skin images

Skin Type: 2

  • Leukemia Cutis

    Leukemia Cutis

    Leukemia Cutis

    Definition: Leukemia cutis (LC) is a rare condition that refers to cutaneous infiltration of neoplastic leukocytes due to peripheral leukemia. 

    Etiology: The etiology of any leukemia can be attributed to genetic and environmental risk factors that promote the expression of neoplastic cells. The proposed etiology of LC involved mechanisms of various chemokines and molecular expression on leukemic cells mediating their migration to the skin through skin0 selective homing processes. Environmental risk factors include benzene exposure, ionizing radiation, viral and alkylating agents. Aneuploidy of chromosome 8, translocation of chromosome 3 and (6;9) have been observed in patients with LC. It has been reported that all-trans retinoic acid to treat promyelocytic leukemia may increase the risk of cutaneous involvement.

    Epidemiology: Exact data on the incidence and specific predilections of LC are unknown. It is believed that LC may affect approximately 3% of individuals with leukemia. However, individuals with adult T- cell leukemia/ lymphoma are more likely to develop LC. Up to 30% of children with congenital leukemia are more likely to develop LC. The subtypes of leukemia that commonly affect the skin are chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML). Cutaneous involvement and the development of chloromas are typically indicative of advanced illness.

    Signs: LC clinical presentation varies, and may be localized or disseminated and occur alone or in combination on any skin site. LC lesions favor previous sites of injury. LC lesions often appear as firm papules, nodules and plaques that are firm or rubbery in consistency. They may range in color from skin- coloured to erythematous to violaceous. In rare cases yellow, blue and gray lesions may be observed. LC lesions may also present with erythroderma, annular erythema, purpura, petechiae, ulceration, gingivitis/ gingival hyperplasia (AML). in infants, LC is a cause of “blueberry muffin syndrome”

    Symptoms: LC lesions are usually not purritic or tender.

    Differentials:  Lymphoma and pseudolymphoma, metastatic solid tumors, pyoderma gangrenosum, urticaria, vasculitis

    Diagnosis: LC[1]  must be diagnosed using a skin biopsy, which will reveal a diffuse infiltration of malignant leukocytes in the dermis of the skin. Further histochemistry may reveal the specific cell type involved.

    Treatment: Care of LC is directed towards addressing the underlying leukemia. Treatment includes electron beam, therapy, localized radiation and phototherapy.

    References:

    1.     Parsi M, Go MS, Ahmed A. Leukemia Cutis. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 17, 2023.

    2.     Leukemia cutis | DermNet. dermnetnz.org. https://dermnetnz.org/topics/leukaemia-cutis

  • Leukemia Cutis

    Leukemia Cutis

    Leukemia Cutis

    Definition: Leukemia cutis (LC) is a rare condition that refers to cutaneous infiltration of neoplastic leukocytes due to peripheral leukemia. 

    Etiology: The etiology of any leukemia can be attributed to genetic and environmental risk factors that promote the expression of neoplastic cells. The proposed etiology of LC involved mechanisms of various chemokines and molecular expression on leukemic cells mediating their migration to the skin through skin0 selective homing processes. Environmental risk factors include benzene exposure, ionizing radiation, viral and alkylating agents. Aneuploidy of chromosome 8, translocation of chromosome 3 and (6;9) have been observed in patients with LC. It has been reported that all-trans retinoic acid to treat promyelocytic leukemia may increase the risk of cutaneous involvement.

    Epidemiology: Exact data on the incidence and specific predilections of LC are unknown. It is believed that LC may affect approximately 3% of individuals with leukemia. However, individuals with adult T- cell leukemia/ lymphoma are more likely to develop LC. Up to 30% of children with congenital leukemia are more likely to develop LC. The subtypes of leukemia that commonly affect the skin are chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML). Cutaneous involvement and the development of chloromas are typically indicative of advanced illness.

    Signs: LC clinical presentation varies, and may be localized or disseminated and occur alone or in combination on any skin site. LC lesions favor previous sites of injury. LC lesions often appear as firm papules, nodules and plaques that are firm or rubbery in consistency. They may range in color from skin- coloured to erythematous to violaceous. In rare cases yellow, blue and gray lesions may be observed. LC lesions may also present with erythroderma, annular erythema, purpura, petechiae, ulceration, gingivitis/ gingival hyperplasia (AML). in infants, LC is a cause of “blueberry muffin syndrome”

    Symptoms: LC lesions are usually not purritic or tender.

