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Body Part: Legs

  • Calciphylaxis

    Calciphylaxis

    Calciphylaxis

    Definition: Patients with end-stage renal disease (ESRD) are disproportionately affected by calciphylaxis, also known as calcific uremic arteriolopathy, an uncommon and frequently fatal syndrome marked by vascular calcification and skin necrosis(1).

    Etiology: Dysregulated metabolism of calcium phosphate causes calcification of small blood arteries, which in turn causes tissue ischemia and necrosis in cases of calciphylaxis (1). Hyperparathyroidism, liver disease, end-stage renal disease (ESRD), and prior use of corticosteroid or vitamin K antagonists are risk factors(1).

    Epidemiology: 

    Cases have been reported worldwide with an estimated mortality rate ranging from 40-80%(1).

    Signs: Patients experience painful, retiform purpuric skin lesions that eventually become ulcerations and necrosis(1).

    Symptoms: Patients may report severe discomfort, frequently out of proportion to the skin findings, at the location of necrotic lesions(1) Sepsis, fever, and indications of organ ischemia are examples of systemic symptoms.

    Differentials: Necrotising fasciitis, cryoglobulinemia, anti phospholipid syndrome, coumarin necrosis and vasculitis (2).

    Diagnosis: A deep wedge skin biopsy demonstrating extravascular and vascular calcium deposits in subcutaneous and dermis layers, fibrin thrombi, ischemic necrosis of the epidermis and fat necrosis supports the clinical diagnosis (1,3). Vascular calcifications may be shown on imaging, and hyperphosphatemia or hypercalcemia may be seen in laboratory tests (2).

    Treatment: The management entails wound care, pain management, and reducing calcium and phosphate levels to address the underlying mineral imbalance (2). Commonly used treatments include bisphosphonates and sodium thiosulfate (2). Necrotic tissue may require surgical debridement, although the prognosis is still not good (2).

    References:

    1. Rick J, Strowd L, Pasieka HB, et al. Calciphylaxis: Part I. diagnosis and pathology. Journal of the American Academy of Dermatology. 2022;86(5):973-982. doi:10.1016/j.jaad.2021.10.064
    2. Calciphylaxis: Causes, symptoms, and management – dermnet. DermNet®. September 23, 2024. Accessed September 26, 2024. https://dermnetnz.org/topics/calciphylaxis.
    3. Gupta S, Baby D, Upadhyay M, et al. Calciphylaxis and its diagnosis: A Review. Journal of Family Medicine and Primary Care. 2019;8(9):2763. doi:10.4103/jfmpc.jfmpc_588_19 
  • Calciphylaxis

    Calciphylaxis

    Calciphylaxis

    Definition: Patients with end-stage renal disease (ESRD) are disproportionately affected by calciphylaxis, also known as calcific uremic arteriolopathy, an uncommon and frequently fatal syndrome marked by vascular calcification and skin necrosis(1).

    Etiology: Dysregulated metabolism of calcium phosphate causes calcification of small blood arteries, which in turn causes tissue ischemia and necrosis in cases of calciphylaxis (1). Hyperparathyroidism, liver disease, end-stage renal disease (ESRD), and prior use of corticosteroid or vitamin K antagonists are risk factors(1).

    Epidemiology: 

    Cases have been reported worldwide with an estimated mortality rate ranging from 40-80%(1).

    Signs: Patients experience painful, retiform purpuric skin lesions that eventually become ulcerations and necrosis(1).

    Symptoms: Patients may report severe discomfort, frequently out of proportion to the skin findings, at the location of necrotic lesions(1) Sepsis, fever, and indications of organ ischemia are examples of systemic symptoms.

    Differentials: Necrotising fasciitis, cryoglobulinemia, anti phospholipid syndrome, coumarin necrosis and vasculitis (2).

    Diagnosis: A deep wedge skin biopsy demonstrating extravascular and vascular calcium deposits in subcutaneous and dermis layers, fibrin thrombi, ischemic necrosis of the epidermis and fat necrosis supports the clinical diagnosis (1,3). Vascular calcifications may be shown on imaging, and hyperphosphatemia or hypercalcemia may be seen in laboratory tests (2).

