skin images

Skin Type: 6

  • Keloid

    Keloid

    Keloid

    Definition: Keloids are hypertrophic, smooth, hard growths or scars that occur on the skin as a result of excessive scar formation. Keloids may rarely occur spontaneously. They may develop on any part of the body and extend beyond the original wound margins. The upper chest, shoulders, ears and neck are especially prone to keloid scar development.

    Etiology: Keloids result from abnormal wound healing in response to skin trauma or inflammation. Their development is dependent on genetic or environmental factors. Keloids are most common in wounds that heal by secondary intention and can arise months to years following injury. The pathogenesis may involve dysregulation of the normal healing process, resulting in excessive production of collagen, elastin, proteoglycans and extracellular matrix proteins. In keloid scars, there is a defect in growth factors and cytokines, with increased TNF-alpha, interferon- beta and interleukin- 6.

    Epidemiology: There is a higher incidence of keloids in darker-skinned individuals of African, Asian and Hispanic descent (Fitzpatrick skin types III-VI). Caucasian and Albino individuals appear to be less affected. A genetic association with HLA haplotypes and blood group A has also been identified. Spontaneously arising keloids have been associated with a variety of conditions like Noonan syndrome and Rubinstein-Taybi syndrome.

    Signs: Keloid scars are benign, derma growths that may appear 1- 12 months following injury. They can develop anywhere but most commonly appear on the deltoid, pre- sternal chest, upper back and ear.  They present as firm, rubbery nodules which project above the underlying skin further than 4 millimeters. They may be pedunculated, or develop into a broad-base plaque. Colour ranges from flesh-coloured, erythematous or hyperpigmented and may change with the evolution of the lesion. 

    Symptoms: Keloids are benign but frequently symptomatic. Patients may experience pruritus, pain, tenderness and burning.

    Differentials: Hypertrophic scars, dermatofibroma, dermatofibrosarcoma protuberans, keloidal variants (morphea and scleroderma), xanthoma disseminatum, lobomycosis.

    Diagnosis: Diagnosis of a keloid is primarily clinical based on the history and features. A biopsy is not required unless the diagnosis is unclear. 

    Treatment: Primary prevention is key. Keloids are difficult to treat as incomplete therapy may result in worsening and growth of the scar. Several modalities alleviate symptoms of existing keloids such as intralesional corticosteroids, cryotherapy, surgical excision, radiotherapy and laser therapy. 

    References:

    1.     Keloids and hypertrophic scars | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/keloid-and-hypertrophic-scar

    2.     McGinty S, Siddiqui WJ. Keloid. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 17, 2023.

  • Androgenetic Alopecia

    Androgenetic Alopecia

    Androgenetic Alopecia

    Definition: Androgenic Alopecia (AGA) is one of the most common types of hair loss and is characterized by the androgen-dependent reduction of terminal hairs into thin vellus hairs (1). 

    Etiology:  AGA is a hereditary disorder for which there is no known cure and is mainly influenced by androgens such as dihydrotestosterone (1). 

    Epidemiology: AGA affects both men and women with different balding patterns (1,3). The prevalence differs with men being more commonly affected (3).

    Signs: In women’s hair the frontal hairline is usually retained with diffuse thinning throughout the crown (2). In males, the thinning starts at the vertex and temples leading to receding in a characteristic “M” shape (2)

    Symptoms: Typically asymptomatic but can have psychological impacts due to the impact on the patient’s appearance. 

    Differentials: Alopecia Areata, Frontal Fibrosing Alopecia, Hereditary hypotrichosis complex, Telogen effluvium, Triangular Alopecia, Trichorhinophalangeal syndrome (1).

    Diagnosis: Advanced AGA is a clinical diagnosis, however in early AGA scalp dermoscopy, pull tests, hair and scalp examinations and biopsies may be used (3). Dermoscopy will show miniaturized hair follicles. (3)

    Treatment: There are only two drugs available, topical Minoxidil (men and women), a pyrimidine derivative and oral finasteride, a SRD5A2 inhibitor (for men only) (1,3).

