Pemphigus Vulgaris


Pemphigus vulgaris is a rare autoimmune disorder characterized by painful blisters and erosions on the skin and mucous membranes, typically seen in the oral cavity. Pemphigus vulgaris is responsible for 70% of all cases of pemphigus globally.


Pemphigus vulgaris can occur in individuals of any race, age, or gender. The condition often manifests itself in individuals aged 30 to 60 and is more prevalent among individuals of Jewish and Indian descent compared to other ethnic groups, perhaps due to hereditary factors.

Drug-induced pemphigus is a recognized condition that is mostly caused by penicillamine, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and cephalosporins.


Pemphigus vulgaris is a blistering autoimmune disease. 

Keratinocytes are adhered together at distinct adhesive sites known as desmosomes. Pemphigus vulgaris is a condition where autoantibodies of the immunoglobulin type G (IgG) attach to a protein called desmoglein 3 (dsg3). This protein is located in the desmosomes of the keratinocytes, which are in the lower part of the epidermis. The outcome is the keratinocytes undergo separation, leading to their replacement by fluid, resulting in the formation of a blister. Approximately half of the individuals diagnosed with pemphigus vulgaris have anti-dsg1 antibodies.

Clinical features:

The majority of individuals with pemphigus vulgaris initially exhibit lesions on the mucous membranes, specifically in areas such as the mouth and genitals. Blisters often form on the skin within a few weeks or months, however in certain cases, only mucosal lesions may be present as a manifestation of the disease. 

Skin lesions manifest as thin-walled flaccid blisters containing transparent fluid that easily rupture resulting in itchy and painful erosions. They primarily occur on the upper chest, back, scalp, and face. Erosions occurring in the skin folds have the potential to progress into vegetative lesions characterized by a granular and crusty appearance, a condition known as pemphigus vegetans.

Characteristics of oral mucosal pemphigus include:

  • Oral lesions are seen in 50-70% of individuals.
  • Shallow blistering and erosion.
  • Widespread engagement inside the oral cavity.
  • Painful, slow-healing ulcers.
  • Difficulty eating and drinking.
  • Spread to the larynx, resulting in hoarseness when talking.


A biopsy of a blister is typically necessary to diagnose pemphigus vulgaris. The histological examination usually reveals keratinocytes that are rounded and separated (acantholytic cells) located immediately above the basal layer of the epidermis.

Pemphigus is confirmed by the use of direct immunofluorescence staining on skin biopsy sections taken from areas surrounding the lesions. This staining process helps to identify the presence of immunoglobulin (Ig)G antibodies or complement on the surfaces of keratinocytes.


The main objective of treating pemphigus vulgaris is to reduce the occurrence of blisters, prevent infections, and facilitate the healing process of blisters and erosions. Systemic corticosteroids are the primary method of medical treatment for managing the condition. Typically, this involves administering moderate to high dosages of oral prednisone or prednisolone or using pulsed intravenous methylprednisolone. Corticosteroids do not provide a cure for the disease, but they enhance the patient’s quality of life by decreasing disease activity. Administering the necessary dosages of corticosteroids to manage pemphigus vulgaris and the duration of treatment might lead to significant adverse effects and potential hazards.

The duration of therapy and the corticosteroid dosages required to manage pemphigus vulgaris can have major risks and adverse effects.

Patients with pemphigus vulgaris may require other immunosuppressive drugs for years in order to lower the dosage of steroids. These are typically:

  • Azathioprine
  • Mycophenolate mofetil
  • Cyclophosphamide
  • Rituximab. 

Topical therapy— refers to the use of medications or treatments that are applied directly to the skin or mucous membranes to treat a specific condition or disease.

Topical treatment for cutaneous pemphigus vulgaris may involve the use of topical corticosteroids and moisturizers.

The management of mucosal pemphigus vulgaris may involve the use of different preparations of a topical corticosteroid, intralesional corticosteroid, topical tacrolimus, or topical ciclosporin.

General management:

Proper wound care is crucial, as it helps facilitate the healing process of blisters and erosions.

  • When changing dressings, it is important to wear surgical gloves and follow the aseptic method.
  • Analgesics may be necessary, particularly when changing dressings.
  • Drain blisters that are still intact, but maintain the blister roof.
  • Apply non-adherent dressings (silicone mesh or gauze soaked in petrolatum, for example). 
  • Patients should limit activities that may damage the skin and mucous membranes while the condition is active. These activities include contact sports and eating food that has the potential to irritate or injure the oral cavity, such as spicy, acidic, hard, and crunchy meals.

Maintaining oral hygiene and practicing adequate dental care are crucial.

Written by:

Mashael Alanazi, Medical student 

Revised by:

Naif Alshehri, Medical Intern



Shiitake Flagellate Dermatitis

What is Shiitake Flagellate Dermatitis?

