Glomus Tumor

3 December، 2024/in Articles, Students Club/by Editorial Team

Definition and Epidemiology:

A glomus tumour is a a rare, benign neoplasm composed of cells resembling the modified smooth muscle cells of the normal glomus body or the Sucquet-Hoyer canal. It is usually located in areas of the skin that are rich in glomus bodies (eg, the subungual regions of digits or the deep dermis of the palm, wrist, forearm, and foot) and can be extremely painful, particularly following change in temperature or pressure.

Solitary glomus tumors can occur at any age, but are most common in young adults. Although these tumors in general show no gender predilection, subungual lesions are more common in women.

Glomus tumors of the fingers and toes occur in approximately 5 percent of patients with neurofibromatosis type 1 (NF1) and are considered NF1-associated neoplasms.

Clinical features:

The glomus tumor is a benign lesion that usually presents in young adults (20–40 years of age) as a small (<2 cm), blue–red papule or nodule in the deep dermis or subcutis of the distal upper or lower extremities. They are tender to touch, and may be associated with severe paroxysmal pain in response to temperature changes and pressure. The hand, especially the nail beds and palm, is most commonly affected, but cutaneous lesions can also occur at other sites. Unusual extracutaneous glomus tumors have been reported in the gastrointestinal tract, bone, mediastinum, trachea, mesentery, cervix, and vagina. Extremely rare instances of malignant transformation within glomus tumors, with documented metastasis, have been described.

Diagnosis:

The diagnosis is suspected on the basis of the clinical appearance and history of paroxysmal pain and cold sensitivity. Histopathologic examination of the excised tumor is necessary to confirm the diagnosis.

Histologically, glomus tumor is a well-circumscribed dermal nodule composed of glomus cells, vasculature, and smooth muscle cells . Solid glomus tumor, with scarce vasculature and scant muscle component, is the most common variant. Less common variants include glomangioma, with prominent vascular component, and glomangiomyoma, with prominent vascular and smooth muscle components.

Treatment:

Treatment is surgical excision. For subungual tumors, preoperative imaging studies with color Doppler ultrasonography and magnetic resonance may provide information on tumor size, shape, and precise anatomic location.

Done by:

Bandar Alharbi, Medical Intern

Revised by:

Naif Alshehri, Medical Intern

Resources:

Dermnetz

UpToDate

Bolognia Textbook

Pityriasis Rosea

26 November، 2024/in Articles, Students Club/by Editorial Team

Definition

Pityriasis rosea is a self-limiting skin condition characterized by an initial “herald patch,” followed by a symmetrical rash of smaller scaly oval lesions, typically distributed along the trunk in a “Christmas tree” pattern. It primarily affects young adults, resolves within 6–10 weeks, and may be associated with a viral trigger, though its exact cause is unknown.

Epidemiology

This condition is most prevalent in healthy individuals aged 10–35, with a slight female predominance. Although it can occur in any season, some studies suggest increased incidence in spring, fall, or winter, depending on geographic location. It affects approximately 0.5% to 2% of the population worldwide and is rarely seen in children under two years old.

Etiology

The exact cause of pityriasis rosea remains uncertain. A viral origin is widely hypothesized, with human herpesvirus types 6 and 7 (HHV-6/7) being the most strongly associated, though evidence is inconclusive. Other possible triggers include H1N1 influenza, SARS-CoV-2, and certain vaccines, such as COVID-19, smallpox, and hepatitis B. Drug-induced cases have also been reported, linked to medications like ACE inhibitors, NSAIDs, and antipsychotics.

Clinical Features

The hallmark of pityriasis rosea is the herald patch, which is a slightly raised, salmon-pink or red lesion 2–5 cm in diameter with a collarette of scaling at the margin. This is followed by the secondary rash, which appears as smaller oval plaques with similar scaling, distributed primarily on the trunk and upper extremities typically distributed along Langer lines in a “Christmas tree” pattern. The rash often spares the face, palms, and soles. In some cases, prodromal symptoms such as mild fever, headache, or malaise precede the rash. About 25% of patients experience pruritus, ranging from mild to severe.

Variants of the condition may involve atypical features, including inverse patterns affecting the axillae or groin, or more severe forms with pustules, vesicles, or purpuric lesions.