    References: (AMA)

    1.     Khan Mohammad Beigi P. Alopecia areata. Published online 2018. doi:10.1007/978-3-319-72134-7

    2.     Androgenetic alopecia: Medlineplus genetics. MedlinePlus. 2023. Accessed August 18, 2024. https://medlineplus.gov/genetics/condition/androgenetic-alopecia/#resources

    3.      Ntshingila S, Oputu O, Arowolo AT, Khumalo NP. Androgenetic alopecia: An update. JAAD International. 2023;13:150-158. doi:10.1016/j.jdin.2023.07.005 

  • Alopecia Areata

    Alopecia Areata

    Alopecia Areata

    Definition: A common autoimmune condition that is marked by abrupt, non-scarring hair loss on the scalp and other parts of the body go (1)

    Etiology: Many etiologies have been proposed but it is believed that the condition is caused by an autoimmune attack on the hair follicles, leading to hair loss. In addition, environmental factors, genetic predisposition and stress may also play a role (1,2).

    Epidemiology: Alopecia Areat (AA) affects 0.1-0.2% of the overall population with no gender predilection. (1,2).

    Signs: AA is characterized by well-demarcated oval or round patches of hair loss, the lesions may be solitary or multiple with 90% of cases affecting the scalp (2).

    Symptoms: Typically asymptomatic however some patients may experience nail changes, tingling or burning sensation, irritated eyes if loss of hair in eyelashes or eyebrows (3).

    Differentials: Telogen effluvium, Trichotillomania,Tinea capitis, Early scarring Alopecia, Anagen effluvium, Systemic lupus erythematosus, Secondary syphilis and androgenic Alopecia (1,2). 

    Diagnosis: The diagnosis is clinical with a thorough history and routine investigations such as complete hemogram, anemia panel, erythrocyte sedimentation rate, etc (2). Dermoscopic histological examination is a great tool in diagnosing AA and in more uncertain cases a biopsy may also be performed (1).

    Treatment: In a majority of cases the condition is self-limited and regrowth typically will happen within a year (1). In patients where AA is persistent corticosteroids can be prescribed to stimulate hair growth follow by minoxidil to maintain the growth (3).

    References: (AMA)

    1.     Khan Mohammad Beigi P. Alopecia areata. Published online 2018. doi:10.1007/978-3-319-72134-7 

    1. Amin SS, Sachdeva S. Alopecia areata: A Review. Journal of the Saudi Society of Dermatology & Dermatologic Surgery. 2013;17(2):37-45. doi:10.1016/j.jssdds.2013.05.004 
    2. Ludmann P. Hair loss types: Alopecia areata diagnosis and treatment. American Academy of Dermatology. 2023. Accessed August 18, 2024. https://www.aad.org/public/diseases/hair-loss/types/alopecia/treatment. 
  • Hidradenitis Suppurativa

    Hidradenitis Suppurativa

    Hiradentitis Suppurativa

    Definition: Hidradenitis SUppurativa (HS), also known as acne inversa,  is a chronic inflammatory skin condition that affects the apocrine-gland-bearing skin. It is characterized by painful, persistent deep-seated nodules, abscessed as skin tunnels that may develop purulent discharge and result in scarring.

    Etiology: HS development may have genetic, environmental and behavioural influences. There is an autosomal dominant transmission pattern of HS. A loss-of-function mutation of the y- y-secretase complex involved in the Notch signalling pathway has been identified as a cause of HS. Other mutations include the DCD, PSTP 1P1, SOX9 and KLF5 genes. Environmental and behavioural factors are also relevant as individuals with HS often have co-morbidities that may lead to increased skin friction, sweat overproduction and retention and hormonal changes, which can increase the progression and severity of HS.

    Epidemiology: The global prevalence of HS is variable, and may affect up to 4.1% of the population. In North American and European patients, HS is three times more women in females than males. In South Korea and Japan, HS is more common in males. HS typically manifests at puberty and is most active between 20 – 40 years of age. It may resolve at menopause in women. Risk factors include a family history of HS, obesity and metabolic syndromes, cigarette smoking, African ethnicity, IBD- particularly Crohn’s disease and other skin disorders.

    Signs: Characteristic primary HS nodules are deep nodules typically 0.5- 2cm in size and can persist for days to months. The lesions may resemble recurrent, rupture-prone boils and have a serosanguinous discharge which may become purulent. The affected areas include the axilla, neck, inframammary folds, inner upper thighs, and anogenital region. The characteristic features of HS also include double open-ended comedones, painful firm papules and nodules, pustules, abscesses, draining sinuses linked to inflamed lesions, and atrophic and hypertrophic scars. The scars or plaques may cause architectural distortion and “tombstone” comedones.

