
• Oil drop sign (or salmon spot): presents as a well-circumscribed yellow-red discoloration of the nail.

Types of Psoriasis

•  Plaque Psoriasis: This is the most prevalent variant, characterized by symmetrically distributed, thick erythematous lesions covered with silvery scales.
•  Guttate Psoriasis: This variant features lesions resembling the size of drops of water and may progress to plaque psoriasis. It primarily occurs in children and adolescents, often following a streptococcal infection.
•  Erythrodermic Psoriasis: This form presents as generalized erythematous lesions accompanied by diffuse scaling. It has the potential to lead to severe health complications, including fever and dehydration.
• Inverse Psoriasis: This variant predominantly affects skin folds and the flexural creases of large joints, commonly referred to as flexural psoriasis.
•  Pustular Psoriasis: There is a significant association with HLA-B27, with generalized pustular psoriasis being the most common subtype. This variant is characterized by generalized erythroderma and the presence of confluent white pustules over the entire body, potentially involving the oral mucosa and tongue. It typically exhibits a relapsing course, accompanied by pronounced malaise, including fever, weakness, and chills, and can be life-threatening.

Health conditions associated with psoriasis

• Psoriatic Arthritis
• Spondyloarthropathy
• Inflammatory Bowel Disease: Includes Crohn’s disease and ulcerative colitis.
• Uveitis
• Coeliac Disease
• Localised palmoplantar pustulosis, generalised pustulosis, and acute generalised exanthematous pustulosis
• Non-Alcoholic Fatty Liver Disease
• Metabolic Syndrome

Diagnosis of Psoriasis

Psoriasis is a clinical diagnosis based on the patient’s medical and familial history, along with a detailed examination of the skin. Skin biopsy is indicated primarily in cases where the clinical presentation is atypical.

Supporting histological findings include:

• Acanthosis and parakeratosis
• Thickening of the stratum spinosum with thinning of the stratum granulosum
• Presence of Munro microabscesses, which are characterized by the accumulation of neutrophils within the stratum corneum, surrounded by parakeratosis.

Treatment of Psoriasis

Psoriasis currently has no cure; however, symptoms can be effectively managed through various medications tailored to the type, severity, and location of the lesions.

1- Topical therapies:

Mild psoriasis is typically managed with topical agents. Common treatments include:

• Emollients and moisturizers
• Coal tar preparations
• Dithranol treatments
• Salicylic acid
• Vitamin D derivatives (such as calcipotriol)
• Topical steroids
• Combination ointment/gel or foam of calcipotriol and betamethasone dipropionate
• Calcineurin inhibitors (like tacrolimus and pimecrolimus)

2- Phototherapy

3- Systemic therapies:

For moderate to severe psoriasis, treatment typically involves systemic agents and/or phototherapy. The most commonly used systemic treatments include:

• Methotrexate
• Ciclosporin
• Acitretin

Additionally, other medications that are sometimes used for psoriasis are:

•  Apremilast
• Hydroxyurea
• Dimethyl fumarate

4- Biologic therapies: 

Biologic therapy is specifically used for severe cases of psoriasis and psoriatic arthritis that do not respond to standard systemic treatments.

Written by:

Atheer Alhuthaili, Medical Intern.

Revised by: 

 Naif Alshehri, Medical Intern

References:

DermNet.

Amboss 

Medscape 

MOH

Definition:

dermatomyositis is an autoimmune condition that often affects both the skin and the muscles (classic dermatomyositis), but it can alternatively manifest as skin-predominant illness (clinically amyopathic dermatomyositis). While children have no elevated risk of cancer, all adult patients presenting with cutaneous lesions of dermatomyositis should be investigated for concurrent muscle illness, systemic involvement, and/or malignancy.

Epidemiology:

Dermatomyositis exhibits a bimodal age distribution, affecting both adults ( 40-60 years) and children ( 4-14 years). It is a rare condition found worldwide. In adults, women are two to three times more likely to develop dermatomyositis than men. The disease occurs at a rate of 2 to 9 cases per million across different populations.

Etiology:

Dermatomyositis is thought to arise from an immune-mediated process triggered by external factors, such as malignancy, medications, or infections, in individuals with a genetic predisposition. Serum antinuclear autoantibodies are frequently detected, along with other myositis-specific autoantibodies. Antisynthetase antibodies target cytoplasmic antigens, meaning the antinuclear antibody test may sometimes be negative. Patients with antisynthetase antibodies often present with overlap syndromes. The term “antisynthetase syndrome” is used to describe individuals with these autoantibodies who exhibit symptoms like fever, erosive polyarthritis, “mechanic’s hands,” Raynaud’s phenomenon, and interstitial lung disease.