Shiitake dermatitis is a unique rash that can develop after consuming raw or undercooked shiitake mushrooms. It is distinguished by pruritic, erythematous, linear streaks that mimic whiplash marks, hence the name flagellate. It can be referred to as flagellate erythema or toxicodermia.
Shiitake mushrooms are consumed most frequently in China and Japan, and shiitake dermatitis is most common there. It affects approximately 2% of people who eat mushrooms raw or lightly cooked. It has been documented in people of all ages, with men being greater than women.

Causes of Shiitake Flagellate Dermatitis

Shiitake flagellate dermatitis is a toxic reaction to lentinan, which is contained in fresh, powdered, and lightly cooked shiitake mushrooms. Lentinan is a thermolabile polysaccharide that stimulates interleukin-1 secretion, resulting in vasodilation, hemorrhage, and rash. It is not caused by skin contact with the mushrooms.

Clinical features of Shiitake Flagellate Dermatitis

Shiitake dermatitis is characterized by a flagellate rash that typically develops 24 hours after consuming raw or undercooked mushrooms. The symptoms can appear within a few hours or up to 5 days after consuming the mushrooms. Linear streaks of itchy erythematous papules and, occasionally, petechiae appear.There may be localized swelling. It primarily affects the trunk, but it can also affect the limbs, neck, or head. It has no effect on mucousal surfaces.The rash can worsen with sun exposure.

Some people with shiitake flagellate dermatitis experience additional symptoms:

  • Localized oedema.
  • Malaise
  •  Fever
  • Lip tingling
  • discomfort when swallowing
  • Diarrhoea
  • Tingling in the hands and feet

Diagnosis of Shiitake Flagellate Dermatitis

The diagnosis is clinical, based on the typical history of recent mushroom consumption and the development of the rash. There were no specific laboratory findings. Usual tests may include:

  • Full blood count
  • Liver function tests.
  • Urea and electrolytes

Histopathology is nonspecific with hyperkeratosis, spongiosis, dermal oedema, and a perivascular lymphocytic infiltrate containing eosinophils.

Treatment of Shiitake Flagellate Dermatitis

Shiitake flagellate dermatitis is self-limiting. It is unclear whether therapy accelerates the rash’s remission.

  • Oral antihistamines
  • Topical corticosteroids

As the rash heals, those who are affected should avoid exposing their skin to the sun.

There is usually an improvement after two days and a complete resolution after three weeks.

Prevent future attacks by thoroughly cooking shiitake mushrooms before eating.



Written by:

Atheer Alhuthaili, Medical Student.

Revised by:

Maee Barakeh, Medical Student.



Necrolytic Acral Erythema

Necrolytic acral erythema is a skin disease that appears in the toes and the feet. It was first described in the literature in 1996. It is known as the cutaneous marker for hepatitis C infection and is strongly linked with it. The majority of recorded cases, which have an equal sex frequency and a mean onset age of 40–45 years (range 11–78 years), have been in people with skin of color, including Asians and Africans.


Necrolytic acral erythema is thought to be multifactorial, possibly due to low blood levels of albumin, glucagon, and amino acids caused by liver failure, dietary deficiencies (particularly zinc insufficiency), and hereditary factors.

The most common cause is hepatitis C infection, where a study conducted in the USA suggested that necrolytic acral erythema was observed in 1-2% of patients with chronic hepatitis C. The second most common association was found to be zinc deficiency occurring with various other disorders including coeliac disease and Crohn’s disease. It is important to note that for the hepatitis C virus to replicate, zinc is a necessary cofactor. 

Interestingly, the prevalence of chronic hepatitis C infection is high in Japan, in contrast, there are no reported cases of necrolytic acral erythema. This could be a result of genetic predisposition or the prevalent hepatitis C genotypes in that group.

Clinical features:

Usually, the tops of the toes and feet are affected by necrotic acral erythema. The skin lesions are painful most of the time, although they might also occasionally be itchy or burning. 

Acute cases present as erythematous lesions with a margin of erosions or flaccid bullae. 

Chronic cases can be divided into three phases:

  • The initial phase presents with ducky scaly papules or plaques. 
  • The well-developed phase presents with large hyperpigmented well-demarcated papules and plaques. 
  • The late phase presents with thin psoriasiform hyperpigmented lesion with a well-defined dark red rim.

Dermoscopy shows the following findings:

  • Central white and brown peripheral globules. 
  • Irregular red spot in the center. 
  • Brown background.
  • Dull white scale.


  • Laboratory investigations include hepatitis C serology, liver function tests, and serum zinc.
  •  A skin biopsy is used to confirm the diagnosis and it shows inflammatory infiltrate, hyperkeratosis, parakeratosis, epidermal spongiosis, and focal necrosis. 

Differential diagnosis:

Necrolytic migratory erythema is one of the most important differential diagnoses, as it has similar skin biopsy results. Other differentials include psoriasis, pellagra, and biotin-responsive dermatoses. 


