Impetigo

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Overview:

Impetigo is the most common bacterial skin infection in children. It is a highly contagious superficial infection primarily caused by the Staphylococcus aureus and, less commonly, Streptococcus pyogenes. The condition can present in two forms: non-bullous and bullous impetigo.

 

Epidemiology:

  • Primarily affects children <6 years of age. 
  • Highly contagious and spreads through direct contact with an infected individual or contaminated objects (fomites). 

Predisposing factors: 

Several factors increase the risk of developing impetigo, including:

  • Environmental factors: Warm temperature and high humidity 
  • Poor hygiene 
  • Underlying skin conditions: Atopic dermatitis, scabies, and chicken pox.
  • Skin trauma: Lacerations, insect bites, and burns.

 

Pathogenesis:

Infection occurs when bacteria enter through minor skin breaks, such as scratches, trauma, or other skin infections. Disruption of the skin barrier allows bacterial adherence and invasion, leading to infection.

 

Clinical features:

Non-Bullous Impetigo (Most common form):

Lesion characteristics:

  • Commonly appears on the face (especially around the nose and mouth) and extremities.
  • Initially presents as a single erythematous macule, which evolves into vesicle or pustule.
  • Later develops into superficial erosions covered by characteristic honey-colored yellow crusts.
  • Minimal or no surrounding erythema.

Bullous Impetigo:

Lesion characteristics:

  • Affects the face, trunk, buttocks, axillae, and extremities.
  • Begins as small vesicles that enlarge into superfecial Bullae.
  • In late stages, bullae become flaccid and transparent, then ruptures to leave scale with no thick crust.
  • More likely to be associated  with systemic symptoms.

 

Diagnosis:

  • Impetigo is primarily a clinical diagnosis.
  • A skin swab culture (from the exudate beneath crusts or fluid from an intact bullae) may be performed for confirmation.
  • Approximately 50% of patients may have leukocytosis.

 

Treatment:

General Measures:

  • Cleanse the affected area and remove crusts.
  • Maintain proper hand hygiene.

Topical Antibiotics:

For healthy patients with few lesions and no systemic symptoms, the following topical treatments are recommended:

Mupirocin, retapamulin, or ozenoxacin.

Oral Antibiotics:

Systemic antibiotic therapy is required in the following situations: 

  • Bullous impetigo 
  • Widespread non-bullous impetigo 
  • Failure to respond to topical treatment 
  • High risk of complications 
  • Presence of comorbidities 

First line oral antibiotic: flucloxacillin

Prevention:

  • Avoid touching affected areas.
  • Practice regular hand hygiene.
  • Refrain from sharing personal items, such as towels and clothing.
  • Change and wash clothing and bedding daily in hot water.
  • Avoid close contact with others.

 

Done by:

Layan Alshehri, Medical Intern 

Revised by:

Naif Alshehri, Medical Intern

Resources:

Bolognia 5th Edition

DermNet

Reactive perforating collagenosis

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Definition

Reactive perforating dermatoses are characterized by the transepidermal elimination of dermal connective tissue through the epidermis. 

Reactive perforating collagenosis (RPC) is a form of perforating dermatosis involving the extrusion of altered collagen fibers. RPC can be inherited or acquired, with inherited cases often triggered by trauma or cold exposure. 

The acquired form is more common and frequently associated with systemic conditions such as diabetes mellitus or chronic kidney disease, particularly in patients undergoing dialysis, where pruritus-induced trauma exacerbates the condition.

 

Epidemiology : 

RPC occurs globally without a clear racial predilection. The inherited form is rare and often familial, with onset typically in infancy or early childhood. It may follow either an autosomal dominant or autosomal recessive inheritance pattern. In contrast, the acquired form is more prevalent and usually develops later in life, showing a higher incidence in women with a female-to-male ratio of approximately 3:1. Acquired RPC is strongly associated with chronic systemic illnesses such as diabetes and chronic kidney disease,

 

Etiology

The exact pathogenesis of RPC remains uncertain, but key factors include:

  1. Inherited Form:

 – Linked to genetic abnormalities in collagen structure, leading to focal damage and extrusion through the epidermis.

 – Triggers such as trauma or cold weather often exacerbate the condition.