Clinical features:

Cutaneous manifestations:

• The hallmark features of dermatomyositis include the heliotrope sign and Gottron papules. The heliotrope sign is identified by a pink-violet discoloration, mainly affecting the eyelids and periorbital skin, often accompanied by swelling. Dermatomyositis skin lesions are typically more prominent on extensor surfaces, such as the elbows, knees, metacarpophalangeal joints , and both proximal and distal interphalangeal joints (knuckles). When the papules on the knuckles develop a lichenoid texture, they are referred to as Gottron papules, while involvement of the elbows or knees is called Gottron sign.
• A key diagnostic feature of the dermatomyositis skin eruption is poikiloderma, which appears as a pink-violet color in dermatomyositis and a more reddish tone in lupus erythematosus. Photodistributed poikiloderma is highly characteristic of dermatomyositis, often seen on the upper chest (V-neck sign) and upper back (shawl sign). It can also occur in areas not exposed to sunlight, such as the lateral thigh, known as the holster sign. The skin lesions of dermatomyositis are frequently very itchy, which can significantly impact the patient’s quality of life. This itching can sometimes help distinguish dermatomyositis from lupus erythematosus.
• Calcinosis cutis is more common in juvenile dermatomyositis, affecting 25–70% of children. It appears as hard, irregular papules or nodules that may drain a chalky substance. These lesions tend to develop in areas of trauma, like the elbows and knees, but can occur elsewhere and may be painful, potentially interfering with function.

Systemic disease:

In dermatomyositis, skin symptoms often appear before noticeable muscle involvement; however, when muscle disease occurs, it is clinically similar to polymyositis. The myopathy primarily affects proximal muscles, particularly the extensor groups like the triceps and quadriceps, in a symmetrical pattern. In more severe cases, all muscle groups can be impacted. Patients may struggle with simple activities, such as combing their hair or standing up from a seated position. 

Pulmonary complications occur in about 15–30% of dermatomyositis patients and typically present as diffuse interstitial fibrosis, resembling that found in individuals with rheumatoid arthritis or systemic sclerosis. Cardiac involvement is usually asymptomatic, but when it occurs, it typically manifests as arrhythmias or conduction abnormalities.

Diagnosis: 

• A thorough history, including possible triggers and any past malignancies, along with a review of systems, should be conducted.
• Physical examination – This should include an assessment of the skin, muscles, and a complete general examination.

If the patient presents with a characteristic skin eruption, a skin biopsy is recommended to confirm the clinical diagnosis of dermatomyositis. Once histopathological confirmation is obtained, an evaluation for muscle and/or systemic disease should follow, as this will guide treatment decisions. 

The assessment for myositis may involve testing the strength of proximal extensor muscles and other muscles, including the neck flexors, measuring serum muscle enzyme levels, performing an electromyogram, and/or conducting a triceps muscle biopsy. However, MRI or ultrasound of the proximal muscles is increasingly used instead of, or before, a muscle biopsy, especially when classic skin findings and consistent histology are present. 

Additional baseline tests should be carried out to check for pulmonary, cardiac, or symptomatic esophageal diseases.

Management:

Skin-limited disease:

• First-line treatment: Photoprotection, topical corticosteroids (CS), and calcineurin inhibitors with or without antimalarials.
• Second-line treatment: High-dose methotrexate (MTX), mycophenolate mofetil (MMF), intravenous immunoglobulin (IVIG), cyclosporine, and rituximab, particularly for severe skin conditions with ulceration.
• Calcinosis cutis treatment: Diltiazem and possibly surgical removal; early aggressive treatment of juvenile dermatomyositis (JDM) to lower the risk of developing calcinosis cutis.

Disease monitoring:

• • Muscle enzymes and clinical examinations should be rechecked every 2-3 months. If muscle disease develops, systemic steroids should be initiated.
  • Physical exams every 4-6 months to screen for malignancy, especially during the first 2-3 years following diagnosis.

Skin and muscle disease:

• First-line treatment: Systemic corticosteroids (CS), methotrexate (MTX), and azathioprine (AZA).
• Second-line treatment: IVIG, mycophenolate mofetil (MMF), cyclosporine, cyclophosphamide, and rituximab.

Written by:

Mashael Alanazi, Medical Intern

Revised by: 

Naif Alshehri, Medical Intern

Resources:

Bolognia textbook

Review of dermatology textbook

Definition and Epidemiology:

Lupus Erythematosus is an autoimmune multisystem disorder that often affects the skin and other organs such as Kidneys, joints and heart. The cutaneous manifestations can be a source of disability.