Treat the underlying causes mostly hepatitis C with combination therapy with interferon and ribavirin, and oral zinc supplements (220 mg BID) which could enhance the effects of hepatitis C treatment. 


Complications of hepatitis C due to missing the diagnosis. Other complications include lichenification and fissuring. 


The disease follows a relapsing-remission course, with appropriate treatment it can resolve, however, recurrence could be observed if treatment is stopped. 



Written by:

Mohammed Alahmadi, Medical Student. 

Revised by:

Maee Barakeh, Medical Student. 




Andrews’ Diseases of The Skin, Clinical Dermatology 

Dermatology by Bolognia

Transient Acantholytic Dermatosis (Grover Disease)

What is transient acantholytic dermatosis?

Transient acantholytic dermatosis, also known as Grover disease, is a frequent, acquired, itchy, truncal rash that histopathologically shows acantholysis. It is more common in Caucasian men over 50 with sun damaged skin. It is less prevalent in women and young adults.
Sun exposure, sweating, fever, cancer, and being in the hospital or bedridden are all risk factors for transient acantholytic dermatosis.

It is becoming more common with the use of BRAF inhibitors such as vemurafenib and dabrafenib monotherapy, as well as cytotoxic chemotherapeutic agents.


Causes :

The cause of transitory acantholytic dermatosis remains unknown. Because transitory acantholytic dermatosis is frequently associated with skin occlusion, heat, and sweating, one theory suggests that it is caused by sweat duct injury and occlusion. Drug-induced transitory acantholytic dermatosis may be due to medication or its metabolites being secreted in sweat, which has toxic effects on the epidermis, resulting in acantholysis and dyskeratosis. BRAF-induced transitory acantholytic dermatosis may be caused by keratinocyte proliferation triggered by MAP-kinase activation. SARS-CoV-2 was detected on immunohistochemistry in the sweat gland epithelium and cutaneous vasculature of a COVID-19 patient.

Clinical features :

Transitory acantholytic dermatosis frequently begins abruptly. Some (but not all) research indicates that it is more common in the winter than in the summer . The most frequently affected areas are the central back, mid-chest, and upper arms. Lesions consist of tiny red, crusty, or eroded papules and vesicles. The rash is extremely pruritic.

Diagnosis :

Transient acantholytic dermatosis is typically diagnosed clinically; however, a skin biopsy may be required. Transient acantholytic dermatosis has a distinct pathology that includes acantholysis (separated skin cells) and/or dyskeratosis (abnormally rounded skin cells). Spongiotic dermatitis might also be noticed.


Treatment :

Transient acantholytic dermatosis has no cure; however, the following tips may help relieve the itch and speed up the healing process:

  • Keep cool, as sweating may cause more itchy areas.
  • Menthol- and camphor-based moisturizing creams or antipruritic lotions can help lessen the desire to scratch.
  • Cryotherapy
  • Topical trichloroacetic acid
  • Topical steroid
  • Topical steroid/vitamin D analogue combination ointment
  • Oral retinoids
  • Phototherapy and photochemotherapy


Complications :

Dermatitis can complicate transient acantholytic dermatosis, which commonly appears in a discoid pattern with round or oval, dry, or crusted plaques. The plaques begin on the chest and back and may migrate to the limbs.

Prognosis :

Transient acantholytic dermatosis has a variable duration, but it usually resolves spontaneously within 2-4 weeks. It can come and go, with seasonal variations. Transient acantholytic dermatosis, despite being named transient, is frequently recurring and can be chronic, lasting for years.


Written by:

Atheer Alhuthaili , medical student.

Revised by:

Maee barakeh , medical student.




Langerhans Cell Histiocytosis

Langerhans cell histiocytosis (LCH) is a rare multisystem disorder. It is a reactive increase in the number of Langerhans cells which act as antigen-presenting cells in the epidermis. It most commonly affects children from 1 – 3 years of age. It is slightly more common in males. LCH affects 2–5 children per million per year with an estimated prevalence of 1:50 000 children under 15 years of age. LCH has been associated with Epstein-Barr virus in some cases.


This condition can appear in a variety of forms, and several of the well-known patterns have been given unique names. These include:

  • Letterer-Siwe disease: Usually in children less than two years of age, involves many organs including bones, lungs, and the liver. Skin affection can appear in the scalp, trunk, and groin manifesting as pinkish papules or blisters that me crust. It can mimic cradle cap which is seen in seborrheic dermatitis.
  • Hand-Schuller-Christian disease: Usually in children from 2 – 6 years of age, the skin and bone especially the skull. Manifest as a pinkish-crusted papule, with ulcers in the mouth or genitals, and rarely eye protrusion. It often results in diabetes insipidus.
  • Eosinophilic granuloma: Usually in school-age children, less commonly affects the skin, usually present as a single bone lesion.
  • Congenital self-healing reticulohistiocytosis: Usually present at birth as a widespread reddish lump on the skin which breaks and results in a crust that fades with time with no intervention. It is limited to the skin.

