Atopic eruption of pregnancy

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Definition 

Atopic eruption of pregnancy (AEP) is a pruritic skin condition associated with pregnancy, manifesting as eczematous or papular lesions in individuals with an atopic background. It often begins during early pregnancy, with 75% of cases occurring before the third trimester. AEP includes eczema in pregnancy, prurigo of pregnancy, and pruritic folliculitis of pregnancy, previously classified as separate conditions. While most cases involve new-onset atopic changes, some represent exacerbations of pre-existing atopic dermatitis. The disorder is not linked to adverse fetal outcomes and tends to recur in subsequent pregnancies.

 

Epidemiology

AEP is the most common pregnancy-related dermatosis, accounting for over 50% of such cases. Its exact incidence is unclear but may range from 1 in 5 to 1 in 20 pregnancies. It is more prevalent in individuals with a personal or family history of atopy, such as asthma, allergic rhinitis, or atopic dermatitis.

 

Etiology

AEP is linked to immunologic changes during pregnancy. Pregnancy is characterized by reduced T-helper 1 (Th1) cytokine production (e.g., IL-12, interferon-γ) and enhanced T-helper 2 (Th2) cytokine production (e.g., IL-4, IL-10). This shift toward a Th2-dominant immune response exacerbates the existing imbalance in atopic individuals, potentially triggering the development of AEP. While a connection to a history of atopy is recognized, its role remains debated.

 

Clinical Features

AEP typically manifests during the first or second trimester. About 80% of patients experience new-onset atopic changes, while 20% have a recurrence of pre-existing atopic dermatitis.

  • Eczematous Lesions (E-Type AEP):

Most cases involve widespread eczematous eruptions affecting the face, neck, and flexural areas. These lesions may appear as patches or excoriated papules. Severe dryness and signs of atopy are common.

  • Prurigo of Pregnancy (P-Type AEP):

Characterized by grouped erythematous papules or nodules on extensor surfaces, abdomen, and trunk, which may be excoriated or crusted. Lesions typically resolve postpartum.

  • Pruritic Folliculitis:

Rare presentations involve follicular papulopustular eruptions resembling steroid-induced acne. These lesions, initially appearing on the abdomen, may spread and are mildly pruritic. They generally resolve within weeks postpartum.

 

Diagnosis

AEP is primarily diagnosed clinically, based on characteristic lesions and a history of atopy. Skin biopsy is rarely helpful due to nonspecific findings but may be performed if the diagnosis is uncertain or to rule out conditions like pemphigoid gestationis. Elevated serum IgE levels are seen in up to 70% of cases. Folliculitis should be cultured to exclude bacterial or fungal infections.

 

Management

The treatment of AEP focuses on symptom relief:

  1. Topical Corticosteroids:

Low- to mid-potency corticosteroids are the first-line treatment for cutaneous lesions.

  1. Emollients and Hydration:

Regular use of emollients helps maintain skin hydration.

  1. Oral Antihistamines:

Chlorpheniramine, loratadine, or cetirizine can alleviate pruritus.

  1. Other Topical Treatments:

Tacrolimus for sensitive areas (e.g., face, intertriginous zones), urea-based creams, and menthol-containing products are safe during pregnancy.

  1. Severe Cases:

UVB therapy may be considered. Secondary bacterial infections should be treated with pregnancy-safe antibiotics like penicillins or cephalosporins.

 

Prognosis

AEP does not adversely affect the fetus and typically resolves postpartum, although symptoms may persist for a few weeks. The condition often recurs in subsequent pregnancies.

  

Written by: 

Raneem Alahmadi, Medical Intern.

Revised by:

 Naif Alshehri, Medical Intern

Resources:

Bologina 5th edition

UpToDate

Polymorphic eruption of pregnancy

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What is Polymorphic eruption of pregnancy?

Polymorphic eruption of pregnancy, also known as Pruritic Urticarial Papules and Plaques of Pregnancy (PUPPP), is a benign dermatological condition characterized by an intensely pruritic, erythematous rash. It typically manifests in the third trimester of pregnancy, initially presenting in the striae distensae (stretch marks) of the abdomen, and often resolves spontaneously following delivery.

 

 Causes of Polymorphic eruption of pregnancy

The exact cause of Polymorphic Eruption of Pregnancy is not fully understood, although it is believed to be triggered by skin stretching, particularly on the abdomen, which induces an immune response due to connective tissue damage. The condition occurs in about 1 in 160 pregnancies, with a higher incidence in primigravid women. It is more common in women with white skin, and the risk increases with excessive weight gain or multiple gestations. Additionally, carrying a male fetus is associated with a higher risk than carrying a female fetus

 

Clinical features of Polymorphic eruption of pregnancy 

Polymorphic eruption of pregnancy (PEP) typically manifests during the third trimester, often in the final weeks of gestation. Approximately 15% of affected women report the onset of symptoms postpartum. The condition initially presents with small, pink papules, predominantly located within the stretch marks around the umbilicus, frequently accompanied by a pale halo surrounding each lesion. Over time, these papules merge to form large, erythematous, urticated plaques, with occasional vesicular lesions. The rash progressively extends from the abdomen to the buttocks and thighs and may occasionally involve the arms and legs; however, lesions are rarely seen on or above the breasts. PEP is characteristically pruritic, with intense itching that often disrupts sleep.