  1. Acquired Form:

 – Associated with microvascular insufficiency and elevated plasma fibronectin levels, commonly seen in diabetes and chronic kidney disease.

 – Abnormal glycosylation of collagen types I and III in diabetes may alter collagen fibers, contributing to their extrusion.

 – Superficial trauma, scratching, and cold exposure lead to epidermal thinning and necrobiosis in susceptible patients.

 

Clinical Features

RPC typically manifests as a papulonodular mucocutaneous disorder. Lesions appear as red-brown umbilicated papules or nodules with a central keratotic plug and an erythematous halo. The size of the lesions can range from a few millimeters to 10 mm, though rare giant forms measuring up to 10 cm have been reported.

 Lesions are intensely pruritic but are rarely painful or tender. Inherited RPC often affects the hands, elbows, and knees, while the acquired form commonly involves the legs. In both forms, the distribution is generally symmetrical, and lesions may appear more widely scattered or even generalized. A hallmark feature of RPC is the Koebner phenomenon, where new lesions develop in response to trauma or scratching. Lesions typically resolve spontaneously within 6 to 10 weeks, though they may leave post-inflammatory hyperpigmentation or scarring.

 

Diagnosis 

Diagnosis is primarily clinical, based on characteristic lesions and associated systemic conditions.

 – Dermoscopy: May reveal central keratotic plugs and erythematous halos.

 – Skin Biopsy: Multiple biopsies are often required to confirm the histopathological findings, including transepidermal elimination of altered collagen.

 

Management

The management of RPC can be challenging, particularly in the acquired form, as it often involves addressing both the skin lesions and any underlying systemic conditions. Treatment typically focuses on reducing pruritus, minimizing trauma, and promoting lesion healing.

– Topical Treatments:

  • Corticosteroids: Superpotent formulations under occlusion can reduce inflammation.
  • Retinoids: Topical agents like tretinoin may aid in reducing keratotic plugging.
  • Emollients: Improve skin hydration and barrier function.

– Systemic Therapies:

  • Antihistamines: Sedating antihistamines help alleviate itching and improve sleep.
  • Oral Retinoids: Acitretin can reduce lesion severity.
  • Allopurinol: May be considered for refractory cases.

– Procedural Interventions:

  • Intralesional Corticosteroids
  • Cryotherapy or Curettage

– Phototherapy:

  • Broadband or Narrowband UVB: Particularly beneficial for patients with chronic kidney disease, as it can relieve pruritus and improve skin lesions.

– Lifestyle Modifications:

  • Avoid scratching and trauma to the skin to prevent exacerbations. Optimize management of systemic diseases like diabetes and renal dysfunction.

 

 

Written by: 

Raneem Alahmadi, Medical Intern.

Revised by: 

Naif Alshehri, Medical Intern.

Resources:

Bolognia 5th edition

Dermnet

Scabies

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Overview:

Scabies is a contagious skin infestation caused by Sarcoptes scabiei var. hominis mite. It leads to severe pruritus and skin lesions due to the mite burrowing into the epidermis. 

 

Epidemiology:

Scabies is a widespread condition affecting individuals of all ages, ethnicities, and socioeconomic groups. Factors contribute to its spread:

  • Overcrowded living conditions 
  • Delayed diagnosis and treatment 
  • Limited public awareness 
  • Poor hygiene 

Transmission can be through direct skin to skin contact, and indirectly through contaminated objects (fomites). 

A severe form of scabies, crusted scabies (Norwegian scabies), occurs in immunocompromised individuals, and is highly contagious. 

 

Pathogenesis:

The Incubation period varies:

  • First time infestation: symptoms appear within 2 to 6 weeks, 
  • Reinfestation: symptoms develop faster,  within 24 to 48 hours. 

Scabies mites can survive outside the human body for up to 3 days. However, in crusted scabies, mites can survive up to 7 days. 

 

Clinical features:

Itching (pruritus):

  • Often severe and worse at night or with hot showers. 
  • It can be the first symptom before visible skin lesions appear.

