SkinImages.ca

Body Part: Arms

  • Herpes Zoster

    Herpes Zoster

    Herpes Zoster

    Definition: Herpes zoster, also known as shingles, is a localized, painful, blistering rash that is caused by a reactivation of the varicella-zoster virus.

    Etiology: The varicella-zoster virus (VZV) is a member of the Herpesvirales order of double-stranded DNA viruses, that causes chickenpox. The VZV establishes latency in the dorsal root ganglia nerve cells of the spinal cord after primary infection. Once reactivated, the virus replicates in neuronal cell bodies and migrates down sensory nerves to the skin, causing herpes zoster. Pain associated with zoster is due to inflamed nerves that are affected by the virus. The virus can be transmitted via skin-to-skin contact or droplet inhalation.

    Epidemiology: The incidence of herpes zoster is 1.2- 3.4 per 1000 persons per year in individuals younger than 65 years. In individuals older than 65 years, the incidence is 3.9- 11.8  per 1000 persons per year. Recurrences are often seen in immunocompromised patients. 

    Signs: The dermatological involvement of herpes zoster is centripetal and follows a dermatomal distribution pattern. This is typically unilateral and may vary depending on the affected dermatome, age and health of the patient. Following the onset of pain, the rash that erupts is a crop of red papules that is painful, erythematous and blistering. On dark skin, the “shingles band” may appear as gray, dark brown or violaceous papules. The rash then develops forming vesicles which can cause discolouration of the surrounding skin depending on skin tone.The lesions continue to erupt and become pustular and crust over. 

    Symptoms: Early symptoms include localized or widespread pain without tenderness or skin changes. The zoster rash is painful within the associated area of skin. Individuals may feel unwell with a fever and headache. In uncomplicated cases, pain and general symptoms subside as the eruption disappears.

    Differentials: Herpes simplex, dermatitis herpetiformis, impetigo, contact dermatitis, candidiasis.

    Diagnosis: Herpes zoster is diagnosed clinically with pain, characteristic morphology and dermatomal distribution. The rash may form a pattern called the zosteriform herpes simplex. Diagnostic tests include direct fluorescent antibody, PCR and Tzanck smear of vesicular fluid or blood.  

    Treatment: Several antiviral drugs are available to treat shingles such as acyclovir and valacyclovir. They shorten the length and severity of illness. Over-the-counter pain relief medication can also aid in the pain caused by shingles. The CDC recommends 2 doses of the recombinant zoster vaccine to prevent shingles and its complications in individuals 50 years and older. Vaccination is also recommended in younger, immunocompromised patients.

    References:

    1. Nair PA, Patel BC. Herpes Zoster. In: StatPearls. Treasure Island (FL): StatPearls Publishing; September 4, 2023.
    2. Ayoade F, Kumar S. Varicella-Zoster Virus (Chickenpox). In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 15, 2022.
    3. Herpes zoster | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/herpes-zoster
    4. ‌CDC. Shingles. Centers for Disease Control and Prevention. Published 2019. https://www.cdc.gov/shingles/about/index.html
  • Herpes Zoster

    Herpes Zoster

    Herpes Zoster

    Definition: Herpes zoster, also known as shingles, is a localized, painful, blistering rash that is caused by a reactivation of the varicella-zoster virus.

    Etiology: The varicella-zoster virus (VZV) is a member of the Herpesvirales order of double-stranded DNA viruses, that causes chickenpox. The VZV establishes latency in the dorsal root ganglia nerve cells of the spinal cord after primary infection. Once reactivated, the virus replicates in neuronal cell bodies and migrates down sensory nerves to the skin, causing herpes zoster. Pain associated with zoster is due to inflamed nerves that are affected by the virus. The virus can be transmitted via skin-to-skin contact or droplet inhalation.

    Epidemiology: The incidence of herpes zoster is 1.2- 3.4 per 1000 persons per year in individuals younger than 65 years. In individuals older than 65 years, the incidence is 3.9- 11.8  per 1000 persons per year. Recurrences are often seen in immunocompromised patients. 

    Signs: The dermatological involvement of herpes zoster is centripetal and follows a dermatomal distribution pattern. This is typically unilateral and may vary depending on the affected dermatome, age and health of the patient. Following the onset of pain, the rash that erupts is a crop of red papules that is painful, erythematous and blistering. On dark skin, the “shingles band” may appear as gray, dark brown or violaceous papules. The rash then develops forming vesicles which can cause discolouration of the surrounding skin depending on skin tone.The lesions continue to erupt and become pustular and crust over. 

    Symptoms: Early symptoms include localized or widespread pain without tenderness or skin changes. The zoster rash is painful within the associated area of skin. Individuals may feel unwell with a fever and headache. In uncomplicated cases, pain and general symptoms subside as the eruption disappears.

    Differentials: Herpes simplex, dermatitis herpetiformis, impetigo, contact dermatitis, candidiasis.