    Symptoms: Many patients report prodromal symptoms like burning, stinging, pain pruritus or hyperhidrosis which may precede a lesion by 12 hours. Triggers include menstruation, obesity, stress, heat, hormonal changes, and perspiration. 

    Differentials: Staphylococcal skin infection, cysts, Cutaneous Crohn’s disease, Anogenital Crohn’s disease.

    Diagnosis: HS may be diagnosed clinically. Three components of a triad must be met to diagnose HS: characteristic lesions, typical distribution and presence and recurrence of lesions. Skin biopsy can help confirm an HS diagnosis. Histopathological features include follicular occlusion and hyperkeratosis, infundibular follicular epithelial hyperplasia, keratin plugging, epidermal psoriasiform hyperplasia and plasmacytic infiltrate. 

    Treatment: General measures for treatment include smoking cessation, weight reduction, analgesics, loose-fitting clothing and improved hygiene. Specific medical treatment includes topical antibiotics or benzoyl peroxide, systemic antibiotics and oral hormonal therapies and immunomodulatory treatments. Procedural measures include incision and drainage of acute abesses and local excision of persistent nodules. Laser ablation of nodules, hair removal and radical excision of an affected area.

    References:

    1. Ballard K, Shuman VL. Hidradenitis Suppurativa. In: StatPearls. Treasure Island (FL): StatPearls Publishing; May 6, 2024.
    2. Hidradenitis Suppurativa (Acne Inversa): A Complete Picture – DermNet. dermnetnz.org. https://dermnetnz.org/topics/hidradenitis-suppurativa
    3. ‌Bukvić Mokos Z, Markota Čagalj A, Marinović B. Epidemiology of hidradenitis suppurativa. Clin Dermatol. 2023;41(5):564-575. doi:10.1016/j.clindermatol.2023.08.020
  • Acne Keloidalis Nuchae

    Acne Keloidalis Nuchae

    Acne Keloidalis Nuchae

    Definition: Acne keloidalis nuchae (AKN) also known as folliculitis keloidalis nuchae (FKN) is a chronic debilitating condition that is characterized by keloid-life plaques that usually affects the occipital area or nape of the neck. Untreated AKN can lead to scarring folliculitis.

    Epidemiology: Acne keloidalis nuchae is thought to predominantly affect men of African American descent but a few studies have shown it to significantly affect other ethnicities. It is seen in post-pubertal males and is uncommon beyond the age of 55.

    Signs: Firm, flesh-coloured, pink or flesh-coloured papules and nodules may aggregate into sizable plaques resembling keloid. In the afflicted locations, these lesions frequently result in permanent hair loss and scarring.

    Symptoms: Symptoms typically develop from a haircut or irritation from wearing a sports helmet and tend to appear a few hours to days after the irritation. In active lesions, pruritus, discomfort, and contact bleeding are frequent which may cause men to avoid haircuts.

    Differentials: AKN is often mistaken for a keloidal condition and shares some features with cicatricial alopecia.

    Diagnosis: Based mostly on the location and distinctive look of the lesions, the diagnosis is made clinically. In rare circumstances, a biopsy may be done to rule out other disorders.

    Treatment: Treatment options include topical and intralesional corticosteroids, topical retinoids, topical antibacterials, oral antibiotics for secondary infections, and laser therapy. In refractory cases, surgical excision or radiation therapy may be considered as well as oral isotretinoin.

    References: (AMA)

    1. Umar S, Lee DJ, Lullo JJ. A Retrospective Cohort Study and Clinical Classification System of Acne Keloidalis Nuchae. J Clin Aesthet Dermatol. 2021;14(4):E61-E67.
    2. Ogunbiyi A. Acne keloidalis nuchae: prevalence, impact, and management challenges. Clin Cosmet Investig Dermatol. 2016;9:483-489. Published 2016 Dec 14. doi:10.2147/CCID.S99225
    3. Maranda EL, Simmons BJ, Nguyen AH, Lim VM, Keri JE. Treatment of Acne Keloidalis Nuchae: A Systematic Review of the Literature. Dermatol Ther (Heidelb). 2016;6(3):363-378. doi:10.1007/s13555-016-0134-5
  • Acne Keloidalis Nuchae

    Acne Keloidalis Nuchae

    Acne Keloidalis Nuchae

    Definition: Acne keloidalis nuchae (AKN) also known as folliculitis keloidalis nuchae (FKN) is a chronic debilitating condition that is characterized by keloid-life plaques that usually affects the occipital area or nape of the neck. Untreated AKN can lead to scarring folliculitis.