Lesions distribution and appearance: 

  • Lesions present as small erythematous papules with varying degree of excoriations. 
  • Other possible lesions include nodules and vesicles.  
  • Symmetrically affects interdigital web spaces of the hands, wrists, axillae, waist, ankles, feet, and buttocks. 
  • The face and scalp are typically spared, except in infants, elderly, immunocompromised patients, and in crusted scabies cases.
  • Burrows is a pathognomonic sign, representing the tunnels created by female mites as they lay eggs. Burrows appear as grayish-white, thread like lines, measuring 1 to 10 mm in length. 
  • Crusted scabies has a widespread involvement of thick scaling and crusting.

 

Diagnosis:

Diagnosis is clinically, based on history and physical examination. Can be confirmed using diagnostic methods include:

  • Dermoscopy allows visualization of mites and eggs. 
  • Skin scraping and microscopy using mineral oil preparation. 

 

Treatment:

First line treatment: Topical Permethrin 5%

  • Applied from head to toe in infants and elderly. In other age groups, face and scalp are excluded from treatment. Applied overnight for 8 to 12 hours on day 1 and 8. 

Environmental and Preventive Measures:

  • Clothing, bedding, and towels should be washed in hot water and dried in high heat or sealed in a bag for 7 to 10 days. 
  • All close contacts, even asymptomatic, must be treated in the same way. 

Post-Treatment: 

  • After successful treatment, pruritus and skin lesions may persist for 2 to 4 weeks, this is called post scabetic pruritus. 

Oral ivermectin is an option for treatment failures, outbreaks, or non-adherence, with a repeat dose after two weeks. Other alternatives include 25% benzyl benzoate or 0.5% malathion lotion.

 

Done by:

Layan AlShehri, Medical Intern 

Revised by: 

Naif Alshehri, Medical Intern

Resources:

Bolognia 5th Edition. 

DermNet

Dupilumab in Dermatology: Mechanism, Benefits, and Considerations

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Introduction

Dupilumab (Dupixent®) is a monoclonal antibody therapy designed to treat inflammatory conditions, primarily atopic dermatitis. It is the first biologic treatment approved for moderate to severe atopic dermatitis and has since been expanded to other allergic and inflammatory diseases. By blocking specific immune signaling pathways, dupilumab offers an effective alternative for patients who do not respond adequately to conventional therapies.

 

Mechanism of Action

Dupilumab is a human IgG4 monoclonal antibody that specifically binds to the IL-4Rα subunit, a key component of the receptor shared by interleukin-4 (IL-4) and interleukin-13 (IL-13). These two cytokines play a crucial role in Th2-mediated inflammation, which is a major driver of conditions like atopic dermatitis and asthma. By inhibiting IL-4 and IL-13 signaling, dupilumab reduces inflammation, improves skin barrier function, and alleviates symptoms.

 

Indications

Dupilumab is FDA-approved for the treatment of:

  • Atopic dermatitis (eczema) in patients ≥6 months old with moderate-to-severe disease that is inadequately controlled with topical treatments.
  • Prurigo nodularis in adults.
  • Asthma in patients ≥6 years old with moderate-to-severe disease.
  • Eosinophilic esophagitis in patients ≥12 years old.
  • Chronic rhinosinusitis with nasal polyps in adults.

Additionally, off-label uses of dupilumab are being explored for spontaneous chronic urticaria, nummular eczema, allergic contact dermatitis, chronic hand eczema, bullous pemphigoid, and Netherton syndrome.

 

Dosage and Administration

Dupilumab is administered via subcutaneous injection, with dosing dependent on age and weight:

  • Adults and children (≥60 kg): 600 mg loading dose, then 300 mg every 2 weeks.
  • Children (30–59 kg): 400 mg loading dose, then 200 mg every 2 weeks.
  • Children (15–29 kg, ≥6 years old): 600 mg loading dose, then 300 mg every 4 weeks.
  • Children (5–14 kg, ≤5 years old): 200 mg every 4 weeks.

 

Contraindications and Precautions

Dupilumab is contraindicated in patients with a known hypersensitivity to the drug or its components. Additionally, live vaccines should be avoided, and patients should be up to date on their vaccinations before starting therapy.

Patients with serious active helminth infections (parasitic worms) should be treated before starting dupilumab.