    Diagnosis: Herpes zoster is diagnosed clinically with pain, characteristic morphology and dermatomal distribution. The rash may form a pattern called the zosteriform herpes simplex. Diagnostic tests include direct fluorescent antibody, PCR and Tzanck smear of vesicular fluid or blood.  

    Treatment: Several antiviral drugs are available to treat shingles such as acyclovir and valacyclovir. They shorten the length and severity of illness. Over-the-counter pain relief medication can also aid in the pain caused by shingles. The CDC recommends 2 doses of the recombinant zoster vaccine to prevent shingles and its complications in individuals 50 years and older. Vaccination is also recommended in younger, immunocompromised patients.

    References:

    1. Nair PA, Patel BC. Herpes Zoster. In: StatPearls. Treasure Island (FL): StatPearls Publishing; September 4, 2023.
    2. Ayoade F, Kumar S. Varicella-Zoster Virus (Chickenpox). In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 15, 2022.
    3. Herpes zoster | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/herpes-zoster
    4. ‌CDC. Shingles. Centers for Disease Control and Prevention. Published 2019. https://www.cdc.gov/shingles/about/index.html
  • 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.
  • Benign Familial Pemphigus (Hailey Hailey Disease)

    Benign Familial Pemphigus (Hailey Hailey Disease)

    Benign Familial Pemphigus (Hailey Hailey Disease)

    Definition: Benign familial pemphigus (BFP), also known as “Hailey- Hailey Disease”  is a rare autosomal dominant blistering dermatosis that was discovered in 1939.

    Etiology: BPH is a hereditary skin disorder caused by variations or mutations in the ATP2C1 gene. This gene is found on chromosome 3q21-24 and is responsible for encoding the protein hSPCA1 (Human Secretory-Pathway Ca2+/Mn2+-ATPase Isoform 1) localized at the Golgi apparatus. These are primarily loss-of-function mutations. Due to resulting insufficient calcium, keratinocytes cannot stick together due to improper desmosome assembly. 15- 30% of cases are due to sporadic gene mutations or undiagnosed disease in other family members. 

    Epidemiology: The prevalence of BFP is estimated to be 1/50.000. There is no clear predilection for the sexes or any ethnic groups. Clinical findings of BFP typically present in the third and fourth decades of life.

    Signs: Studies suggest that environmental factors and genetic modification may alter the way BFP is expressed clinically. Lesions typically present as symmetrical crusted skin rashes involving the intertriginous regions, inframammary folds and the vulva (female), and rarely, the conjunctival, oral, esophageal, and vaginal mucosa. On fair skin tones, this irregular pattern has pink and white areas separated by pink furrows “cloud pattern”. On deeper skin tones, irregular brown-grayish-black areas with a “crumpled fabric pattern” and crusting may be evident.

    Symptoms: BFP lesions are painful and erosive. Lesions that have been present for a long time may become thickened and macerated, which can worsen pain levels. Lesions are intermittent and may discharge a foul-smelling exudate upon rupture. Patients may experience worse symptoms where heat, sweating and friction exacerbate symptoms.

    Differentials:  Darier disease, Grover disease, Candidiasis, Pemphigus vulgaris/vegetans

    Diagnosis: Diagnosis of BFP is made clinically and supported by skin histopathology. Dermoscopy may be used in early diagnosis.

    Treatment: There is no cure for BFP. Treatment focuses on alleviating symptoms and preventing flare-ups. You may be advised to avoid trigger factors such as heat and tight clothing. Topical corticosteroids and antibiotics may be prescribed to treat inflamed lesions.

    References:

    1.     Hailey-Hailey disease (benign familial pemphigus) | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/benign-familial-pemphigus

    2.     ‌Konstantinou MP, Krasagakis K. Benign Familial Pemphigus (Hailey-Hailey Disease). In: StatPearls. Treasure Island (FL): StatPearls Publishing; August 14, 2023.

    3.     Żychowska M, Kołt-Kamińska M, Kijowski R, Reich A. Hailey-Hailey disease exacerbated by scabies: the role of dermatoscopy in preventing misdiagnosis. Postepy Dermatol Alergol. 2023;40(4):567-570. doi:10.5114/ada.2023.130477

    4.     Ben Lagha I, Ashack K, Khachemoune A. Hailey-Hailey Disease: An Update Review with a Focus on Treatment Data. Am J Clin Dermatol. 2020;21(1):49-68. doi:10.1007/s40257-019-00477-z

  • Benign Familial Pemphigus (Hailey Hailey Disease)

    Benign Familial Pemphigus (Hailey Hailey Disease)

    Benign Familial Pemphigus (Hailey Hailey Disease)

    Definition: Benign familial pemphigus (BFP), also known as “Hailey- Hailey Disease”  is a rare autosomal dominant blistering dermatosis that was discovered in 1939.