    Epidemiology: Acne keloidalis nuchae is thought to predominantly affect men of African American descent but a few studies have shown it to significantly affect other ethnicities. It is seen in post-pubertal males and is uncommon beyond the age of 55.

    Signs: Firm, flesh-coloured, pink or flesh-coloured papules and nodules may aggregate into sizable plaques resembling keloid. In the afflicted locations, these lesions frequently result in permanent hair loss and scarring.

    Symptoms: Symptoms typically develop from a haircut or irritation from wearing a sports helmet and tend to appear a few hours to days after the irritation. In active lesions, pruritus, discomfort, and contact bleeding are frequent which may cause men to avoid haircuts.

    Differentials: AKN is often mistaken for a keloidal condition and shares some features with cicatricial alopecia.

    Diagnosis: Based mostly on the location and distinctive look of the lesions, the diagnosis is made clinically. In rare circumstances, a biopsy may be done to rule out other disorders.

    Treatment: Treatment options include topical and intralesional corticosteroids, topical retinoids, topical antibacterials, oral antibiotics for secondary infections, and laser therapy. In refractory cases, surgical excision or radiation therapy may be considered as well as oral isotretinoin.

    References: (AMA)

    1. Umar S, Lee DJ, Lullo JJ. A Retrospective Cohort Study and Clinical Classification System of Acne Keloidalis Nuchae. J Clin Aesthet Dermatol. 2021;14(4):E61-E67.
    2. Ogunbiyi A. Acne keloidalis nuchae: prevalence, impact, and management challenges. Clin Cosmet Investig Dermatol. 2016;9:483-489. Published 2016 Dec 14. doi:10.2147/CCID.S99225
    3. Maranda EL, Simmons BJ, Nguyen AH, Lim VM, Keri JE. Treatment of Acne Keloidalis Nuchae: A Systematic Review of the Literature. Dermatol Ther (Heidelb). 2016;6(3):363-378. doi:10.1007/s13555-016-0134-5
  • Hemangioma

    Hemangioma

    Hemangioma

    Definition: A hemangioma is a benign proliferative blood vessel neoplasm. Hemangiomas can arise early or later in life, and there are several hemangiomas. The most common type is a cherry angioma. Congenital hemangiomas are present at birth while infantile hemangiomas appear later within the first few weeks of life.

    Etiology: Hemangiomas are caused by endothelial cell proliferation. Studies suggest this may occur in three ways: increased GLUT- 1 and VEGF expression, stem cells originating from trophoblasts or de novo formation.

    Epidemiology: Hemangiomas are the most common benign tumours of infancy, affecting approximately 4-5% of newborns. Infantile hemangiomas appear more frequently in Caucasian infants. Premature infants, infants with elder mothers and low birth weight infants are also more susceptible to developing hemangiomas. Most cases of hemangiomas are sporadic but are associated with an autosomal dominant inheritance pattern with no specific gene implicated.

    Signs: Cherry hemangiomas typically appear as multiple firm erythematous or violaceous papules less than 1 cm in diameter. They can be scattered across any body surface If thrombosed, they can appear darker in colour before close dermatoscopic inspection when the red or purple colour is more easily seen. Infantile hemangiomas are usually solitary and appear on the head and neck. Clinical features are determined by the lesion’s depth, distribution pattern (usually facial in 77% of cases) and growth phases.

    Symptoms: Cherry angiomas may be asymptomatic. Superficial, deep and mixed infantile hemangiomas are usually non-tender.