 

Adverse Effects

While generally well-tolerated, dupilumab can cause certain side effects, the most common being:

  • Injection site reactions
  • Ocular diseases (conjunctivitis, dry eyes, blepharitis, keratitis)
  • Herpes infections
  • Atopic dermatitis exacerbation
  • Nasopharyngitis (common cold symptoms)
  • Headache and upper respiratory infections

Ocular side effects occur in approximately 10% of patients and usually develop within the first few weeks to months of treatment. Artificial tears, antihistamine eye drops (e.g., ketotifen), corticosteroids, cyclosporine, and tacrolimus ointment may be used for management.

Some patients may also experience facial or neck erythema, or dermatitis that is possibly linked to rosacea, allergic contact dermatitis, or Malassezia related dermatitis. 

Rare but reported conditions associated with dupilumab include psoriasiform eruptions, lichen planus-like reactions, and eosinophilic granulomatosis with polyangiitis.

 

Clinical Outcomes and Efficacy

Clinical trials have demonstrated that 40–50% of adolescents and adults receiving dupilumab alone, and 60–70% of children or adults receiving it in combination with topical corticosteroids, achieve a 75% improvement in their Eczema Area and Severity Index (EASI-75).

 

Conclusion

Dupilumab has revolutionized the management of atopic dermatitis and other Th2-driven inflammatory conditions, offering a safe and effective option for patients with moderate-to-severe disease. While its side effects, particularly ocular symptoms, should be monitored, its benefits in reducing inflammation and improving quality of life make it a cornerstone therapy in dermatology and beyond.

 

Written by: 

Naif Alshehri, Medical Intern 

Resources: 

Saudi MOH Atopic Dermatitis Guidelines

Dermnet

Bolognia Dermatology Textbook 5th Edition

Muñoz-Bellido FJ, Moreno E, Dávila I. Dupilumab: A Review of Present Indications and Off-Label Uses. J Investig Allergol Clin Immunol. 2022;32(2):97-115. doi:10.18176/jiaci.0682

Second Picture Resource:

Bolognia Dermatology Textbook 5th Edition

Pustular psoriasis of Pregnancy

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Introduction

Pustular psoriasis of pregnancy (PPP), formerly known as impetigo herpetiformis, is a rare, severe variant of generalized pustular psoriasis uniquely associated with pregnancy. It most commonly arises during the third trimester but can occur earlier or postpartum and has a tendency to recur in subsequent pregnancies, often at an earlier stage. Hormonal factors, such as oral contraceptive use and menstrual cycles, are believed to contribute to its onset. Additionally, a personal or family history of psoriasis highlights the role of genetic and immunological predisposition. 

 

Clinical Manifestation

PPP typically presents with symmetrical, annular, or polycyclic erythematous plaques surrounded by sterile pustules at their margins. These lesions begin in intertriginous areas and gradually spread to the trunk and extremities, sparing the face, palms, and soles. Over time, pustules coalesce to form large plaques with scaling and residual red-brown pigmentation. Oral mucosal involvement is rare but may cause erosive lesions.

Systemic symptoms are common and include fever, malaise, nausea, vomiting, diarrhea, and arthralgia. Severe cases may present with life-threatening complications such as tachycardia, delirium, tetany, or seizures. While pruritus is uncommon, nail changes like onycholysis and pitting may occur.

 

Diagnosis

The diagnosis of PPP is primarily clinical, based on the characteristic pustular rash and associated systemic symptoms. Microbiological swabs of pustules, often negative, are useful in excluding infectious causes. Laboratory tests typically show leukocytosis, elevated inflammatory markers, and metabolic abnormalities such as hypocalcemia and hypoalbuminemia. Histopathological examination of a skin biopsy remains the definitive diagnostic tool, revealing hallmark features such as spongiform pustules of Kogoj, psoriasiform hyperplasia, and neutrophilic infiltration in the epidermis. Accurate diagnosis is vital to ensure timely management and reduce maternal and fetal complications.

 

Treatment

The goal of management in Pustular Psoriasis of Pregnancy is to alleviate mother symptoms and protect fetal health.