    Etiology: BPH is a hereditary skin disorder caused by variations or mutations in the ATP2C1 gene. This gene is found on chromosome 3q21-24 and is responsible for encoding the protein hSPCA1 (Human Secretory-Pathway Ca2+/Mn2+-ATPase Isoform 1) localized at the Golgi apparatus. These are primarily loss-of-function mutations. Due to resulting insufficient calcium, keratinocytes cannot stick together due to improper desmosome assembly. 15- 30% of cases are due to sporadic gene mutations or undiagnosed disease in other family members. 

    Epidemiology: The prevalence of BFP is estimated to be 1/50.000. There is no clear predilection for the sexes or any ethnic groups. Clinical findings of BFP typically present in the third and fourth decades of life.

    Signs: Studies suggest that environmental factors and genetic modification may alter the way BFP is expressed clinically. Lesions typically present as symmetrical crusted skin rashes involving the intertriginous regions, inframammary folds and the vulva (female), and rarely, the conjunctival, oral, esophageal, and vaginal mucosa. On fair skin tones, this irregular pattern has pink and white areas separated by pink furrows “cloud pattern”. On deeper skin tones, irregular brown-grayish-black areas with a “crumpled fabric pattern” and crusting may be evident.

    Symptoms: BFP lesions are painful and erosive. Lesions that have been present for a long time may become thickened and macerated, which can worsen pain levels. Lesions are intermittent and may discharge a foul-smelling exudate upon rupture. Patients may experience worse symptoms where heat, sweating and friction exacerbate symptoms.

    Differentials:  Darier disease, Grover disease, Candidiasis, Pemphigus vulgaris/vegetans

    Diagnosis: Diagnosis of BFP is made clinically and supported by skin histopathology. Dermoscopy may be used in early diagnosis.

    Treatment: There is no cure for BFP. Treatment focuses on alleviating symptoms and preventing flare-ups. You may be advised to avoid trigger factors such as heat and tight clothing. Topical corticosteroids and antibiotics may be prescribed to treat inflamed lesions.

    References:

    1.     Hailey-Hailey disease (benign familial pemphigus) | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/benign-familial-pemphigus

    2.     ‌Konstantinou MP, Krasagakis K. Benign Familial Pemphigus (Hailey-Hailey Disease). In: StatPearls. Treasure Island (FL): StatPearls Publishing; August 14, 2023.

    3.     Żychowska M, Kołt-Kamińska M, Kijowski R, Reich A. Hailey-Hailey disease exacerbated by scabies: the role of dermatoscopy in preventing misdiagnosis. Postepy Dermatol Alergol. 2023;40(4):567-570. doi:10.5114/ada.2023.130477

    4.     Ben Lagha I, Ashack K, Khachemoune A. Hailey-Hailey Disease: An Update Review with a Focus on Treatment Data. Am J Clin Dermatol. 2020;21(1):49-68. doi:10.1007/s40257-019-00477-z

  • 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.

  • 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.

  • Eczema Herpeticum

    Eczema Herpeticum

    Eczema Herpeticum

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

    Definition: Eczema herpeticum (also known as Kaposi varicelliform eruption) is a severe, potentially life-threatening skin infection caused by the herpes simplex virus (HSV) in individuals with atopic dermatitis or other underlying skin conditions. 

    Epidemiology: It typically occurs in children and young adults but can affect individuals of any age. 

    Symptoms: Eczema herpeticum usually presents with clusters of painful, monomorphic, punched-out erosions that rapidly spread over eczematous skin areas. The affected areas may become swollen, and the lesions can develop into pustules, vesicles, and crusts. Systemic symptoms such as fever, malaise, and lymphadenopathy may also be present. 

    Diagnosis: Early diagnosis and treatment are crucial to prevent complications. Antiviral medications, such as acyclovir or valacyclovir, are the primary treatment options and should be administered promptly. In severe cases, hospitalization may be required for intravenous antiviral therapy and supportive care. Corticosteroids and antibiotics may be used to manage concurrent inflammation and bacterial infections.

    References:

    1.     Eichenfield, L. F., Tom, W. L., Chamlin, S. L., Feldman, S. R., Hanifin, J. M., Simpson, E. L., & Paller, A. S. (2014). Guidelines of care for the management of atopic dermatitis. Journal of the American Academy of Dermatology, 71(1), 116-132.

    2.     Wollenberg, A., Oranje, A., Deleuran, M., Simon, D., Szalai, Z., Kunz, B., … & Taïeb, A. (2016). ETFAD/EADV eczema task force position paper on diagnosis and treatment of atopic dermatitis. Journal of the European Academy of Dermatology and Venereology, 30(5), 729-747.

    3.     Hebert, A. A., & Rodriguez, L. A. (2016). Management of eczema herpeticum in children. Pediatric Dermatology, 33(4), 357-361.