    Differentials: Port-wine stain, Congenital hemangioma, Angiokeratoma, Pyogenic granuloma, Kaposiform hemangioendothelioma

    Diagnosis: Hemangiomas are diagnosed clinically. A skin biopsy may also be performed. Infantile hemangiomas are positive for GLUT-1 staining. Ultrasound, CT and MRI may be performed to determine the depth of infantile hemangiomas where there are no superficial skin changes.

    Treatment: Cherry angiomas are typically harmless and are left untreated. In some cases, they must be excised to rule out nodular melanoma.  Infantile hemangiomas may resolve on their own. Complicated infantile hemangiomas may require treatment. This is in the form of beta-blockers, oral prednisone, and topical corticosteroids.

    References:

    1. Infantile haemangioma: Definition and pathogenesis | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/infantile-haemangioma-definition-and-pathogenesis
    2. Chamli A, Aggarwal P, Jamil RT, Litaiem N. Hemangioma. In: StatPearls. Treasure Island (FL): StatPearls Publishing; June 12, 2023.
    3. ‌Angiomas. Spider naevus | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/cherry-angioma
    4. Dicko A, Safi T, Tounkara TM, et al. Prevalence des hemangiomes infantiles sur peau noire au Mali [Prevalence of infantile haemangiomas on black skin]. Mali Med. 2017;32(4):18-20.
  • Pemphigus Vulgaris

    Pemphigus Vulgaris

    Author: Shahnawaz Towheed MS2, Y, Miller-Monthrope, Dermatologist/Dermatopathologist, Toronto, Canada, 2024

    Definition: Pemphigus Vulgaris is an autoimmune blistering disorder affecting the skin and mucous membranes. 

    Epidemiology: It has an incidence of approximately 1-5 cases per million people per year and predominantly affects middle-aged and older adults, with a higher prevalence in certain ethnic groups, such as the Ashkenazi Jewish population and patients of East Indian descent. 

    Etiology: The condition is caused by autoantibodies against desmogleins, which are essential proteins in skin cell adhesion. 

    Signs/ Symptoms: Clinically, it presents with flaccid blisters and erosions, particularly in the mouth, and can progress to involve the skin. 

    Diagnosis: Diagnosis is confirmed through biopsies of involved skin and a biopsy for direct immunofluorescence of uninvolved skin, which shows IgG antibodies against the keratinocyte cell surface in a “chicken wire pattern”. 

    Treatment: The treatment typically requires high-dose corticosteroids, and immunosuppressive agents like azathioprine, and rituximab.

    Complications: The prognosis is generally favourable with appropriate management, though the condition can be chronic and require long-term treatment. Corticosteroids first used for PV in the 1950s reduced the mortality from 75% to 30%. This was further reduced to below 5% with the addition of other immunosuppressive agents introduced in the 1980s. 

    References:

    1.     Alpsoy E, Akman-Karakas A, Uzun S. Geographic variations in epidemiology of two autoimmune bullous diseases: pemphigus and bullous pemphigoid. Arch Dermatol Res. 2015;307(4):291-298. doi:10.1007/s00403-014-1531-1

    2.     Russo I, De Siena FP, Saponeri A, Alaibac M. Evaluation of anti-desmoglein-1 and anti-desmoglein-3 autoantibody titers in pemphigus patients at the time of the initial diagnosis and after clinical remission. Medicine (Baltimore). 2017;96(46):e8801. doi:10.1097/MD.0000000000008801

    3.     Kridin K, Sagi SZ, Bergman R. Mortality and Cause of Death in Patients with Pemphigus. Acta Derm Venereol. 2017 May 8;97(5):607-611. doi: 10.2340/00015555-2611. PMID: 28093595.

    4.     Joly P, Maho-Vaillant M, Prost-Squarcioni C, et al. First-line rituximab combined with short-term prednisone versus prednisone alone for the treatment of pemphigus (Ritux 3): a prospective, multicentre, parallel-group, open-label randomised trial. Lancet. 2017;389(10083):2031-2040. doi:10.1016/S0140-6736(17)30070-3

  • Pemphigus Vulgaris

    Pemphigus Vulgaris

    Author: Shahnawaz Towheed MS2, Y, Miller-Monthrope, Dermatologist/Dermatopathologist, Toronto, Canada, 2024

    Definition: Pemphigus Vulgaris is an autoimmune blistering disorder affecting the skin and mucous membranes. 