Diagnosis

Diagnosis is primarily clinical, based on the characteristic appearance and distribution of lesions. When uncertain, histology may confirm subacute dermatitis, particularly for drug-induced cases. It is essential to differentiate pityriasis rosea from other conditions, especially when atypical lesions or palm/sole involvement occurs.

Management

Treatment focuses on symptom control and patient reassurance, as the condition is self-resolving. Common interventions include:

General measures: Using moisturizers, gentle bathing practices, and limited sun exposure.
Topical treatments: Low to Medium-strength corticosteroids and antipruritic lotions to alleviate itching.
Systemic treatments: Oral antihistamines for itching; acyclovir for faster lesion resolution in severe cases; and, in rare instances, oral corticosteroids or phototherapy.

For pregnant women, caution is advised as pityriasis rosea may increase the risk of miscarriage during the first trimester if associated with active HHV-6 infection.

Written by:

Raneem Alahmadi, Medical Intern

Revised by:

Naif Alshehri, Medical Intern

Resources:

Bolognia 5th edition

Dermnet

Scarlet Fever

19 November، 2024/in Articles, Students Club/by Editorial Team

What is Scarlet Fever?

Scarlet fever is an infectious disease mediated by exotoxins, characterized by a distinctive erythematous rash affecting the skin and tongue. It typically arises from an infection of the throat, or less frequently, the skin, caused by Group A Streptococcus (GAS). Although scarlet fever can occur at any age, it predominantly affects children between the ages of 1 and 10 years, with the highest incidence observed in those aged 3 to 6 years. It is relatively rare in infants under 1 year of age and in adults.

Risk factors of Scarlet Fever

Group A Streptococcus (GAS) Pharyngitis
Presence in crowded environments
People in close contact with someone who has a strep throat or skin infection
Age range of 1 to 10 years
Seasonal prevalence, particularly during winter and spring months

Causes of Scarlet Fever

Scarlet fever is caused by a bacterial infection Streptococcus group A (Streptococcus pyogenes), a type of bacteria that is commonly found in the throat and on the skin. This group of bacteria can produce toxins that trigger the symptoms of scarlet fever, including a red rash, fever, and a sore throat.

Clinical features of Scarlet Fever

Scarlet fever typically manifests with abrupt onset of fever, often accompanied by pharyngitis, cervical lymphadenopathy, headache, nausea, vomiting, anorexia, swollen and red strawberry tongue, abdominal pain, myalgia, and general malaise.

The characteristic erythematous rash usually emerges 12 to 48 hours following the onset of fever, initially affecting areas such as the neck, below the ear, chest, axillae, and groin, before progressively spreading to the remainder of the body within the subsequent 24 hours.

The initial rash in scarlet fever often manifests as erythematous spots or blotches, giving the skin a “boiled lobster” appearance. As the lesions expand and become more widespread, they may resemble sunburn, with goose pimples. The affected skin often develops a rough, sandpaper-like texture. In skin folds, particularly in the axillary and cubital areas, capillary rupture can lead to the formation of characteristic red streaks, known as Pastia’s lines, which may persist for 1 to 2 days after the generalized rash has resolved. A typical red, flushed appearance of the cheeks accompanied by pallor around the mouth.

In untreated patients, the fever typically reaches its peak by the second day and gradually returns to baseline over a period of 5 to 7 days. However, when appropriate antibiotic therapy is administered, the fever generally abates within 12 to 24 hours. By the sixth day of infection, the rash begins to to fade and peeling, resembling that of sunburned skin. The peeling is most prominent in areas such as the axillae, groin, and the tips of the fingers and/or toes, and it may persist for up to 6 weeks.

Diagnosis of Scarlet Fever

Scarlet fever is typically diagnosed based on clinical history and physical examination findings. Diagnostic confirmation is supported by throat swab culture or a rapid streptococcal antigen test, ideally obtained from the posterior pharynx or tonsils.

Additionally, elevated titers of anti-deoxyribonuclease B (anti-DNase B) and antistreptolysin O (ASO) may further support the diagnosis.