General measures

  • Ensure adequate hydration and maintain electrolyte balance
  • Provide pain relief 
  • Emollients 
  • Monitor fetal well-being closely via ultrasound and non-stress tests

Medications

  • High dose systemic steroids 
  • Suitable alternatives like cyclosporine and biologics agents like infliximab may be used in refractory cases 
  • Narrowband UVB is an option for mild disease
  • Retinoids or methotrexate can be used postpartum in non-breastfeeding patients

Prognosis 

Pustular psoriasis of pregnancy usually settles quickly after delivery of the baby, although some changes of psoriasis may persist long-term.

Pustular psoriasis of pregnancy can recur with subsequent pregnancies, and may present earlier in the next pregnancy and in a more severe form. Pustular psoriasis of pregnancy carries a poor prognosis for mother and/or fetus if untreated.

 

Written by: 

Dr. Renad Alkaanan

Revised by: 

Naif Alshehri, Medical Intern 

Resources: 

UpToDate

Dermnet

Pyogenic Granuloma

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Introduction

Pyogenic granuloma, also known as lobular capillary hemangioma, granuloma gravidarum, or pregnancy tumor, is a benign vascular lesion characterized by the rapid proliferation of capillary blood vessels in the skin or mucosa. Despite its name, it is neither pyogenic nor granulomatous. Modern research shows it arises due to reactive neovascularization without any infectious involvement.

 

Epidemiology

Pyogenic granulomas (PGs) can develop at any age but are most common in children, teenagers, and young adults. A slight male predominance is observed overall, except for oral lesions, which are more frequent in females due to hormonal influences like pregnancy or oral contraceptive use. Rare presentations include neonates with multifocal PGs or adults with eruptive disseminated forms.

 

Etiology and Pathogenesis

PGs are often linked to pre-existing trauma or irritation, hormonal changes, or specific medications. Minor trauma accounts for 7% of cases, while oral lesions are commonly associated with chronic irritation and poor dental hygiene. Hormonal changes during pregnancy or contraceptive use are significant factors, with 5% of pregnant women developing gingival PGs.
Medications like retinoids, protease inhibitors, and cancer-targeted therapies can also trigger PGs. Additionally, molecular studies have identified mutations in the BRAF and NRAS genes, which activate the MAPK signaling pathway, suggesting a neoplastic component in some cases.

 

Clinical Features

PGs typically present as painless, red nodules or polyps that grow rapidly over weeks. The lesions are highly friable, frequently ulcerating or bleeding after minor trauma. They stabilize at sizes usually under 1 cm but may persist indefinitely if untreated. Common sites include the gingiva, lips, fingers, face, and tongue.

Oral mucosal PGs often develop as pedunculated or sessile nodules on the gums or lips. These lesions may ulcerate, develop a yellow fibrinous surface, and cause minor discomfort. Rarely, satellite lesions may arise near a primary PG after trauma or irritation.

 

Dermoscopy and Histology

Dermoscopy
Dermoscopy reveals a distinct keratinized border forming a white collarette around the lesion. Vascular structures are prominent, with red homogeneous areas and white linear “rail lines” being hallmark features.

Histological Findings
Histologically, PGs are characterized by a lobular arrangement of capillaries in the dermis surrounded by inflammatory cells and fibromyxoid stroma. The epidermis is often thinned or ulcerated, and a peripheral collarette formed by elongated rete ridges is typically present. Signs of hemorrhage and inflammatory infiltrates, including lymphocytes and plasma cells, are common. Oral PGs may show an additional granulation tissue-like vascular proliferation pattern.

 

Differential Diagnosis

The differential diagnosis for PG depends on its location and presentation:

Cutaneous Differential Diagnosis

  • Amelanotic melanoma: Most critical to exclude due to overlapping features.
  • Bacillary angiomatosis: Especially in immunosuppressed patients.
  • Kaposi sarcoma: Seen in HIV-positive individuals.
  • Cherry angioma: Benign capillary proliferation.
  • Irritated melanocytic nevus or wart: May mimic PG due to irritation.