    Differentials:  Lymphoma and pseudolymphoma, metastatic solid tumors, pyoderma gangrenosum, urticaria, vasculitis

    Diagnosis: LC[1]  must be diagnosed using a skin biopsy, which will reveal a diffuse infiltration of malignant leukocytes in the dermis of the skin. Further histochemistry may reveal the specific cell type involved.

    Treatment: Care of LC is directed towards addressing the underlying leukemia. Treatment includes electron beam, therapy, localized radiation and phototherapy.

    References:

    1.     Parsi M, Go MS, Ahmed A. Leukemia Cutis. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 17, 2023.

    2.     Leukemia cutis | DermNet. dermnetnz.org. https://dermnetnz.org/topics/leukaemia-cutis

  • Lichen Planopilaris

    Lichen Planopilaris

    Lichen Planopilaris

    Definition: Lichen Planopilaris (LP) is an inflammatory primary cicatricial alopecia that can result in permanent hair loss. LP is a follicular variant of lichen planus that results in progressive, patchy and permanent hair loss on the hair-bearing skin surfaces. 

    Etiology: LP is believed to be a hair-specific autoimmune disorder caused by activated T-lymphocytes targeting follicular antigens. This is theorized to be a part of a cytotoxic autoimmune response to an unknown antigen present in hair follicles. The use of nilotinib and pembrolizumab has been linked to LP.

    Epidemiology: The incidence of LP is not precisely known. LP has been reported as the most frequent primary scarring alopecia. Variants of LP include Graham-Little syndrome and frontal fibrosing alopecia. LP often affects women more than men. The peak age range of LP is between 40- 60 years.

    Signs: Many individuals with LP may develop characteristics affecting the skin, mucous membranes and nails. LP typically presents as multifocal areas with smooth white patches of scalp hair loss. There may be perifollicular erythema and perifollicular scale at the edge of the patches, and these may be spiny upon palpation. There may be cutaneous, nail and mucous membrane involvement before LP manifests on the scalp. Hairs may be easily extracted anywhere on the scalp, indicating active disease requiring treatment. The clinical course of hair loss in LP may be insidious or fulminant. Clinical features of LP do not vary in different skin types. Complications of LP include alopecia, psychological distress and reduced quality of life.

    Symptoms: Individuals with active LP may experience severe itching, burning and tenderness. 

    Differentials: Discoid lupus erythematosus, folliculitis decalvans, central centrifugal cicatricial alopecia, seborrheic dermatitis.

    Diagnosis: LP is assessed using trichoscopy, which reveals absent follicles, tubular perifollicular scale, white dots and perifollicular erythema. Diagnosis may be confirmed through scalp biopsy

    Treatment: as no treatment restored the original hair loss due to scarring, treatment aims to slow the progression of LP and relieve its associated symptoms. Anti- inflammatory agents such as corticosteroids, tacrolimus and hydroxychloroquine may be indicated. Non pharmacological measures include scalp reductions and hair transplantation in end- stage inactive disease.

    References:

    1.     Lepe K, Nassereddin A, Syed HA, Salazar FJ. Lichen Planopilaris. In: StatPearls. Treasure Island (FL): StatPearls Publishing; May 1, 2024.

    1. Lichen Planopilaris — DermNet. dermnetnz.org. https://dermnetnz.org/topics/lichen-planopilaris
  • Lentigo Maligna

    Lentigo Maligna

    Lentigo Maligna

    Definition: Lentigo maligna (LM), also known as Hutchinson melanotic freckle, is a slow-growing precursor of lentigo maligna melanoma (LMM). LM often occurs in sun-damaged skin of the head and neck region, usually in the elderly.

    Etiology: LM occurs due to the proliferation of malignant melanocytes within the hair follicle and the basal layer of the epidermis. Solar damage to the skin results in the abnormal melanocytes proliferating unchecked. Major risk factors for LM include cumulative lifetime UVR exposure, x-ray radiation, estrogen/progesterone therapy, nonpermanent hair dyes and genetic conditions predisposing to sun sensitivity. UVR exposure causes oxidative damage which affects genes involved in KIT CCND1, MITF, NRAS, and p53 pathways.

    Epidemiology:  LM is the precursor to the third most common subtype of melanoma (LMM), comprising up to 15% of all melanomas and up to 26% of melanomas on the head and neck. Women are often more affected by LM than men, with the ratio being 1.7: 1. LM occurs often in those with very fair skin (Fitzpatrick types 1,2), and is rare in brown or black skin (Fitzpatrick types 4,5,6). LM is more common in males, and the mean age of diagnosis is between 66- 72 years.