Treatment of Scarlet Fever

Upon confirmation of a streptococcal infection, a 10-day course of antibiotics, typically penicillin, is prescribed. In patients with a penicillin allergy, macrolides serve as an appropriate alternative antibiotic .In cases of recurrence caused by antibiotic resistance, cephalosporins may be used

Additional management strategies include:

Administering paracetamol as needed to alleviate fever, headache.
Encouraging the consumption of soft foods and adequate fluid intake, particularly cool liquids, in cases of severe throat pain.
Utilizing oral antihistamines and emollients to alleviate pruritus associated with the rash.

Fever typically improves within 12-24 hours after starting antibiotics, and most patients recover within 4-5 days, although skin symptoms may take several weeks to fully resolve

Written by:

Atheer Alhuthaili, Medical Intern.

Revised by:

Naif Alshehri, Medical Intern

References:

DermNet.

Amboss

BMJ

Anaphylaxis

12 November، 2024/in Articles, Students Club/by Editorial Team

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

Urticaria

5 November، 2024/in Articles, Students Club/by Editorial Team

Definition:

Urticaria is a common terminology used to describe recurring wheals on the skin, with angioedema typically seen as a physical manifestation. However, it is increasingly recognized that “urticaria” is more accurately defined as a disease, which can be either acute or chronic. Consequently, urticaria may present with wheals, angioedema, or a combination of both.

Wheals are itchy, erythematous or pale swellings that occur in the superficial layer of the dermis, initially surrounded by a red flare. These lesions can range in size from a few millimeters to several centimeters, with numbers varying from a few to many. A defining feature of wheals is that each lesion appears and disappears quickly, typically within 24 hours.

In contrast, angioedema involves deeper layers of the dermis, as well as subcutaneous or submucosal tissues. Affected areas are usually normal or light pink in color, tend to be painful rather than itchy, and are generally larger and less distinct than wheals, often persisting for 2 to 3 days.

Classification of Urticaria:

Urticaria is categorized based on its duration:

Acute urticaria, lasting less than 6 weeks and frequently resolving within hours to days.
Chronic urticaria, persisting for over 6 weeks, with wheals occurring daily or intermittently.

Chronic urticaria can be either spontaneous or triggered by specific factors, and both forms may occur simultaneously.

Chronic inducible urticaria includes:

Dermographism
Cold urticaria
Cholinergic urticaria
Contact urticaria
Delayed pressure urticaria
Solar urticaria
Heat urticaria
Vibratory urticaria
Vibratory angioedema
Aquagenic urticaria

Etiology:

Many cases of urticaria are idiopathic, with various potential causes, including allergies, autoimmune responses, infections, and medications. In children, viral infections or idiopathic factors are the most common triggers, although other causes include:

Infectious: Evaluate for symptoms of urinary tract, respiratory, or gastrointestinal infections.
Allergic: Foods, medications, and environmental allergens.
Physical stimuli: Pressure, sunlight, exercise-induced (cholinergic), and cold exposure.
Arthropod bites: Can cause reactions known as “papular urticaria.”
Malignancy: Often associated with lymphoma.

The primary cell involved in urticaria is the mast cell, with basophils and eosinophils also contributing. These cells release proinflammatory mediators:

Preformed mediators: Include histamine, proteases, and heparin.
Newly synthesized mediators: Such as prostaglandin D2, leukotrienes C4, D4, E4, platelet-activating factor, and various cytokines (e.g., TNF-a, IL-1, IL-4, IL-5, IL-6, and IL-8).

Clinical features:

Urticaria is categorized based on its duration:

Acute urticaria, lasting less than 6 weeks and frequently resolving within hours to days.
Chronic urticaria, persisting for over 6 weeks, with wheals occurring daily or intermittently.

Chronic urticaria can be either spontaneous or triggered by specific factors, and both forms may occur simultaneously.

Urticarial wheals vary in size, from a few millimeters to several centimeters in diameter, and can appear white or red, with or without an erythematous flare. Each wheal may last from a few minutes to several hours, often changing shape. Wheals may be round or take on ring shapes, map-like patterns, or even form large patches.

Urticaria can affect any area of the body, typically presenting in widespread distribution, whereas angioedema tends to be more localized. Angioedema frequently involves the face (particularly the eyelids and areas around the mouth), hands, feet, and genital regions, and may extend to the tongue, uvula, soft palate, or larynx.