 

Diagnosis of Polymorphic eruption of pregnancy

Polymorphic eruption of pregnancy is typically diagnosed based on clinical history and characteristic findings. There are no definitive diagnostic tests for this condition, and skin biopsy results are generally nonspecific.

 

Treatment of Polymorphic eruption of pregnancy

 Polymorphic eruption of pregnancy does not have a curative treatment. Symptomatic management typically includes:

  • Emollients
  • Topical corticosteroids: Applied sparingly once or twice daily to alleviate pruritus and erythema.
  • Systemic corticosteroids: A short course (e.g., prednisone) may be considered in severe cases.
  • Antihistamines: Oral antihistamines are generally safe in late pregnancy.

 

Prognosis of Polymorphic eruption of pregnancy

Polymorphic eruption of pregnancy typically persists until delivery and generally resolves within 4 to 6 weeks postpartum. However, in rare instances, the condition may persist beyond this period

Recurrence of polymorphic eruption of pregnancy is rare; when it does occur, it is typically less severe.

 

 

Written by:

Atheer Alhuthaili, Medical Intern.

Revised by:

Naif Alshehri, Medical Intern.

References:

DermNet.

Medscape

Leukonychia

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Background

Leukonychia, or white nail, is defined as partial or complete whitening of the nail plate affecting one or more fingernails or toenails. The nail loses its natural pink color, taking on a white appearance. It can be classified according to the underlying pathology, its distribution, or its mode of onset.

 

Classification according to pathology

  • True leukonychia: 
    • Due to abnormal nail plate keratinisation. 
    • The white nail will not be hidden by pressure application of the nail plate.
  • Apparent leukonychia: 
    • Secondary to disease of the nail bed. 
    • Disappears with pressure application on the nail.

Classification according to distribution

Leukonychia can be partial or total.

  • Total leukonychia: whitening of the entire nail plate.
  • Partial leukonychia: 3 subtypes are described.
    • Punctate
    • Longitudinal
    • Striate

Classification by development timeline

White nails can be acquired or congenital.

  • Congenital: Familial leukonychia is more commonly inherited recessively, although dominant patterns are possible
  • Acquired: Secondary to systemic disease. 

 

Causes

  • Trauma
  • Poisoning and drugs
    • Heavy metal poisoning (eg lead, arsenic)
    • Chemotherapy
    • Sulphonamides
  • Systemic illness
    • Liver cirrhosis
    • Chronic kidney disease
    • Heart failure
    • Hypoalbuminemia 
    • Protein-losing enteropathy
    • Diabetes
    • Iron deficiency (anaemia)
    • Zinc deficiency
    • Hyperthyroidism.

 

Diagnosis

History and physical examination are typically adequate.

The following can provide additional insight:

  • Nail clippings to rule out fungal infections
  • Nail biopsy
  • Blood tests to evaluate systemic disease.

 

Treatment 

  • Management varies based on the underlying cause.
  • Trauma-induced leukonychia has no specific treatment.
  • Punctate lesions will disappear as the nail follows its natural growth pattern.

 

 

Written by:

Dr. Renad Alkanaan

Revised By: 

Naif Alshehri, Medical Intern

Resources: 

Dermnet

UpToDate

Nail Psoriasis

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Definition

Nail psoriasis, also known as psoriatic nail dystrophy, is a manifestation of psoriasis affecting the nail bed, nail matrix, or both. It presents specific and non-specific clinical changes, including pitting, onycholysis, subungual hyperkeratosis, and nail discoloration. Nail involvement is often associated with psoriatic arthritis and can significantly impact quality of life due to pain, functional limitations, and psychological distress.

 

Epidemiology

Nail psoriasis occurs in 10–90% of psoriasis patients, with higher prevalence in adults compared to children. It often coincides with skin or joint psoriasis but may also present as the sole manifestation of the disease. Up to 80–90% of patients with psoriatic arthritis exhibit nail changes. Although nail psoriasis affects all ages and sexes, a slight male predominance has been noted. Severe or chronic plaque psoriasis increases the likelihood of nail involvement.