    Signs: LM is slow-growing and may resemble a lentigo in its early stages. Over several years it may develop the following characteristics: smooth, flat surface, size >6 mm and irregular shape with variable pigmentation ranging from light brown, tan, dark brown, pink, red or white. 86% of LM lesions occur on the head and neck, with a predilection for the cheek. Extrafacial lesions may be seen on the extremities of women and the back in men.

    Symptoms: LM lesions are usually asymptomatic. In 3-10% of cases, invasive melanoma may arise from LM in which symptoms include thickened portions of the lesion, increasing number of colours, ulceration, bleeding, itching or stinging.

    Differentials: Solar lentigo, Melanocytic naevi, seborrheic keratosis, lichen planus-like keratosis, and pigmented actinic keratosis

    Diagnosis: The clinical diagnosis of LM is by dermoscopy or confocal microscopy. If a lesion if suspicious of LM, an excisional biopsy is indicated for histopathological diagnosis.

    Treatment: The treatment of choice is surgical excision. For poor surgical candidates, radiotherapy, or a topical imiquimod 5% cream may be indicated.

    References:

    1. Oakley A. Lentigo maligna and lentigo maligna melanoma | DermNet NZ. dermnetnz.org. Published 2011. https://dermnetnz.org/topics/lentigo-maligna-and-lentigo-maligna-melanoma
    2. ‌Xiong M, Charifa A, Chen CSJ. Lentigo Maligna Melanoma. In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 31, 2022.
  • 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.

  • Kaposi Sarcoma

    Kaposi Sarcoma

    Kaposi Sarcoma

    Definition: Kaposi sarcoma (KS) is a rare disease of the endothelial cells of blood vessels and the lymphatic system. There are four types of Kaposi sarcoma: Classic KS, Human immunodeficiency virus (HIV)- associated KS, endemic or African KS and iatrogenic KS.

    Etiology: Kaposi sarcoma herpesvirus (KSHV) or Human herpesvirus-8- 8 (HHV-8) is present in all forms of KS. HHV-8 is a double-stranded enveloped DNA virus with 6 major subtypes (A-F). HHV-8 interferes with many normal cell functions and requires co-factors that result in the decrease in CD4 cells and the development of Kaposi sarcoma. HHV-8 may be found in men who have sex with men (MSM), and heterosexuals and may be transmitted through saliva or arthropod bites. Iatrogenic KS occurs as a result of drug treatment leading to immunosuppression.

    Epidemiology: Classic KS affects patients over 50 years old of Sub-Saharan African, Middle European and Mediterranean descent. It is associated with Diabetes Mellitus. The male-to-female ratio is 17:1. Prevalence in the United States is 1: 100,000, and mirrors the distribution of HHV-8. HIV- HIV-associated KS mainly affects MSM, and is the most common malignancy affecting children in Uganda and Zambia. HIV- positive MSM have a 5 to 10-fold increased risk of developing KS. Endemic KS arises in Africa and has a unique predilection for the pediatric population. The male-to-female ratio is 2:1. Iatrogenic KS has a male-to-female ratio of approximately 3:1. Over 5% of transplant patients who develop a de-novo malignancy have a 400- 500 fold increased risk of developing KS when compared to the general population.

    Signs: KS presents with erythematous to violaceous macules, papules and nodules on the skin or mucous membranes. KS lesions begin small and eventually ulcerate. Early KS lesions appear as flat patches with associated lymphedema. These eventually evolve into plaques, nodules or scaly tumors. Patients with HIV- HIV-associated KS may develop lesions at any time during the illness. The aggression of KS is directly related to the degree of immunosuppression a patient is experiencing.

    Symptoms: External KS lesions ulcerate and become painful. Internal KS lesions may be associated with bleeding, hematemesis, hematochezia, melena, shortness of breath, and peripheral edema.

    Differentials: Interstitial granuloma annulare, spindle cell hemangioma, gasiform hemangioendothelioma, cutaneous angiosarcoma, pyogenic granuloma

    Diagnosis: A biopsy shoring characteristic features of KS is required for a definitive diagnosis. Histologically, KS presents as a spindle cell vascular neoplasm with extravasated red blood cells and hyaline globules. Immunohistochemistry positivity for LANA-1 also differentiates KS from similar lesions.