Serum sickness, which can occur following a blood transfusion, and serum sickness-like reactions triggered by certain medications, can lead to acute urticaria with accompanying bruising, fever, swollen lymph nodes, joint pain, and swelling.

In chronic inducible urticaria, wheals generally appear about five minutes after exposure to a trigger and may last from a few minutes to an hour. These wheals are characterized as follows:

Linear wheals in dermographism
Small wheals in cholinergic urticaria
Restricted to contact areas in contact urticaria
Diffuse in cold urticaria; in cases where large areas are involved, fainting may occur, posing a risk during cold-water swimming.

In chronic spontaneous urticaria, wheals tend to persist longer, although each individual lesion typically resolves within 24 hours and may recur at specific times of the day

Diagnosis:

Urticaria is diagnosed in individuals with a history of wheals lasting less than 24 hours, with or without angioedema. Assessment includes reviewing medication and family history, as well as performing a comprehensive physical examination.

For acute urticaria, if allergies to drugs, latex, or food are suspected, skin prick testing and specific allergen blood tests like RAST or CAP fluoroimmunoassay may be conducted. In chronic spontaneous urticaria, routine diagnostic tests are usually limited to blood counts and C-reactive protein (CBC, CRP); however, further tests may be performed if an underlying condition is suspected. Sometimes, the autologous serum skin test is used, showing a positive result if the patient’s serum injection under the skin produces a red wheal, although its effectiveness is debated.

Inducible urticaria is often confirmed by directly inducing the response, such as scratching for dermographism or applying an ice cube in suspected cases of cold urticaria. Additional tests are recommended for patients presenting with fever, joint or bone pain, or malaise to rule out systemic or autoinflammatory conditions. Patients with angioedema without wheals should be checked for ACE inhibitor usage and tested for complement C4, C1-INH levels, function, antibodies, and C1q.

Histopathological examination through biopsy may be non-specific, generally showing dermal edema, dilated blood vessels, and mixed inflammatory infiltrates. If vessel wall damage is present, urticarial vasculitis may be indicated.

Management:

The primary treatment for all types of urticaria in adults and children is an oral second-generation H1-antihistamine, like cetirizine or loratadine. If the standard dose (e.g., 10 mg of cetirizine) is ineffective, it may be increased up to four times (e.g., 40 mg daily). Antihistamines are discontinued once acute urticaria subsides, and adding a second antihistamine generally offers no additional benefit.

Systemic treatments are generally avoided during pregnancy and breastfeeding, second-generation antihistamines, particularly loratadine and cetirizine, are preferred if necessary, as they have shown no link to birth defects.

Avoidance of triggers

Avoiding known triggers can help manage urticaria. For example, avoiding allergens identified through testing can clear urticaria within 48 hours. Additionally, chronic infections, such as H. pylori, should be treated, and medications like aspirin, opiates, and NSAIDs should be avoided when possible, with paracetamol being a safer option. A temporary trial of a low pseudoallergen diet for at least three weeks may also be beneficial.

Physical triggers for inducible urticaria should be minimized, though symptoms may persist:

Symptomatic dermographism: Avoid friction and tight clothing.
Cold urticaria: Dress warmly and avoid cold-water swimming.
Delayed pressure urticaria: Broaden contact areas, such as with heavy bags.
Solar urticaria: Use protective clothing and broad-spectrum sunscreen.

Some individuals may benefit from daily, controlled exposure to triggers to build tolerance, and phototherapy can reduce itching in symptomatic dermographism.

Written by:

Mashael Alanazi, Medical Intern

Revised by:

Naif Alshehri, Medical Intern

Resources:

Bologina textbook

Review of dermatology textbook

DermNet

Psoriasis

29 October، 2024/in Articles, Students Club/by Editorial Team

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

Epidermolysis bullosa

22 October، 2024/in Articles, Students Club/by Editorial Team

Definition:

Epidermolysis bullosa (EB) is defined by mechanical fragility of the skin, it is a group of genetically inherited disorders characterized by the formation of blisters on the skin and mucous membranes, often triggered by minimal trauma or friction, particularly on areas like the hands and feet, in severe cases, blistering can also affect internal organs such as the esophagus, stomach, and respiratory tract, even in the absence of external friction.