 

Etiology

Nail psoriasis arises from psoriatic inflammation in the nail matrix or nail bed:

  • Matrix involvement causes pitting, leukonychia, red spots in the lunula, and nail crumbling.
  • Nail bed involvement leads to oil-drop discoloration, onycholysis, subungual hyperkeratosis, and splinter hemorrhages.

 Theories on etiology include dysregulated immunity (e.g., IL-10 expression), trauma (Koebner phenomenon), and secondary infections like onychomycosis. Genetic factors, such as the HLA-Cw6 allele, contribute to cutaneous psoriasis but may differ in nail disease.

 

Clinical Features

Nail psoriasis can affect fingernails, toenails, or both, and patients often experience pain, tenderness, and difficulty with fine motor tasks. Common manifestations include:

  • Matrix-related changes:

–  Pitting (punctate depressions)

–  Leukonychia (white discoloration)

–  Red spots in the lunula

–  Nail crumbling

  • Nail bed-related changes:

–  Oil-drop discoloration or salmon patches

–  Onycholysis (distal nail separation)

–  Subungual hyperkeratosis (keratin accumulation)

–  Splinter hemorrhages

Severe cases may involve all 20 nails, with additional complications like paronychia and acrodermatitis continua of Hallopeau.

 

Diagnosis

Diagnosis is primarily clinical, especially in patients with cutaneous psoriasis or psoriatic arthritis. The Nail Psoriasis Severity Index (NAPSI) helps quantify disease severity. Fungal infections (onychomycosis) must be ruled out through microscopy or culture, as they can mimic or exacerbate nail psoriasis. In rare cases, a proximal nail matrix biopsy is needed to confirm the diagnosis or exclude malignancy, though this may cause permanent nail deformity. 

 

Management 

Treatment depends on severity:

  1. Mild Disease

– Topical corticosteroids (e.g., betamethasone, clobetasol)

– Vitamin D analogs (e.g., calcipotriol)

– Combination therapies

  1. Moderate to Severe Disease

– Systemic treatments:

– Methotrexate

– Acitretin

– Biologics (e.g., infliximab, adalimumab, ustekinumab)

– Small molecules (e.g., apremilast, tofacitinib)

– Non-pharmacologic interventions: Phototherapy ,Laser treatments.

  1. General Measures:

– Minimize nail trauma and keep nails short.

– Address coexisting onychomycosis before initiating psoriasis treatments.

 

Written by: 

Raneem Alahmadi, Medical Intern

Revised by:

Naif Alshehri, Medical Intern

Resources:

Bologina 5th edition

Dermnet

UTD

Parakeratosis Pustulosa

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What is Parakeratosis Pustulosa?

Parakeratosis pustulosa is a condition characterized by the deformation of the fingernail or toenail, accompanied by surrounding erythema and often scaling of the overlying skin. It predominantly affects the thumb or index fingernail in young children, although it can occasionally involve other digits, including toenails. The condition is approximately three times more prevalent in females.

Initial manifestations typically involve erythema beneath the free margin of the nail, which subsequently extends to the nail fold, resulting in swelling and the loss of the cuticle. As the condition progresses, thickened skin pushes upward, leading to deformities in the nail plate. Parakeratosis pustulosa is generally not pruritic, though it may cause mild pain .

 

 Causes

The exact cause of parakeratosis pustulosa is not fully understood. While it may be associated with various skin conditions, the specific mechanisms remain unclear in many cases.

 

Clinical features 

An affected nail may exhibit a variety of clinical signs, including:

  • Subungual hyperkeratosis 
  • Onycholysis
  • Onychomadesis 
  • Pitting 
  • Transverse ridging 
  • Ragged or absent cuticles
  • Erythema of the periungual skin
  • Blister formation on the fingertips

These signs can complicate the differentiation from other dermatological conditions, such as psoriasis and atopic dermatitis, leading to frequent misdiagnosis despite their common occurrence

 

Diagnosis

 Parakeratosis pustulosa is primarily a clinical diagnosis, with diagnostic investigations conducted to exclude other potential nail disorders.

  • Swab cultures may aid in identifying microorganisms associated with paronychia.
  • Tinea infection can be diagnosed through the detection of fungal hyphae in skin scrapings.
  • Biopsy  can distinguish between atopic dermatitis and psoriasis, it is infrequently required in clinical practice.

 

Treatment

 There is no specific treatment for Parakeratosis pustulosa .However, most cases tend to improve gradually over time. The following treatments have been occasionally found to be beneficial:

  • Emollients
  • High-potency topical corticosteroids
  • Topical retinoids
  • Calcipotriol

The duration of lesions can vary, ranging from one week to several years, although recurrences are infrequent.                                                                     

 

Written by:

Atheer Alhuthaili, Medical Intern

Revised by:

Naif Alshehri, Medical Intern

References:

DermNet

Medscape

Glomus Tumor

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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

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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

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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

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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

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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

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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

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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