    Treatment: Skin involvement of KS is treated by local excision, liquid nitrogen and vincristine infections. Chemotherapy is used to treat endemic and systemic forms. HIV- HIV-associated KS is treated with Highly active antiretroviral therapy (HAART) and is combined with chemotherapy in severe cases. Iatrogenic KS treatment requires a reduction in immunosuppression to reduce levels of tumor growth-promoting proteins.

    References:

    1.     Kaposi sarcoma | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/kaposi-sarcoma

    2.     Bishop BN, Lynch DT. Kaposi Sarcoma. In: StatPearls. Treasure Island (FL): StatPearls Publishing; June 5, 2023.

    3.     Grabar S, Costagliola D. Epidemiology of Kaposi’s Sarcoma. Cancers (Basel). 2021;13(22):5692. Published 2021 Nov 14. doi:10.3390/cancers13225692

  • Bullous Pemphigoid

    Bullous Pemphigoid

    Bullous Pemphigoid

    Definition: Bullous Pemphigoid is a chronic autoimmune bullous disease that is characterized by tense bullae on normal or erythematous skin (1).

    Etiology: Bullous Pemphigoid is caused by autoantibodies against hemidesmosomal proteins BP180 (type XVII collagen) and BP230 that lead to the production of subepidermal blisters (1).

    Epidemiology: Bullous Pemphigoid is the most common autoimmune subepidermal blistering condition  and it commonly affects older adults usually above 70 years old(1,2).

    Signs: It is characterized by severe pruritus along with tense blisters over urticaria plaques typically seen in the limbs and trunks (1). It is not typically seen in mucosal areas (1). 

    Symptoms: Patients typically face intense pruritus and discomfort or pain at the site of active lesions (1,2).

    Differentials: Pemphigus foliaceus, pemphigus herpetiformis, bullous lupus erythematosus, eczema, urticaria, prurigo, impetigo, erythema multiforme, Sweet syndrome, toxic epidermal necrolysis, and autotoxic pruritus (1).

    Diagnosis: The diagnosis is based on three factors; histopathological evaluation showing eosinophilic spongiosis or a subepidermal detachment with eosinophils, use of direct or indirect immunofluorescence assays to detect IgG and/or C3 deposition at the basement membrane and ELISA measurement of circulating autoantibodies (1).

    Treatment: The treatment is based on the patient’s clinical status and disease severity  (1). Systemic and topical high potency steroids are the current treatment options (1).

    References: (AMA)

    1.      Miyamoto D, Santi CG, Aoki V, Maruta CW. Bullous pemphigoid. Anais Brasileiros de Dermatologia. 2019;94(2):133-146. doi:10.1590/abd1806-4841.20199007 

    1. Miyamoto D, Santi CG, Aoki V, Maruta CW. Bullous pemphigoid. Anais Brasileiros de Dermatologia. 2019;94(2):133-146. doi:10.1590/abd1806-4841.20199007 
  • Bullous Pemphigoid

    Bullous Pemphigoid

    Bullous Pemphigoid

    Definition: Bullous Pemphigoid is a chronic autoimmune bullous disease that is characterized by tense bullae on normal or erythematous skin (1).

    Etiology: Bullous Pemphigoid is caused by autoantibodies against hemidesmosomal proteins BP180 (type XVII collagen) and BP230 that lead to the production of subepidermal blisters (1).

    Epidemiology: Bullous Pemphigoid is the most common autoimmune subepidermal blistering condition  and it commonly affects older adults usually above 70 years old(1,2).

    Signs: It is characterized by severe pruritus along with tense blisters over urticaria plaques typically seen in the limbs and trunks (1). It is not typically seen in mucosal areas (1). 

    Symptoms: Patients typically face intense pruritus and discomfort or pain at the site of active lesions (1,2).

    Differentials: Pemphigus foliaceus, pemphigus herpetiformis, bullous lupus erythematosus, eczema, urticaria, prurigo, impetigo, erythema multiforme, Sweet syndrome, toxic epidermal necrolysis, and autotoxic pruritus (1).

    Diagnosis: The diagnosis is based on three factors; histopathological evaluation showing eosinophilic spongiosis or a subepidermal detachment with eosinophils, use of direct or indirect immunofluorescence assays to detect IgG and/or C3 deposition at the basement membrane and ELISA measurement of circulating autoantibodies (1).

    Treatment: The treatment is based on the patient’s clinical status and disease severity  (1). Systemic and topical high potency steroids are the current treatment options (1).