It is classified into four major subtypes: EB simplex, junctional EB, dystrophic EB, and Kindler EB, each distinguished by the specific layer of tissue where blistering occurs. Collectively, these subtypes encompass over 30 distinct clinical phenotypes.

Epidemiology:

According to data from the National EB Registry, the estimated prevalence of epidermolysis bullosa (EB) in the U.S. is 11.1 cases per 1 million people, with an incidence of 19.6 per 1 million live births.

The prevalence and incidence for major EB subtypes are as follows: EB simplex (6.0 and 7.9), junctional EB (0.5 and 2.7), dominant dystrophic EB (1.5 and 2.1), and recessive dystrophic EB (1.4 and 3.0) per 1 million population and live births, respectively.

Etiology:

EB results from genetic mutations in proteins essential for skin adhesion. These mutations determine where blistering occurs. For example:

Epidermolysis Bullosa Simplex: Mutations disrupt proteins within the epidermis
Junctional Epidermolysis Bullosa: Mutations affect the dermal-epidermal junction
Dystrophic Epidermolysis Bullosa: Mutations impair structures in the upper dermis

The structural weakness in these layers leads to blister formation even with minor friction or trauma.

Clinical Features:

Clinically, EB manifests as fragile skin prone to blistering and erosions.

Fragile Skin and Blisters: Skin easily blisters and erodes, especially in areas prone to friction. Scarring is minimal in localized EBS but severe in recessive DEB.
Nail and Hair Abnormalities: Dystrophic or missing nails are common, along with scarring alopecia.
Extracutaneous Involvement:
Eye: Repeated eye blistering may cause neovascularization and blindness.
Gastrointestinal: Esophageal strictures, malabsorption, and constipation can develop.
Genitourinary: Blistering may result in urethral or bladder strictures.
Rare Presentations: Some forms of JEB and EBS may present with pyloric atresia at birth.

Approach to Diagnosis of Epidermolysis Bullosa (EB):

Diagnosing EB requires a combination of clinical evaluation and specialized testing. In cases with a known family history, a dermatologist can often make a preliminary diagnosis based on the patient’s symptoms. However, more precise diagnostic tools are often necessary. Skin biopsy with immunofluorescence antigen mapping (IFM) is used to examine newly formed blisters, identifying the defective skin proteins involved. Transmission electron microscopy (TEM) can reveal the ultrastructural level where blistering occurs, although this technique is typically available only in specialized laboratories. With the advancements in genetic testing, next-generation sequencing has become a valuable tool for confirming the diagnosis, pinpointing the exact mutation, and providing genetic counseling for families.

Management:

Currently, there is no cure for EB, and treatment focuses on symptom relief, skin protection, and preventing complications. Key management strategies include:

Daily Care:

Prevent Friction: Use soft clothing, padding, and non-irritating footwear. Handle infants and children with care to prevent skin damage.
Maintain a Cool Environment: Avoid overheating, which can trigger blistering.
Blister Care: Blisters should be drained and dressed by trained professionals using non-adhesive or silicone-based dressings.

Wound Management:

Bathing Solutions: Sodium hypochlorite or acetic acid baths help prevent bacterial infections.
Wound Dressings: Use low-tack silicone dressings or Vaseline®-impregnated gauze to promote healing and prevent trauma during dressing changes.

Medications:

Topical Treatments: Diacerein cream for EBS, and aluminum chloride for managing hyperhidrosis.
Systemic Treatments: Antibiotics for infections and drugs like tetracycline or erythromycin for EBS. Emerging therapies, such as retinoids and losartan, aim to reduce severe complications in DEB.
Innovative Therapies in Research: Therapies such as Gene Therapy and Stem Cell Therapy are being explored to repair defective genes and improve skin integrity.
Specialized Care:Multidisciplinary care teams address complications affecting the esophagus, eyes, and gastrointestinal system.

Written by:

Raneem Alahmadi, Medical Intern.

Revised by:

Naif Alshehri, Medical Intern

Resources:

Bolognia 5th edition

Dermnet

Dermatomyositis

15 October، 2024/in Articles, Students Club/by Editorial Team

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

Systemic Sclerosis

8 October، 2024/in Articles, Students Club/by Editorial Team

What is Systemic Sclerosis?

Systemic Sclerosis (SSc) is an autoimmune inflammatory disorder that can cause extensive fibrosis and vascular abnormalities, affecting various organs such as the skin, lungs, gastrointestinal tract, heart, and kidneys.