A newer classification is also used where it is based on the number of involved organs in a single system (SS-LCH) and multisystem (MS-LCH) disease.


The diagnosis is suspected with the described rash and X-ray scans of internal organs. LCH is confirmed by skin biopsy. When histiocytosis is diagnosed in one organ, other organs should be checked to detect if it was affected.


If the disease was limited to the skin the following therapies could be utilized: topical corticosteroids, topical antibiotics, photochemotherapy, and thalidomide. In cases of pain lesions, the following medications can be used non-steroidal anti-inflammatory drugs, steroids injection, and radiotherapy.

In cases of multisystem involvement, starting with oral corticosteroids, then chemotherapy is warranted. The choice of treatment depends on several factors including age, and organ involvement. BRAF-V600 inhibitors may be beneficial such as vemurafenib and dabrafenib.


Many people may have little or no symptoms of a minor disease that is limited to one organ. There is an excellent prognosis for these individuals. In cases of several organ involvement, it could be fatal. In those younger than two years, a disease involving multiple organs, and vital organs such as the liver are the predictor of poor outcomes in LCH. The mortality rate for children under two years old who have multiple organ involvement from LCH is between 40-50%.

Written by:

Mohammed Alahmadi, Medical Student.

Revised by:

Maee Barakeh, Medical Student.




Dermatology by Bolognia

Practical Guide to Dermatology, The Henry Ford Manual

Primary Care Dermatology Society

Erythema Nodosum


Erythema nodosum is a form of panniculitis, which is an inflammatory condition that specifically targets the subcutaneous fat. It appears on the anterior shins as painful red nodules. Occasionally, they affect the thighs and forearms.



Erythema nodosum is a type of hypersensitivity reaction that occurs in approximately 55% of patients, and its etiology is currently unknown. In some situations, there is an association to an infection, medication, inflammatory disease, or cancer.

  • Pharyngitis: caused by streptococcal bacteria or viral pathogen.
  • Yersinia infection: can lead to symptoms such as diarrhea and stomach pain.
  • Chlamydia infection.
  • Fungal infections: histoplasmosis and coccidioidomycosis.
  • Parasitic infection: amoebiasis and giardiasis.
  • Viral: such as herpes simplex, viral hepatitis and human immunodeficiency virus (HIV) infection.


Clinical features:

Erythema nodosum is characterized by the presence of painful, red, and swollen nodules that appear under the skin. These nodules can range in size from 3 to 20 cm and typically develop over a period of one to several weeks. The symptoms include fever and joint pain. Swelling and pain in the ankle occur in 50% of cases and might last for many weeks. It may also affect other joints, such as the knees.

The nodules are primarily located on the anterior lower legs, knees and arms.
Their shape can be described as ill-defined, warm, oval, round, or arciform, and they do not exhibit ulceration.
The nodules exhibit an initial color ranging from bright to deep red.
Erythema contusiformis is a term used to describe the development of violaceous, brownish, or yellowish bruise-like marks that dissolve on their own within eight weeks.
Erythema nodosum does not result in permanent scarring.



Erythema nodosum is primarily diagnosed through clinical examination and confirmed by laboratory tests and histology. Erythema nodosum pathology primarily manifests as inflammation of the septa between subcutaneous fat lobules in the absence of vasculitis.


Differential diagnosis:

Panniculitis can manifest as either mainly septal, characterized by inflammation between lobules, or lobular, characterized by inflammatory cells within subcutaneous fat lobules. Septal and lobular inflammation can coexist.

The nodules caused by mostly septal panniculitis include:

-Different types of scleroderma
-Medium vessel vasculitis, such as that caused by polyarteritis nodosa, is characterized by the presence of sensitive subcutaneous nodules accompanied by ulceration, necrosis, livedo racemosa, fever, joint discomfort, myalgia, and peripheral neuropathy.
-Necrobiosis lipoidica
-Eosinophilic panniculitis
-Rheumatoid nodule.

The nodules caused by mostly lobular panniculitis include:

-Connective tissue illness, such as panniculitis linked with cutaneous lupus erythematosus.
-Erythema nodosum leprosum.
-Pancreatic panniculitis is a condition characterized by the development of subcutaneous nodules that may become ulcerated or fluctuant. The laboratory tests reveal increased levels of lipase, amylase, and trypsin.
-Traumatic panniculitis
-Nodular vasculitis, also known as erythema induratum, is a condition characterized by the presence of ulcerated and draining nodules that specifically affect the posterior calves.
-Lipodermatosclerosis is a condition that occurs as a result of venous insufficiency.
-Subcutaneous fat infection caused by bacteria, mycobacteria, or fungus, resulting in the formation of ulcerated, fluctuant, and draining abscesses.



