Body Part: Foot

  • 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

  • Granuloma Annulare

    Granuloma Annulare

    Granuloma annulare 

    Condition Name: Granuloma annulare

    Definition: Granuloma annulare is a benign, chronic skin condition characterized by the formation of annular plaques or papules.

    Etiology: The exact cause of granuloma annulare is unknown, though it is believed to involve an immune-mediated response.

    Epidemiology: Granuloma annulare affects individuals of all ages but is more commonly seen in children and young adults. It is slightly more prevalent in females than in males. The prevalence in the general population is relatively low, and the condition is not typically associated with significant morbidity.

    Signs: The appearance of small, firm, flesh-colored or erythematous papules that coalesce to form rings with a central depression. These lesions most commonly appear on the hands, feet, elbows, and knees but can occur on any part of the body.

    Symptoms: The lesions are usually asymptomatic but can occasionally cause mild itching.

    Differentials: Conditions such as tinea corporis, sarcoidosis, and necrobiosis lipoidica should be considered.

    Diagnosis: Diagnosis is primarily clinical, based on the characteristic appearance of the lesions. A skin biopsy can confirm the diagnosis by revealing necrobiotic collagen surrounded by histiocytes and multinucleated giant cells.

    Treatment: Treatment is often unnecessary as granuloma annulare can resolve spontaneously, particularly in localized cases. Treatment options for persistent or widespread cases include topical or intralesional corticosteroids, cryotherapy, or laser therapy. Systemic treatments, such as dapsone, isotretinoin, or hydroxychloroquine, may be considered for more severe cases.

    References:

    ●       Piette, E. W., & Rosenbach, M. (2016). Granuloma annulare: Pathogenesis, disease associations, and triggers, and therapeutic options. Journal of the American Academy of Dermatology, 75(3), 467-479. doi:10.1016/j.jaad.2016.02.1222

    ●       Marneros, A. G., & Bruckner, A. L. (2010). “Granuloma annulare.” Journal of the American Academy of Dermatology, 62(2), 207-222. doi:10.1016/j.jaad.2009.03.044

  • Allergic Contact Dermatitis

    Allergic Contact Dermatitis

    Allergic Contact Dermatitis 

    Definition: Allergic contact dermatitis (ACD) is a skin condition that occurs when the skin comes into contact with an allergen, leading to an immune response and subsequent inflammation(1).

    Etiology: ACD is caused by an allergic reaction to substances that come into direct contact with the skin. Common allergens include nickel, fragrances, preservatives, latex, and certain plants like poison ivy (1,3). The immune system recognizes these substances as harmful, triggering an inflammatory response(1).

    Epidemiology: ACD affects individuals of all ages, but it is more prevalent in adults due to cumulative exposure to allergens over time. It is common with some studies demonstrating a prevalence rate of 20% in the general population (2). It is particularly common in certain occupations that involve frequent contact with irritants and allergens, such as healthcare workers, hairdressers, and construction workers (2). 

    Signs: Key signs of ACD include erythema, edema, vesicles, and lichenification in chronic cases (1). These signs typically appear in areas directly exposed to the allergen(1,2).

    Symptoms: Symptoms of ACD include intense itching, burning, and discomfort at the site of contact(3). The skin may also become dry, cracked, and scaly if exposure continues or if the dermatitis becomes chronic(3)

    Differentials: Differential diagnoses for ACD include irritant contact dermatitis, atopic dermatitis, psoriasis, fungal infections, and seborrheic dermatitis (1).

    Diagnosis: Diagnosis of ACD is primarily clinical, based on the history of exposure and characteristic skin findings(1). Patch testing is the gold standard and is used to identify the allergens that cause allergic contact dermatitis (1).

    Treatment: The cornerstone of ACD treatment is identifying and avoiding the offending allergen(1). Topical corticosteroids are commonly prescribed to reduce inflammation and alleviate symptoms(1). In severe cases, systemic corticosteroids may be required. Avoidance necessitates thorough label-checking for the allergen and related cross-reactive substances. Understanding these cross-reactive ingredients and knowing where a particular allergen is commonly found can aid in effectively advising the patient (1).

    References: (AMA)

    1. Kanwaljit K. Brar MD, AbstractObjectiveTo familiarize the reader with the mechanisms and causes of contact dermatitis.Data SourcesRecent research articles, Dhingra N, et al. A review of contact dermatitis. Annals of Allergy, Asthma & Immunology. October 20, 2020. Accessed August 10, 2024. https://www.sciencedirect.com/science/article/pii/S1081120620310802.
    2. Stacy Nassau MD, Jacob SE, Warshaw EM, et al. Allergic contact dermatitis. Medical Clinics of North America. October 28, 2019. Accessed August 10, 2024. https://www.sciencedirect.com/science/article/pii/S0025712519300884. 
    3. Brandon L. Adler M. Allergic contact dermatitis. JAMA Dermatology. March 1, 2021. Accessed August 10, 2024. https://jamanetwork.com/journals/jamadermatology/article-abstract/2775575.