Systemic sclerosis is classified into subtypes based on the pattern of skin involvement:

Diffuse Cutaneous Systemic Sclerosis (dcSSc)
Limited Cutaneous Systemic Sclerosis (lcSSc)
Systemic sclerosis sine scleroderma

Causes of Systemic Sclerosis

The exact cause of systemic sclerosis remains unclear, but it is believed to result from a combination of genetic, environmental, and immunological factors:

Genetic Factors: Specific genetic loci that are associated with the disease have been identified.
Environmental Triggers: Exposure to certain environmental factors, such as silica dust, vinyl chloride, trichloroethylene, and some drugs (e.g., penicillamine), may trigger the disease in genetically predisposed individuals.
Immune pathways: Several pathways are likely implicated in the development of systemic sclerosis. These include cytokines that damage blood vessels, growth factors that promote collagen production, integrin signaling, morphogen pathways, co-stimulatory pathways, and others.

Clinical features of Systemic Sclerosis

Generally there is thickening and hardening of the skin, which appears smooth, shiny, and puffy.

Hands

Sclerodactyly
Puffy Fingers
Raynaud’s Phenomenon: Reduced blood flow to fingers in response to cold or stress.
Nail Changes: abnormal capillaries at the nail fold, smaller fragile nails with ragged cuticles, and digital pitted scars.
Digital Ulcers
Palmar erythema affecting thenar/hypothenar eminence

Face

Matt Telangiectases
Peri-Oral Furrowing
Microstomia
Beaked Nose

Other Features

Calcinosis: Deposits affecting fingers and extensor surfaces, which can break down and discharge chalky material (calcium)
Salt and Pepper Dyspigmentation: of hyperpigmentation and vitiligo-like depigmentation.
Pruritus

Rarer Cutaneous Features

Morphoea: Often appears as plaque, nodular, or linear lesions; more common in limited cutaneous systemic sclerosis.
Panniculitis

Organ Involvement:

It can affect the lungs, heart, kidneys, and gastrointestinal tract.
Constitutional symptoms are common, such as fatigue, arthralgia, and myalgia.

Diagnosis of Systemic Sclerosis

Diagnosing systemic sclerosis (SSc) involves a combination of clinical evaluation, laboratory tests, and imaging studies.

Key Features for Diagnosis

Sclerodactyly
Abnormal Nail Fold Capillaries are detected through capillaroscopy or dermatoscopy.
Autoantibodies: Testing for specific autoantibodies:
Anti-Scl70
Anticentromere antibodies
Internal Organ Involvement: Evidence of fibrosis or damage in internal organs, such as the lungs, heart, or kidneys.

Laboratory Tests

Antinuclear Antibodies (ANA): Often positive in SSc patients.
Inflammatory Markers: CRP and ESR
BNP

Additional Investigations

Pulmonary Function Tests
High-Resolution CT (HRCT) Chest
Echocardiogram
Gastrointestinal Studies: Such as EGD to assess esophageal involvement
In some cases, a skin biopsy may be performed

Treatment of Systemic Sclerosis

There is no cure for systemic sclerosis, treatment is mainly symptomatic and organ system specific.

Supportive care

Protect hands from trauma and cold exposure (e.g., by wearing gloves)
Keep skin moisturized (e.g., with warm oil, paraffin baths, and emollients)
Promote smoking cessation
Consider vasodilatory physical therapy and lymphatic drainage
Provide antihistamines for pruritus

Cutaneous Disease Management:

Raynaud Phenomenon (RP): First-line treatment includes calcium channel blockers.

For severe or refractory cases, consider adding oral PDE-5 inhibitors (e.g., sildenafil) or IV iloprost.

Digital Ulceration (DU): PDE-5 inhibitors (e.g., tadalafil) or IV iloprost.

For severe or refractory cases, bosentan may be considered.

Cutaneous Fibrosis: In early diffuse systemic sclerosis, treatment options include phototherapy and pharmacotherapy such as methotrexate or mycophenolate mofetil.

For severe or refractory fibrosis, cyclophosphamide or autologous hematopoietic stem cell transplantation (HSCT) may be necessary.