Systemic lupus Erythematosus (SLE) is a common disease with significant morbidity and mortality. The reported prevalence of SLE in the United states is  20 to 150 cases per 100,000. The strongest affecting risk factor is gender. The increased frequency of SLE in women especially in the childbearing age has been attributed to the estrogen hormonal effect.

Ethnicity is also a major risk factor. The prevalence of SLE in African American women is fourfold higher than Caucasian women. In addition, African American and Hispanic individuals in the US have a poorer renal prognosis than Caucasian individuals.

Pathogenesis:

The pathogenesis of SLE is complex and multifactorial. It involves the interaction between genetic and environmental factors. The genetic factors include HLA-B8-DR3 and The environmental factors include ultraviolet radiation, medications, cigarette smoking and possibly viruses. This interplay triggers an inflammatory  cascade of cytokines, chemokines and inflammatory cell response that ends with cytotoxic keratinocyte damage.

Clinical features:

Discoid Lupus Erythematousus: discoid lesions represents one of the most common skin manifestations of lupus and commonly found on the face, scalp and ears. Discoid lesions has the potential of scarring, and over time, a substantial portion of patients develop disfiguring scars. Active lesions are intensely inflammatory with a pronounced superficial and deep dermal infiltrate. On palpation, they feel thicker and firmer than surrounding skin. The adnexa are prominently involved, with follicular plugging and scarring alopecia. Dyspigmentation is a common complication in longstanding lesions, with hypopigmentation in the center and hyperpigmentation in the periphery.

Subacute Cutaneous Lupus Erythematosus: patients with subacute cutaneous lupus Erythematosus (SCLE) typically exhibit photosensitivity. Their lesions most frequently occur in sun-exposed areas. Lesions of SCLE may have an annular configuration with raised pink borders and central clearing, or a papulosquamous presentation with chronic psoriasiform or eczematous appearance.

In 20-30% of patients with SCLE, the disease is linked to medications including terbinafine, thiazide diuretics, anti-TNF, and proton pump inhibitors.

Since Anti-SSA/Ro antibodies are associated with both Sjogren syndrome and SCLE. Some patients have features of both diseases and may have some internal manifestations of Sjogren such as pulmonary or neurologic disease.

Acute Cutaneous Lupus Erythematosus: the lesions of ACLE are exemplified by the development of Malar rash (“butterfly rash”). These lesions tend to be transient following sun exposure and resolve without scarring. Patients presenting with this type of eruptions must be carefully evaluated for internal manifestations.

The morphology of lesions ranges from mild erythema to intense edema. The face is most commonly affected and there is often sparing of the nasolabial folds.

Lupus panniculitis: intense inflammation of the subcutaneous tissue leading to indurated plaques that can evolve into disfiguring, depressed areas. Lesions are frequently distributed over the face, scalp, upper arms, breast and thighs.

Chilblain lupus: chilblain lupus consists of dusky purple papules and plaques on the toes, fingers and sometimes the nose. These lesions are exacerbated by cold exposure.

Systemic manifestations: the organ systems that are commonly affected are joints, kidneys, hematologic and Central nervous system as well as pleural and pericardial serosal surfaces. Many of the internal organs manifestaitons are included in the diagnostic criteria.

Diagnosis:

Diagnostic criteria: using the SLICC criteria, SLE is diagnosed if the patient has either of the following:

• Four criteria including at least more than one clinical criterion and one immunological criterion
• Biopsy proven lupus nephritis and antinuclear antibody (ANA) or anti double stranded DNA anitbody

Clinical criteria

1. Acute or subacute cutaneous lupus
2. Chronic cutaneous lupus (discoid, lupus panniculitis)
3. Oral ulcers
4. Nonscarring alopecia
5. Synovitis involving 2 or more joints
6. Serositis involving lungs and heart
7. Renal involvement 
8. Neurological involvement 
9. Hemolytic anemia
10. Leukopenia or lymphopenia
11. Thrombocytopenia

Immunological criteria:

1. Raised ANA titers
2. Raised Anti-double stranded DNA
3. Presence of anti smith antibody
4. Positive antiphospholipid antibody
5. Low complement levels
6. Positive direct Coombs test

Management:

General measures:

• Sun protection using clothing, accessories and SPF 50+ sunscreens.
• Smoking cessation

Topical treatments:

• Topical and intralesional corticosteroids are a mainstay of therapy. They offer a high degree of safety profile as well as a relatively rapid response. Particularly in active discoid lesions, intralesional triamcinolone can be very effective.
• Topical calcineurin inhibitors such as Tacrolimus can also be used.