Treatment for erythema nodosum is determined by the primary cause of the condition. It is necessary to address any underlying infection.

Methods for pain management may involve prolonged periods of rest, administration of colchicine, use of NSAIDs, and application of venous compression therapy.
After infection, sepsis, and cancer have been ruled out, a prescription for systemic corticosteroids (1 mg/kg daily) may be prescribed until the erythema nodosum resolves.



Written by:

Mashael Alanazi, Medical Student.

Revised by:
Maee Barakeh, Medical Student.


Flegel Disease

What is Flegel disease?

Flegel disease is often referred to as hyperkeratosis lenticularis perstans. Flegel described for the first time in 1958. It is distinguished by red-brown papules with irregular, horny scales found primarily on the top surface of the feet and lower legs.


Causes of Flegel disease 

The exact cause of the condition is uncertain. It is assumed to be a hereditary disorder.

It is assumed to be an inherited disorder, although the disease has been found in people with no family history. Sun exposure has also been linked, but not proven.

Clinical features of Flegel disease

Lesions are tiny, red-brown, scaly papules ranging in size from 1 to 5 mm that typically cover the surface of the foot and lower legs. When the scale is removed, a bright red base appears, typically with pinpoint bleeding. In rare cases, the outer ear lobes, arms, palms, soles, and oral mucosa may be impacted. The papules are usually painless.


Diagnosis of Flegel disease

Flegel disease is sometimes clinically diagnosed, particularly if there is a family history of the condition. Otherwise, a biopsy could reveal a pathological diagnosis of Flegel disease.

Treatment for Flegel disease

Lesions are benign and are primarily treated for cosmetic reasons. Treatment for Flegel illness includes:

– 5% fluorouracil cream was used topically for several months.
– Dermabrasion
– Cryotherapy
– Topical Retinoids
– Oral retinoid like isotretinoin or acitretin


Written by:

Atheer Alhuthaili , medical student.



Capillaritis (Pigmented Purpura)

Capillaritis also known as pigmented purpura is a benign skin disease characterized by reddish-brown patches that are caused by leaky capillaries. While it can afflict anyone, children are rarely affected by capillaritis. It usually affects healthy individuals, but multiple factors including medications, foods, viral infections, and exercise could trigger it.


Capillaritis is thought to be idiopathically caused by a mechanism that irritates the capillaries which are near the skin’s surface. The pathophysiology behind this disease is due to the passage of blood cells through the gaps between the capillary walls resulting in petechial hemorrhage which fades away depositing haemosiderin in the the dermis’ uppermost part.

Clinical features:

Red-brown purpuric macules “cayenne pepper spots” are the characteristic features of capillaritis. These may be distributed over the body or cluster together forming a red patch that gradually disappears over weeks to months.

Types and variants:

Progressive pigmented purpura (schamberg disease): The most common type of capillaritis, presented by cayenne pepper spots which appear suddenly. Most commonly on the lower leg, with irregular distribution and no associated symptoms.

Doucas-Kapetanakis eczematid-like purpura (itching purpura): Similar to schamberg disease bit with itching. It can affect the trunk and upper limbs.

Gougerot-Blum purpura (pigmented purpuric lichenoid dermatosis): Characterized by thick and itchy patches similar to eczema.

Majocchi purpura (purpura annularis telangiectodes): Characterized by annular patches that spread gradually and form concentric rings.

Lichen aureus: Overlies varicose vein and is characterized by a persistent single brown patch.

Exercise-induced capillaritis: common in prolonged exercise during the summer. The lesions fade with time. The appearance of the lesions is associated with a burning sensation.


The diagnosis is made clinically. It can be confirmed by skin biopsy and dermatoscopy. Histology may reveal red cell extravasation, hemosiderin, perivascular lymphocytic infiltrate, and lichenoid infiltrate, these findings could be found in one or more variants.  In immunocompromised patients always rule out cutaneous T-cell lymphoma.


Usually, no treatment is required, and unfortunately, no cure is known. However, avoiding possible risk factors including medications, food preservatives, and artificial coloring agents could result in improvements. Topical steroids can be used for symptomatic treatment. Ascorbic acid and rutoside can be used also. Phototherapy may be effective but with recurrence risk. Elastic compression socks can be used in exercise-induced capillaritis. Ascorbic acid and rutoside can be used also.


Capillaritis can go away in a few weeks, come back occasionally, or last for years.


Written by:

Mohammed Alahmadi, Medical Student.

Revised by:

Maee barakeh, Medical student.


Andrews’ Diseases of The Skin, Clinical Dermatology

Dermatology, Illustrated Study Guide and Comprehensive Board Review by Sima Jain

British Association of Dermatologists

Tinea Corporis

What is tinea corporis?

Tinea corporis is a superficial fungal infection of the skin that affects any region of the body, excluding the hands and feet, scalp, face and beard, groin, and nails. It is often known as ‘ringworm’ because of its distinctive ring-shaped lesions.