Calcinosis Cutis: Treatment options include carbon dioxide laser therapy or surgical removal of symptomatic lesions.

For scleroderma renal crisis: use of ACE inhibitors ( captopril ).

For gastrointestinal disease: use proton pump inhibitors for GERD.GI motility disorder: prokinetic therapy, e.g., metoclopramide.

Cardiopulmonary disease requires targeted treatment for heart and lung conditions.

Written by:

Atheer Alhuthaili, Medical Intern

Revised by:

Naif Alshehri, Medical Intern

References:

DermNet

Amboss

Medscape

Systemic Lupus Erythematosus (SLE)

1 October، 2024/in Articles, Students Club/by Editorial Team

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

Acute or subacute cutaneous lupus
Chronic cutaneous lupus (discoid, lupus panniculitis)
Oral ulcers
Nonscarring alopecia
Synovitis involving 2 or more joints
Serositis involving lungs and heart
Renal involvement
Neurological involvement
Hemolytic anemia
Leukopenia or lymphopenia
Thrombocytopenia

Immunological criteria:

Raised ANA titers
Raised Anti-double stranded DNA
Presence of anti smith antibody
Positive antiphospholipid antibody
Low complement levels
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

Hand eczema

24 September، 2024/in Articles, Students Club/by Editorial Team

Definition:

Hand dermatitis, also known as hand eczema, is a common inflammatory skin condition affecting the palms and backs of the hands.

It can be acute or chronic, often presenting with redness, thickened skin, scaling, swelling, and cracks. Chronic hand eczema (CHE) refers to cases lasting over three months or recurring frequently within a year.

Epidemiology:

Hand dermatitis accounts for 20–35% of all dermatitis cases, though it is particularly common in young adult females it can occur at any age. It is more prevalent in individuals with a history of atopic dermatitis.

Chronic hand eczema (CHE) affects an estimated 10–15% of the population, frequently observed in occupations involving wet work or chemical exposure.

Etiology:

Hand eczema results from a combination of genetic and environmental factors:

Genetic susceptibility (such as mutations in the filaggrin gene (FLG) impairs the skin barrier, leading to increased water loss and susceptibility to irritants and allergens.

Environmental factors like repeated exposure to water, detergents, and chemicals, especially through occupational tasks.
Additionally, allergic contact dermatitis can contribute to the condition.

Clinical features:

Hand eczema is typically bilateral, affecting both the palmar and dorsal surfaces of the hand. Common symptoms include burning, stinging, and itching. The condition can alternate between acute flare-ups, which cause redness, swelling, weeping, and the formation of vesicles, and a chronic phase that is marked by nail changes (such as cuticle loss, thickening of nail folds (chronic paronychia), and nail plate ridging), lichenification, dry, thickened skin, and fissures.

Diagnosis:

The diagnosis of hand eczema is primarily clinical and involves a comprehensive approach, starting with a detailed personal and occupational history to identify any personal or family history of atopy and potential exposure to irritants or allergens, A physical examination assesses the extent of hand involvement, along with a complete skin examination.

Patch testing is crucial for identifying allergens in patients with CHE unresponsive to treatment.
Additional tests, such as skin prick tests, KOH preparation, and bacterial cultures, may be used to rule out other conditions. Also, in some cases, a skin biopsy is necessary to exclude other causes.

Management:

The management of hand eczema focuses on educating patients about proper Hand care, avoiding irritants and allergens, using non-soap cleansers, and applying thick emollients frequently.

For mild to moderate cases, high-potency topical corticosteroids are recommended, alongside liberal use of emollients. Steroid-sparing options like topical Calcineurin inhibitors (e.g., Tacrolimus) can also be used as an alternative.
In severe or unresponsive cases, a short course of oral corticosteroids may be necessary. Alternative treatments include phototherapy, oral immunosuppressants (such as methotrexate, cyclosporin, or azathioprine), or alitretinoin.
Dupilumab is an option for atopic CHE, and systemic antibiotics are prescribed if secondary bacterial infections are present.

Written by:

Raneem Alahmadi, Medical Intern.

Revised by:

Naif Alshehri, Medical Intern

Resources:

Dermnet

UpToDate

Seborrheic dermatitis

18 September، 2024/in Articles, Students Club/by Editorial Team

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

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

Specific Measures

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