    Treatment: The management entails wound care, pain management, and reducing calcium and phosphate levels to address the underlying mineral imbalance (2). Commonly used treatments include bisphosphonates and sodium thiosulfate (2). Necrotic tissue may require surgical debridement, although the prognosis is still not good (2).

    References:

    1. Rick J, Strowd L, Pasieka HB, et al. Calciphylaxis: Part I. diagnosis and pathology. Journal of the American Academy of Dermatology. 2022;86(5):973-982. doi:10.1016/j.jaad.2021.10.064
    2. Calciphylaxis: Causes, symptoms, and management – dermnet. DermNet®. September 23, 2024. Accessed September 26, 2024. https://dermnetnz.org/topics/calciphylaxis.
    3. Gupta S, Baby D, Upadhyay M, et al. Calciphylaxis and its diagnosis: A Review. Journal of Family Medicine and Primary Care. 2019;8(9):2763. doi:10.4103/jfmpc.jfmpc_588_19 
  • 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 
  • Pityriasis Rubra Pilaris

    Pityriasis Rubra Pilaris

    Pityriasis Rubra Pilaris

    Pityriasis Rubra Pilaris (PRP) is a group of rare, chronic, inflammatory skin disorders characterized by follicular hyperkeratotic papules, waxy yellow palmoplantar keratoderma, and erythematous plaques with islands of sparing. It can affect individuals of all ages, with bimodal peaks in the first and fifth to sixth decades of life, and occurs equally in males and females.

    Clinically, PRP typically presents with red-orange scaly patches that begin on the head, neck, and upper trunk. These patches often spread to cover most of the body, including the palms and soles, which become thickened and yellow. The condition can cause significant discomfort, including itching and pain, which may interfere with daily activities. Diagnosis is primarily clinical, supported by biopsy if needed to rule out other conditions. Treatment for PRP is challenging and varies depending on the severity and type of PRP. Options include topical therapies like emollients, corticosteroids, and vitamin D analogs, as well as systemic treatments such as retinoids and immunosuppressants. Biologic agents have also shown promise in treating refractory cases. The prognosis varies: classical adult-onset PRP often resolves within three years, while other types may persist for longer periods​.

    References

    1. Wang D, Chong VC, Chong WS, Oon HH. A Review on Pityriasis Rubra Pilaris. Am J Clin Dermatol. 2018;19(3):377-390. doi:10.1007/s40257-017-0338-1
    2. Napolitano M, Abeni D, Didona B. Biologics for pityriasis rubra pilaris treatment: A review of the literature. J Am Acad Dermatol. 2018;79(2):353-359.e11. doi:10.1016/j.jaad.2018.03.036
  • Pityriasis Rubra Pilaris

    Pityriasis Rubra Pilaris

    Pityriasis Rubra Pilaris

    Pityriasis Rubra Pilaris (PRP) is a group of rare, chronic, inflammatory skin disorders characterized by follicular hyperkeratotic papules, waxy yellow palmoplantar keratoderma, and erythematous plaques with islands of sparing. It can affect individuals of all ages, with bimodal peaks in the first and fifth to sixth decades of life, and occurs equally in males and females.

    Clinically, PRP typically presents with red-orange scaly patches that begin on the head, neck, and upper trunk. These patches often spread to cover most of the body, including the palms and soles, which become thickened and yellow. The condition can cause significant discomfort, including itching and pain, which may interfere with daily activities. Diagnosis is primarily clinical, supported by biopsy if needed to rule out other conditions. Treatment for PRP is challenging and varies depending on the severity and type of PRP. Options include topical therapies like emollients, corticosteroids, and vitamin D analogs, as well as systemic treatments such as retinoids and immunosuppressants. Biologic agents have also shown promise in treating refractory cases. The prognosis varies: classical adult-onset PRP often resolves within three years, while other types may persist for longer periods​.