    References: (AMA)

    1.      Miyamoto D, Santi CG, Aoki V, Maruta CW. Bullous pemphigoid. Anais Brasileiros de Dermatologia. 2019;94(2):133-146. doi:10.1590/abd1806-4841.20199007 

    1. Miyamoto D, Santi CG, Aoki V, Maruta CW. Bullous pemphigoid. Anais Brasileiros de Dermatologia. 2019;94(2):133-146. doi:10.1590/abd1806-4841.20199007 
  • Bullous Pemphigoid

    Bullous Pemphigoid

    Bullous Pemphigoid

    Definition: Bullous Pemphigoid is a chronic autoimmune bullous disease that is characterized by tense bullae on normal or erythematous skin (1).

    Etiology: Bullous Pemphigoid is caused by autoantibodies against hemidesmosomal proteins BP180 (type XVII collagen) and BP230 that lead to the production of subepidermal blisters (1).

    Epidemiology: Bullous Pemphigoid is the most common autoimmune subepidermal blistering condition  and it commonly affects older adults usually above 70 years old(1,2).

    Signs: It is characterized by severe pruritus along with tense blisters over urticaria plaques typically seen in the limbs and trunks (1). It is not typically seen in mucosal areas (1). 

    Symptoms: Patients typically face intense pruritus and discomfort or pain at the site of active lesions (1,2).

    Differentials: Pemphigus foliaceus, pemphigus herpetiformis, bullous lupus erythematosus, eczema, urticaria, prurigo, impetigo, erythema multiforme, Sweet syndrome, toxic epidermal necrolysis, and autotoxic pruritus (1).

    Diagnosis: The diagnosis is based on three factors; histopathological evaluation showing eosinophilic spongiosis or a subepidermal detachment with eosinophils, use of direct or indirect immunofluorescence assays to detect IgG and/or C3 deposition at the basement membrane and ELISA measurement of circulating autoantibodies (1).

    Treatment: The treatment is based on the patient’s clinical status and disease severity  (1). Systemic and topical high potency steroids are the current treatment options (1).

    References: (AMA)

    1.      Miyamoto D, Santi CG, Aoki V, Maruta CW. Bullous pemphigoid. Anais Brasileiros de Dermatologia. 2019;94(2):133-146. doi:10.1590/abd1806-4841.20199007 

    1. Miyamoto D, Santi CG, Aoki V, Maruta CW. Bullous pemphigoid. Anais Brasileiros de Dermatologia. 2019;94(2):133-146. doi:10.1590/abd1806-4841.20199007 
  • Bullous Pemphigoid

    Bullous Pemphigoid

    Bullous Pemphigoid

    Definition: Bullous Pemphigoid is a chronic autoimmune bullous disease that is characterized by tense bullae on normal or erythematous skin (1).

    Etiology: Bullous Pemphigoid is caused by autoantibodies against hemidesmosomal proteins BP180 (type XVII collagen) and BP230 that lead to the production of subepidermal blisters (1).

    Epidemiology: Bullous Pemphigoid is the most common autoimmune subepidermal blistering condition  and it commonly affects older adults usually above 70 years old(1,2).

    Signs: It is characterized by severe pruritus along with tense blisters over urticaria plaques typically seen in the limbs and trunks (1). It is not typically seen in mucosal areas (1). 

    Symptoms: Patients typically face intense pruritus and discomfort or pain at the site of active lesions (1,2).

    Differentials: Pemphigus foliaceus, pemphigus herpetiformis, bullous lupus erythematosus, eczema, urticaria, prurigo, impetigo, erythema multiforme, Sweet syndrome, toxic epidermal necrolysis, and autotoxic pruritus (1).

    Diagnosis: The diagnosis is based on three factors; histopathological evaluation showing eosinophilic spongiosis or a subepidermal detachment with eosinophils, use of direct or indirect immunofluorescence assays to detect IgG and/or C3 deposition at the basement membrane and ELISA measurement of circulating autoantibodies (1).

    Treatment: The treatment is based on the patient’s clinical status and disease severity  (1). Systemic and topical high potency steroids are the current treatment options (1).

    References: (AMA)

    1.      Miyamoto D, Santi CG, Aoki V, Maruta CW. Bullous pemphigoid. Anais Brasileiros de Dermatologia. 2019;94(2):133-146. doi:10.1590/abd1806-4841.20199007 

    1. Miyamoto D, Santi CG, Aoki V, Maruta CW. Bullous pemphigoid. Anais Brasileiros de Dermatologia. 2019;94(2):133-146. doi:10.1590/abd1806-4841.20199007