Systemic treatments:

• Antimalarials such as hydroxychloroquine remains the gold standard for systemic therapy.
• Systemic corticosteroids such as prednisone. These are the mainstay of treatment in acutely ill patients.
• Methotrexate
• Immunosuppressive agents such as azathioprine, mycophenolate and cyclophosphamide 
• Targeted biological treatments that have been FDA approved such as anifrolumab and belimumab 

Written by: 

Bandar Alharbi, Medical Intern.

Revised by: 

Naif Alshehri, Medical Intern

Resources:

Dermnet

UpToDate

Bolognia

What is Seborrheic dermatitis?

Seborrheic dermatitis (SD) is a chronic inflammatory skin condition characterized by erythematous, scaly patches primarily in seborrheic areas—regions rich in sebaceous glands such as the scalp, face, and upper trunk. There are infantile and adult forms of seborrhoeic dermatitis.

 Who gets Seborrheic dermatitis?

Seborrhoeic dermatitis affects 3% to 12% of the population and has two main age distributions:   

Infants: Under 3 months old; usually resolves by 6-12 months.

Adults: It typically begins in late adolescence, is more common in males, and tends to peak during young adulthood and later in life. Various factors are linked to more severe cases in adults, including having oily skin, a family history of seborrhoeic dermatitis or psoriasis, and conditions causing immunosuppression, such as organ transplants, HIV, or lymphoma. Additionally, neurological and psychiatric disorders like Parkinson’s disease, depression, and epilepsy, as well as the use of neuroleptic medications, can contribute to its severity. Other contributing factors include PUVA therapy for psoriasis, lack of sleep, and stressful life events.

Causes of seborrhoeic dermatitis

The exact cause of seborrhoeic dermatitis is not fully understood. However, various factors are thought to be associated with the condition, including hormonal changes, fungal infections, nutritional deficiencies, and neurogenic factors. The proliferation of Malassezia yeast is believed to contribute to its development. Malassezia, a normal skin saprophyte, produces lipases and phospholipases that break down triglycerides in sebum into free fatty acids, which may trigger inflammation. Differences in skin barrier lipid composition and function may account for the varying manifestations of the condition. 

Clinical features of Seborrhoeic dermatitis

Infantile seborrhoeic dermatitis

Seborrhoeic dermatitis in infants, also known as cradle cap, features:

• Diffuse, greasy, yellow scaling on the scalp.
• The rash may extend to the armpit and groin folds.
• Salmon-pink patches that may flake or peel.
• Generally not itchy

Adult seborrhoeic dermatitis

Seborrheic dermatitis typically follows a chronic course characterized by episodic phases. Active phases may include symptoms such as burning and itching, while these are interspersed with inactive, asymptomatic periods. The condition usually flares in winter and improves with sun exposure in the summer. It manifests with a range of symptoms, from erythematous plaques with patchy scaling to greasy yellow crusts, and is commonly distributed in areas with hair and oily skin. The affected regions include:

• Scalp (dandruff and itching)
• Forehead/hairline and retro auricular area
• Nasolabial fold, eyebrows, and periocular region (blepharitis with scaly, red eyelid margins)
• Cheeks and chin
• Presternal and interscapular regions
• Axillae, under the breasts, umbilicus, and groin area

People with darker skin may show scaly, hypopigmented macules and patches in affected areas.

Diagnosis of Seborrhoeic dermatitis

Seborrhoeic dermatitis is usually diagnosed clinically based on lesion location, appearance, and behavior. If uncertain, a biopsy may be performed. Histological findings in seborrhoeic dermatitis typically include:

• Parakeratosis in the epidermis
• Plugged follicular ostia
• Spongiosis (intercellular edema in the epidermis)
• A sparse, perivascular, lymphohistiocytic inflammatory infiltrate in the dermis

Treatment of Seborrhoeic dermatitis

General Measures

1. Patient Education:
   • Explain the nature of the condition and appropriate skincare routines.
2. Lifestyle Modifications:
   • Diet: A high fruit intake may reduce symptoms.
   • Stress Management: Stress can trigger flare-ups, so managing stress is important.
3. Many herbal remedies are used, but their effectiveness is unclear.