Oral Differential Diagnosis

  • Peripheral giant cell granuloma
  • Peripheral ossifying fibroma

Histological Differential Diagnosis

  • Cherry angioma
  • Bacillary angiomatosis

 

Treatment

Treatment focuses on lesion removal and addressing contributing factors to prevent recurrence. Options include:

    • General Measures: Improving oral hygiene, removing trauma sources, and discontinuing triggering medications.
    • Topical Treatments: Timolol gel, imiquimod cream, cryotherapy, or table salt therapy (applied under occlusion).
  • Procedural Treatments:
    • Shave excision with electrosurgery: The most common approach.
    • Curettage and cautery: Effective but with recurrence risk.
    • Pulsed dye laser: Safe and effective for smaller lesions, particularly in children.
    • Sclerotherapy: Using monoethanolamine oleate for minimal scarring.
    • Surgical excision: Offers lower recurrence rates, especially in gingival lesions.

 

Prognosis

Pyogenic granulomas are benign and rarely resolve spontaneously, except in postpartum cases. Recurrence is common, particularly in gingival lesions or cases with persistent irritation or inadequate treatment. With appropriate intervention, the prognosis is excellent.

 

Written by: 

Naif Alshehri, Medical Intern. 

Resources: 

Dermnet

Bolognia Textbook 5th Edition

Pemphigoid  Gestationis

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Epidemiology:

Pemphigoid  Gestationis  is  a  rare,  self-limited,  autoimmune  bullous disease.  It  is  the  most  clearly  characterized  dermatosis  of  pregnancy and the only type of dermatosis of pregnancy that may also affect the skin of the newborn. The  incidence  of  pemphigoid  gestationis  has  been  estimated  at 1:20,000–1:50,000  pregnancies.

 

Pathogenesis:

Pemphigoid gestationis is caused by circulating immunoglobulin G1 (IgG1) autoantibodies directed against the 180 kilodalton bullous pemphigoid antigen (BP180 or collagen XVII), a transmembrane hemidesmosomal glycoprotein expressed in the basement membrane zone of the skin. As in bullous pemphigoid, the binding of antibodies to antigens within the basement membrane zone stimulates an inflammatory cascade that results in separation of the epidermis from the dermis. In pemphigoid gestationis, the primary site of autoimmunity seems to be the placenta, as antibodies bind not only to the basement membrane zone of the epidermis, but also to that of chorionic and amniotic epithelia, both of ectodermal origin.

 

Clinical features:

Pemphigoid gestationis most often present in the second or third trimester of pregnancy. Intense pruritus may precede the onset of visible skin lesions. The rash typically begins on the trunk as urticarial plaques or papules surrounding the umbilicus. Vesicles may also be present. Lesions may be seen on the palms and soles but rarely on the face or mucous membranes. The eruption spreads rapidly and forms tense blisters. The entire body surface may be involved, but the mucous membranes are usually spared.

Pemphigoid gestationis may remit prior to delivery. However, 75 percent of patients have a flare postpartum, and at least 25 percent of patients subsequently have a flare with use of oral contraceptive pills or during menses. Most cases spontaneously resolve in the weeks to months following delivery. The disease usually recurs with subsequent pregnancies and is often worse but may also skip pregnancies.

 

Diagnosis: 

The diagnosis of pemphigoid gestationis is based upon the combination of clinical findings, examination of a lesional skin biopsy for routine histopathology and a perilesional skin biopsy for direct immunofluorescence (DIF). DIF reveals a homogeneous, linear deposit of complement C3 at the basement membrane zone. The presence of C3 is pathognomonic for pemphigoid gestationis in a pregnant patient.

 

Management:

The main goals of treatment of pemphigoid gestationis are to decrease blister formation, promote the healing of blisters and erosions, and relieve pruritus. In mild cases, the use of potent topical corticosteroids combined with emollients and systemic antihistamines may be adequate. However, systemic corticosteroids remain the cornerstone  of  therapy.  Most  patients  respond  to  0.5 mg/kg  of prednisolone  daily;  the  dose  is  tapered  as  soon  as  blister  formation  is suppressed. The common flare associated with delivery usually requires a  temporary  increase  in  dosage.  Those  rare  patients  with  refractory disease  may  benefit  from  plasmapheresis  during  pregnancy.

 

Done by: 

Bandar Alharbi, Medical Intern

Revised by:

Naif Alshehri, Medical Intern

Resources: 

Dermnet

UpToDate

Bolognia

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