Risk factors for tinea corporis

  • Previous or concomitant tinea infections
  • Diabetes mellitus
  • Immunodeficiency
  • Hyperhidrosis
  • Xerosis
  • Ichthyosis
  • Hot, humid climates
  • Household crowding
  • Keeping house pets
  • Recreational activities that include close contact with people.


Causes of tinea corporis

Tinea corporis is mostly caused by dermatophyte fungi of the genera Trichophyton and Microsporum .The most prevalent cause of tinea corporis is T. rubrum. It can also be caused by T. interdigitale, T. tonsurans, M. canis, T. verrucosum, T. equinum, and T. erinacei species. Infection can be acquired through direct skin contact with an infected person or animal, contact with fomites, or secondary dissemination from other sites of dermatophyte infection.

Clinical features of tinea corporis

Tinea corporis first appears as a single circular red patch with a raised, scaly leading edge. A lesion spreads from the center to form a ring with central hypopigmentation and a scaly red rim (ringworm). The border may be papular or pustular. Itching is common. Multiple lesions can develop over time, which may lead to the formation of a polycyclic pattern. The distribution of lesions is often asymmetric.

Diagnosis of tinea corporis

Tinea corporis is usually diagnosed clinically after taking a complete history and physical examination. However, tests can be performed to confirm the diagnosis. Skin scrapings are examined under a microscope with KOH preparation, which will show branching, segmented hyphae. A fungal culture is another method to confirm the diagnosis. Tinea corporis is sometimes diagnosed with a skin biopsy.

Treatment for tinea corporis

General Measures:

The skin should be kept clean and completely dried. In hot and humid areas, loose-fitting, light clothes are recommended. Avoid close contact with infected people and the sharing of fomites.

Specific measures:

Topical antifungal treatments like imidazoles and terbinafine. It’s used to treat localized tinea corporis.

Oral antifungal treatment is often needed if tinea corporis affects a hair-bearing site, is widespread, or has not responded to topical antifungals. Terbinafine and itraconazole are the recommended oral antifungal medications.

Written by:

Atheer Alhuthaili , medical student.

Revised by:

Maee Barakeh , medical student.






Erythema Multiforme 


Erythema multiforme is an immune-mediated illness that usually resolves on its own. It affects the skin and mucous membranes, and is characterized by the presence of “target” lesions. Erythema multiforme major can be distinguished from multiforme minor by the presence of significant mucosal involvement. Episodes can manifest as either solitary, recurrent, or persistent.


1-Approximately 90% of cases are triggered by infection, with HSV type 1 being the predominant cause. Additional infectious triggers include:

  • HSV type 2
  • Cytomegalovirus
  • Epstein-Barr virus
  • Influenza virus
  • Vulvovaginal candidiasis
  • SARS-CoV-2
  • Orf.

2-Medications that can potentially cause erythema multiforme include:

  • Antibiotics (including erythromycin, nitrofurantoin, penicillins, sulfonamides, and tetracyclines)
  • Anti-epileptics
  • Non-steroidal anti-inflammatory drugs
  • Vaccinations (most common cause in infants).

3-Additional disorders that are commonly linked to erythema multiforme, particularly in cases of chronic disease, include:

  • Inflammatory bowel disease
  • Hepatitis C
  • Leukaemia
  • Lymphoma
  • Solid organ cancer malignancy

Clinical features:

Cutaneous features:

  • Cutaneous lesions initially appear on the periphery and then move centrally.
  • The distribution is typically symmetrical, with a tendency to favor extensor surfaces.
  • May cause pain, itching, or swelling.
  • Initial lesions manifest as circular, red papules that subsequently progress into target-shaped lesions.

Target lesions are characterized by three concentric rings of color variation:

-A dark, central region of epidermal necrosis

-Encircled by a less swollen area

-Surrounded by an erythematous periphery.

Atypical lesions can coexist alongside typical lesions. Atypical lesions exhibit elevated surfaces with indistinct boundaries.

In severe disease, up to hundreds of lesions in varying developmental stages may be present making it challenging to distinguish characteristic lesions.

Mucosal features:

  • Lesions form as blisters, which then rupture to reveal superficial erosions covered by a white pseudo-membrane.
  • Erythema multiforme primarily affects the oral membranes, but can also manifest with urogenital and, infrequently, ocular lesions.
  • When the mucous membrane is affected, it can cause pain and greatly restrict the ability to eat; these lesions may occur before or after skin lesions. 


The symptoms are anticipated to resolve spontaneously after 4 weeks from the start of the condition (or up to 6 weeks in cases of severe disease).


The diagnosis of acute erythema migrans (EM) is often established by evaluating the patient’s history and thorough physical examination of their clinical symptoms. Skin biopsies are helpful in confirming the diagnosis when there is uncertainty. Direct immunofluorescence studies may be necessary to rule out the presence of autoimmune blistering disease.