Specific Measures

1. Keratolytics:
   • Salicylic Acid, Lactic Acid, Urea, Propylene Glycol: Used to remove scales.
2. Topical Antifungal Agents:
   • Ketoconazole, Ciclopirox: Reduce Malassezia.
   • If resistant: Zinc Pyrithione or Selenium Sulfide.
3. Mild Topical Corticosteroids:
   • Use for 1–3 weeks to reduce inflammation during acute flare-ups.
4. Topical Calcineurin Inhibitors:
   • Pimecrolimus Cream, and Tacrolimus Ointment: Alternatives for long-term use, especially on the face.
5. Resistant Cases in Adult :
   • Oral Itraconazole, tetracycline antibiotics, or phototherapy.
   • Low-Dose Oral Isotretinoin: Effective for severe cases.
6. Roflumilast 0.3% Foam: Recently FDA-approved for use in patients aged 9 years and older.

Written by:

Atheer Alhuthaili, Medical Intern.

Revised by:

Naif Alshehri, Medical Intern.

References:

DermNet.

Amboss

Definition:

Atopic dermatitis, also known as atopic eczema, is the most prevalent inflammatory skin condition that is observed globally. It manifests as widespread dryness, itching, and a rash.

Epidemiology:

Approximately 230 million individuals worldwide suffer from atopic dermatitis, with a lifetime prevalence exceeding 15%, particularly in more affluent cultures. It usually impacts individuals who have a tendency for atopic conditions, which often tend to coincide with hay fever, asthma, and food allergies.

Typically, atopic dermatitis begins during infancy and can impact up to 20% of children. Around 80% of children who are affected experience the disease before they reach the age of 6. People of all age groups can be affected. 5–15% of young adults up to the age of 26 have it, despite the fact that it can settle in late childhood and adolescence.

Etiology:

Atopic dermatitis arises from a complex interaction of environmental and genetic aspects. 

Atopic dermatitis (eczema) is a complex condition with multiple factors contributing to its development, making it difficult to identify a single cause. There are numerous theories concerning the underlying mechanisms. Ongoing research is exploring various factors, including the immune system, mutations in skin structural genes, abnormalities in skin cells (keratinocytes), and the presence of bacteria, viruses, and yeasts on the skin surface.

Clinical features:

The hallmark symptoms of AD at every stage include dry skin and pruritus. Subacute and chronic AD is characterized by dry, scaly, or excoriated papules or skin thickening (lichenification) from persistent scratching, but acute AD is characterized by erythematous papules and vesicles with exudation and crusting. 

Clinical course and complications: AD progresses over months to years in a chronic, relapsing manner. Individuals who have mild disease may go through periods of intermittent flares followed by spontaneous remission. However, those with moderate to severe dermatitis typically do not experience complete clearance without receiving treatment.

Diagnosis:

The diagnosis of AD is clinical, which is established by evaluating the history, morphology, location of skin lesions, and related clinical symptoms. The diagnostic criteria include: 

• Pruritus 
• Eczematous dermatitis (acute, subacute, chronic) with characteristic morphology and age-specific patterns:

Facial, neck, and extensor involvement in neonates and young children

Flexural lesions in any age group, either present or past

Sparing the groin and axillary regions.

• History of chronic or relapsing conditions

Management:

The primary objectives of managing atopic dermatitis (AD) are to alleviate symptoms (pruritus and dermatitis), avoid worsening of the condition, and minimize the potential risks associated with therapy. 

Management includes the removal of aggravating factors, restoration of the skin barrier function and moisturization of the skin, patient education, and pharmacological intervention for skin inflammation. 

• Patient education is a crucial element of effective management. Patients are advised to: 

– Regularly apply emollients to maintain skin hydration. 

– Minimize aggravating elements such as: excessive bathing/washing without then moisturizing, exposure to cold, low-humidity conditions, excessive heat and perspiration, exposure to solvents, and strong detergents.

• Patient with mild to moderate atopic dermatitis: 

Topical therapies: Patients presenting with mild to moderate symptoms are treated with topical treatments.

The recommendation for the majority of patients with mild to moderate AD is to use topical corticosteroids and emollients instead of other topical anti-inflammatory medications. 

Topical calcineurin inhibitors like pimecrolimus and tacrolimus are topical immunomodulators and work in a different way from corticosteroids, they are suitable for treating atopic dermatitis in sensitive sites such as the eyelids, skin folds, and genital area. It can be used interchangeably with topical corticosteroids.  

• Patients with moderate to severe atopic dermatitis:

Patients with chronic, moderate to severe disease that does not improve with the best available topical therapy need a systemic treatment. For the majority of these patients, administration of a biologic immunomodulatory agent (dupilumab, tralokinumab, or lebrikizumab) instead of traditional immunosuppressants, other immunomodulators, or phototherapy is recommended 

Written by:

Mashael Alanazi, Medical Intern

Revised by:

Naif Alshehri, Medical Intern

Resources:

DermNet

UpToDate