    Epidemiology: It has an incidence of approximately 1-5 cases per million people per year and predominantly affects middle-aged and older adults, with a higher prevalence in certain ethnic groups, such as the Ashkenazi Jewish population and patients of East Indian descent. 

    Etiology: The condition is caused by autoantibodies against desmogleins, which are essential proteins in skin cell adhesion. 

    Signs/ Symptoms: Clinically, it presents with flaccid blisters and erosions, particularly in the mouth, and can progress to involve the skin. 

    Diagnosis: Diagnosis is confirmed through biopsies of involved skin and a biopsy for direct immunofluorescence of uninvolved skin, which shows IgG antibodies against the keratinocyte cell surface in a “chicken wire pattern”. 

    Treatment: The treatment typically requires high-dose corticosteroids, and immunosuppressive agents like azathioprine, and rituximab.

    Complications: The prognosis is generally favourable with appropriate management, though the condition can be chronic and require long-term treatment. Corticosteroids first used for PV in the 1950s reduced the mortality from 75% to 30%. This was further reduced to below 5% with the addition of other immunosuppressive agents introduced in the 1980s. 

    References:

    1.     Alpsoy E, Akman-Karakas A, Uzun S. Geographic variations in epidemiology of two autoimmune bullous diseases: pemphigus and bullous pemphigoid. Arch Dermatol Res. 2015;307(4):291-298. doi:10.1007/s00403-014-1531-1

    2.     Russo I, De Siena FP, Saponeri A, Alaibac M. Evaluation of anti-desmoglein-1 and anti-desmoglein-3 autoantibody titers in pemphigus patients at the time of the initial diagnosis and after clinical remission. Medicine (Baltimore). 2017;96(46):e8801. doi:10.1097/MD.0000000000008801

    3.     Kridin K, Sagi SZ, Bergman R. Mortality and Cause of Death in Patients with Pemphigus. Acta Derm Venereol. 2017 May 8;97(5):607-611. doi: 10.2340/00015555-2611. PMID: 28093595.

    4.     Joly P, Maho-Vaillant M, Prost-Squarcioni C, et al. First-line rituximab combined with short-term prednisone versus prednisone alone for the treatment of pemphigus (Ritux 3): a prospective, multicentre, parallel-group, open-label randomised trial. Lancet. 2017;389(10083):2031-2040. doi:10.1016/S0140-6736(17)30070-3

  • Epidermal Nevus

    Epidermal Nevus

    Author: Kawaroreet Karwal MS2, Y, Miller-Monthrope, Dermatologist/Dermatopathologist, Toronto, Canada, 2024

    Definition: Epidermal nevus is a benign skin condition characterized by the overgrowth of epidermal cells, resulting in the formation of warty or verrucous plaques. 

    Etiology: These lesions typically present at birth or develop early in childhood and can persist throughout life.

    Epidemiology: Epidermal nevi are rare, occurring in approximately 1 in 1,000 live births. They are most commonly found on the trunk, limbs, and neck. 

    Signs: The lesions are often linear or segmental, following the lines of Blaschko, and can vary in colour from flesh-toned to brown.

    Symptoms: Symptoms associated with epidermal nevus include pruritus and irritation, particularly if the lesions are inflamed or become secondarily infected. In rare cases, epidermal nevi can be part of broader syndromes, such as epidermal nevus syndrome, which may involve neurological, skeletal, and ocular abnormalities.

    Treatment: Treatment for epidermal nevus is primarily aimed at managing symptoms and improving cosmetic appearance. Options include topical treatments, such as keratolytics and retinoids, and surgical interventions like excision, laser therapy, or cryotherapy. The choice of treatment depends on the size, location, and symptoms associated with the nevus.

    References:

    1.     Hafner, C., & Vogt, T. (2008). Sebaceous Gland Disorders. In Harper’s Textbook of Pediatric Dermatology (Vol. 2, pp. 235-246). Wiley-Blackwell.

    2.     Happle, R. (2000). The group of epidermal nevus syndromes part I. Well-defined phenotypes. Journal of the American Academy of Dermatology, 42(2), 171-183.

    3.     Patel, S., Zirwas, M., & English, J. C. (2010). Treatment of epidermal nevi: a systematic review. Journal of the American Academy of Dermatology, 62(1), 19-28.