    References

    1. Wang D, Chong VC, Chong WS, Oon HH. A Review on Pityriasis Rubra Pilaris. Am J Clin Dermatol. 2018;19(3):377-390. doi:10.1007/s40257-017-0338-1
    2. Napolitano M, Abeni D, Didona B. Biologics for pityriasis rubra pilaris treatment: A review of the literature. J Am Acad Dermatol. 2018;79(2):353-359.e11. doi:10.1016/j.jaad.2018.03.036
  • 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
  • Pityriasis Rosea

    Pityriasis Rosea

    Pityriasis Rosea

    Pityriasis Rosea is an acute, self-limiting skin condition characterized by an initial herald patch followed by a widespread rash on the trunk and proximal extremities. It commonly affects individuals aged 10 to 35 years, with a slight female predominance. The exact cause is unknown, but it is believed to be associated with the reactivation of human herpesvirus 6 or 7.

    Clinically, the condition begins with a single large, scaly, pink patch (herald patch), typically on the chest, back, or abdomen. This is followed by smaller, oval, scaly patches that appear in a “Christmas tree” pattern. Some patients may experience mild prodromal symptoms such as headache, fever, or malaise before the rash appears. Diagnosis is primarily clinical, and possible differentials include tinea corporis, secondary syphilis, and psoriasis, among others. Treatment is usually unnecessary as the condition resolves on its own within 6–8 weeks. However, symptomatic management may include topical corticosteroids, oral antihistamines, and moisturizers to alleviate itching. The prognosis is excellent, with most cases resolving without complications. Recurrences are rare, but the condition can occasionally lead to prolonged skin discoloration​.

    References

    1. Villalon-Gomez JM. Pityriasis Rosea: Diagnosis and Treatment. Am Fam Physician. 2018;97(1):38-44.
    2. El-Hussein M, El-Tawil C, Nakhle R, Souaiby N. HHV 6-7 reactivation causing Pityriasis Rosea and labyrinthitis: A case report. Am J Emerg Med. 2020;38(9):1969.e1-1969.e3. doi:10.1016/j.ajem.2020.05.005
    3. Contreras-Ruiz J, Peternel S, Jiménez Gutiérrez C, Culav-Koscak I, Reveiz L, Silbermann-Reynoso ML. Interventions for pityriasis rosea. Cochrane Database Syst Rev. 2019;2019(10):CD005068. doi:10.1002/14651858.CD005068.pub3
  • Erythema Nodosum

    Erythema Nodosum

    Erythema Nodosum

    Erythema nodosum (EN) is an inflammatory condition characterized by the sudden appearance of painful, red nodules, typically on the shins. It is considered a hypersensitivity reaction to a variety of stimuli, including infections, medications, and systemic diseases.

    EN most commonly affects young adults, particularly women aged 20-40. The condition can be associated with infections such as streptococcal pharyngitis, tuberculosis, and fungal infections. It is also linked to systemic conditions like sarcoidosis, inflammatory bowel disease, and pregnancy. Certain medications, including oral contraceptives, can also trigger EN.

    Symptoms include the development of tender, erythematous nodules that usually measure between 1-5 cm in diameter. These nodules typically appear on the extensor surfaces of the lower legs but can also affect the thighs and forearms. The nodules evolve over several weeks, starting as firm and red, then becoming softer and less red before eventually resolving without ulceration or scarring.

    Treatment for erythema nodosum focuses on addressing the underlying cause and providing symptomatic relief. NSAIDs and potassium iodide can be used to reduce inflammation and pain. Bed rest and elevation of the affected limbs are recommended for severe cases. Identifying and treating any underlying infections or discontinuing causative medications are also crucial in managing EN.

    References:

    • Schwartz, R. A., Nervi, S. J., & Nervi, S. J. (2007). Erythema nodosum: A sign of systemic disease. American Family Physician, 75(5), 695-700.
    • Bohn, S., & Buchner, R. (2006). Erythema nodosum: Etiology, diagnosis, and treatment. Journal of the American Academy of Dermatology, 55(6), 1133-1146.
    • Mert, A., Kumbasar, H., Ozaras, R., Erten, S., Tasdelen, F., & Bilir, M. (2007). Erythema nodosum: An evaluation of 100 cases. Clinical and Experimental Rheumatology, 25(4), 563-570.