Differential diagnosis:

  • Urticaria
  • Viral exanthem
  • Stevens-Johnson syndrome
  • Fixed drug eruption
  • Bullous pemphigoid
  • Paraneoplastic pemphigus
  • Polymorphous light eruption
  • Rowell syndrome (erythema multiforme-like lesions in systemic lupus erythematosus)


Treatment is frequently unnecessary as episodes are generally self-limiting without any persistent complications. However, the presence of ocular involvement should always result in a referral to an ophthalmologist due to the potential for more severe consequences.

Management of symptomatic mild cases:

  • Itch: To relieve itch or discomfort caused by skin lesions, oral antihistamines and/or topical steroids might be used.
  • Pain: For mild mucosal involvement, oral washes containing antiseptic or local anesthetic might be used to relieve pain.

Additional therapies are dependent on the underlying cause:

  • Infection: treat precipitating infections appropriately (notice that treating HSV does not change the course of a single episode of erythema multiforme significantly). 
  • Offending medication: stop any offending medication and avoid in future.

Severe mucosal disease:

  • Admission to the hospital might be necessary to support oral intake.

Chronic illness:

  • A minimum duration of 6 months of continuous oral antiviral treatment (usually acyclovir/aciclovir), regardless of whether a definite cause has been determined.
  • Achieving remission might be challenging and may necessitate trying a longer course of treatment or a different antiviral medication.



Written by:

Mashael Alanazi, Medical Student.

Revised by:

Maee Barakeh, Medical Student.




Central Centrifugal Cicatricial Alopecia

Central Centrifugal Cicatricial Alopecia (CCCA) is a type of scarring alopecia that causes permanent hair loss, it affects middle-aged black women the most. It can be observed in men and people of various racial and hair color backgrounds.


The cause of CCCA is idiopathic, but most likely multifactorial is the precise cause of CCCA. It has been proposed that there is a genetic component, linked to mutations in the gene PADI3, which codes for peptidyl arginine deiminase, type III (PADI3), an enzyme that alters proteins necessary for the development of the hair shaft. Although hair care procedures including using a hot comb, and tight extensions have been linked for decades, research has not consistently demonstrated this connection. Infections with fungi, bacteria, autoimmune diseases, and heredity disorders are some other variables that have been suggested as causes. 

Clinical features:

Usually, hair loss starts at the vertex or middle of the scalp and moves outward in a centrifugal motion. There is loss of the follicular openings on examination of the scalp. As a result, the scalp could seem shiny. Tenderness, itching, and burning are frequent, while some people do not experience any symptoms. Breakage of the hair may potentially be a precursor to CCCA. The loss of hair happens gradually. A photographic rating system has been devised to assess the degree of hair loss in the central region.


Early detection of CCCA is crucial because treatment can stop the condition’s progression, frequently leading to significant, irreversible hair loss. Clinical characteristics, a scalp biopsy, and ruling out other hair loss conditions are used to make the diagnosis.

Rather than the middle of a scarred region, a scalp biopsy should be collected from the active edge of an alopecia patch. Histopathology indicates fibrosis and a lymphocytic inflammatory infiltrate surrounding the infundibulum, the root of the hair follicle. One typical trait is premature desquamation, or pealing, of the inner root sheath.

Differential diagnosis:

Any disorder that might cause progressive alopecia that affects the crown can mimic CCCA. These include lichen planopilaris, discoid lupus erythematosus, and even male and female pattern alopecia. True bacterial scalp infections and tinea capitis are additional entities in the differential diagnosis. 


Therapy aims to stop the disease’s progression and stop more hair loss. Regrowth is not possible in locations where fibrosis has replaced the hair follicle. There is no approved targeted therapy for CCCA because the precise etiology is unknown. We can divide it as follows: 

Gentle hair care:

  • Minimizing heat application.
  • Avoiding tight bands/extensions.
  • Avoiding tight bands/extensions.
  • Avoiding hairstyle practices associated with discomfort, and scalp irritation. 

Topical medications:

  • Corticosteroids.
  • Topical minoxidil.

Intralesional therapy:

  • Triamcinolone.

Oral therapy:

  • Doxycycline 100 mg daily for at least 6 months.
  • Hydroxychloroquine 200 mg BID (or 5 mg/kg/d).

Surgical therapy:

  • Hair transplantation, once inflammation has been controlled for at least 1 year.


Written by:

Mohammed Alahmadi, Medical Student.

Revised by:

Maee Barakeh, Medical Student.

Practical Guide to Dermatology

The Henry Ford Manual
British Association of Dermatologists

Topical Steroids Withdrawal (TSW)

Topical corticosteroid withdrawal is an infrequent rebound reaction that happens in patients who have excessively used topical steroids and occurs following cessation.

This condition is typically a result of long-term application of topical corticosteroids with moderate to high potency. Withdrawal symptoms might manifest as skin burning, itching, redness, scaling, swelling, papules, or pustules.


The etiology of topical steroid withdrawal may be explained by the following mechanisms:

  • Tachyphylaxis, which is a decrease in response, occurs with continued application, resulting in the need for higher doses.
  • Patients with atopic dermatitis who do not respond well to topical steroids have an upregulation of glucocorticoid receptor b.
  • Following the withdrawal of topical steroids, keratinocytes continue to suppress the formation of self-cortisol.
  • Topical corticosteroids induce vasoconstriction, however, upon discontinuation, there is a rebound effect of vasodilation due to an increase in the release of nitric oxide, resulting in skin redness (erythema).
  • Disruption of the barrier leads to a subsequent release of cytokines, triggering a cascade of immune responses, after the anti-inflammatory effects of topical corticosteroids are stopped.

Clinical manifestations:

The withdrawal symptoms might begin anytime from 48 hours to more than 3 months after discontinuation. 

Withdrawal generally manifests in four distinct stages:

  • Typically, a few days after stopping the treatment, there is a sudden eruption of intensely red and oozing skin, which may spread to places that were not previously treated.
  • The skin experiences dryness and itchiness accompanied by shedding, also known as desquamation.
  • The skin begins to regenerate, although it becomes more sensitive and may experience occasional flare-ups.
  • The skin returns to the state that it was before topical corticosteroid cessation. The duration of the recovery process can range from several weeks to several years.


  • Severe itch
  • Intense itching
  • Burning pain 
  • Insomnia
  • Depressed state
  • skin hypersensitivity
  • Intolerance to emollients.

Skin characteristics:

  • Erythematous skin
  • Elephant wrinkles refer to the thicker skin with decreased flexibility that typically affects the extensor surfaces of the body.
  • The red sleeve sign refers to the presence of erythema (redness) on the limbs, but the palms and soles are not affected.
  • The headlight sign is characterized by redness (erythema) across the face, but specifically excluding the nose and the area around the mouth (perioral skin).
  • Skin shedding (desquamation)
  • Edema
  • Exudate.
  • Telangiectasia
  • Papules with or without nodules
  • Pustules. 


One of the challenges is determining whether the observed skin reaction is a result of discontinuing topical corticosteroids or a deterioration of the underlying skin condition for which the steroids were given.

The diagnostic criteria for topical corticosteroid withdrawal lack consensus. However, recent literature highlights the following key features: 

  • Frequent and prolonged topical steroid use on the area of initial eruption
  • Frequent topical steroids  use on the face or genital area
  • Sensation of burning or itching

Often associated with:

  • Atopy history, particularly atopic dermatitis
  • History of using oral prednisone to treat skin conditions
  • sensitivity 
  • Skin shedding 
  • Swelling, particularly in the eyelids or ankles, and the presence of ‘elephant wrinkles’ on the back of the elbows and front of the knees (extensors).
  • Red sleeve sign.

Patch testing is a valuable tool for ruling out contact dermatitis caused by topical corticosteroids, cream excipients, or other topical treatments such as emollients. However, this can be challenging if there is not enough healthy skin available for testing.

Histology is not a reliable method for diagnosing topical corticosteroid withdrawal because the histological signs it presents, such as epidermal atrophy, spongiosis, and parakeratosis, are not specific enough.


General measures:

  • Emollients and moisturizers.
  • cold compresses, the use of ice, and the administration of gabapentin for burning pain.
  • Antihistamines are used to alleviate itching.
  • Pain management with simple analgesic.

Specific measures: 

  • The primary treatment approach is discontinuing the use of topical corticosteroids, while closely monitoring for any rebound reactions. 
  • There is controversy around tapering vs abrupt withdrawal.
  • Gradually reducing the dosage of oral corticosteroids.
  • Dupilumab should be taken into consideration for people with atopic dermatitis.
  • Prevention and treatment of any subsequent infection.
  • Phototherapy.
  • Immunosuppressants. 


  • Gradually decrease the frequency and potency of topical corticosteroids once the inflammatory skin conditions have resolved.
  • Avoid prolonged use of strong topical corticosteroids on the face.
  • Reduce the length of continuous and prolonged corticosteroid treatment, for example, to less than 2 weeks. Certain disorders, including vulval lichen sclerosus, may require a therapy duration beyond 4 weeks in order to optimize the favorable response.
  • Decrease the strength and frequency of topical steroid usage from daily to twice weekly after 2-4 weeks of treatment.

Finally, atopic dermatitis and other skin disorders should be well treated despite concerns about the risk of topical corticosteroid withdrawal, since a considerably higher proportion of patients react to effective topical steroid use than have withdrawal symptoms.

Written by:

Mashael Alanazi, Medical student

Revised by:

Maee Barakeh, Medical student