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Body Part: Arms

  • 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

  • Burns from Laser Hair Removal with an Inappropriately Used Devices

    Burns from Laser Hair Removal with an Inappropriately Used Devices

    Burns from Laser Hair Removal with inappropriately used devices

    Definition: When laser hair removal devices are handled incorrectly, it can cause thermal injury to the skin and results in burns (1).

    Etiology: These burns are caused by overly high energy settings, an improper laser wavelength, or insufficient cooling of the skin, which allows heat to damage the epidermis and dermis (1,3).

    Epidemiology:  Burns from laser hair removal devices are a rare side effect but are more common in people with darker skin types (1).

    Signs: Blisters, crusts, or erythema where the laser was applied(1,3) Full-thickness burns with necrosis could occur in severe cases (2,3).

    Symptoms: The patient may experience acute pain, burning or discomfort (2). Scarring, hyperpigmentation or hypopigmentation could also develop (3).

    Differentials: Chemical burns, thermal burns from other sources, scalds (2).

    Diagnosis: Diagnosis is clinical based on history of recent laser therapy and characteristic skin findings (2,3)

    Treatment: A hydrocolloid dressings can be applied a week as topical antimicrobials (2). Exposure to direct sunlight should also be avoided (2).

    References: (AMA)

    1.      Finlayson HW, Kim WA, Dheansa B. Case report: Full thickness Burns from intense pulsed light hair removal. Burns Open. 2023;7(2):26-27. doi:10.1016/j.burnso.2023.02.002 

    1. Kester S. Laser hair removal burns: Prevention, treatment, and more. Healthline. June 1, 2021. Accessed September 2, 2024. https://www.healthline.com/health/beauty-skin-care/laser-hair-removal-burns#Why-burns-can-happen.
    2. Braynova I, Timonov P, Fasova A, Alexandrov A. Severe burns of the genital area after laser hair removal: A case report. Cureus. Published online October 21, 2023. doi:10.7759/cureus.47429 
  • Burns from Laser Hair Removal with Inappropriately Used Devices

    Burns from Laser Hair Removal with Inappropriately Used Devices

    Burns from Laser Hair Removal with inappropriately used devices

    Definition: When laser hair removal devices are handled incorrectly, it can cause thermal injury to the skin and results in burns (1).

    Etiology: These burns are caused by overly high energy settings, an improper laser wavelength, or insufficient cooling of the skin, which allows heat to damage the epidermis and dermis (1,3).

    Epidemiology:  Burns from laser hair removal devices are a rare side effect but are more common in people with darker skin types (1).

    Signs: Blisters, crusts, or erythema where the laser was applied(1,3) Full-thickness burns with necrosis could occur in severe cases (2,3).

    Symptoms: The patient may experience acute pain, burning or discomfort (2). Scarring, hyperpigmentation or hypopigmentation could also develop (3).

    Differentials: Chemical burns, thermal burns from other sources, scalds (2).

    Diagnosis: Diagnosis is clinical based on history of recent laser therapy and characteristic skin findings (2,3)

    Treatment: A hydrocolloid dressings can be applied a week as topical antimicrobials (2). Exposure to direct sunlight should also be avoided (2).

    References: (AMA)

    1.      Finlayson HW, Kim WA, Dheansa B. Case report: Full thickness Burns from intense pulsed light hair removal. Burns Open. 2023;7(2):26-27. doi:10.1016/j.burnso.2023.02.002 

    1. Kester S. Laser hair removal burns: Prevention, treatment, and more. Healthline. June 1, 2021. Accessed September 2, 2024. https://www.healthline.com/health/beauty-skin-care/laser-hair-removal-burns#Why-burns-can-happen.
    2. Braynova I, Timonov P, Fasova A, Alexandrov A. Severe burns of the genital area after laser hair removal: A case report. Cureus. Published online October 21, 2023. doi:10.7759/cureus.47429 
  • Bites, Bullous Insect Bites

    Bites, Bullous Insect Bites

    Bites, Bullous Insect Bites

    Definition: Bullous insect bites are delayed hypersensitivity reactions that occur in people who are already sensitized (2). They are characterized by blisters packed with fluid that appear on the skin (1).

    Etiology: The bites arise from an immune response to toxins being released at the bite site (1). The most common bites come from spiders, fleas, bed bugs and mosquitos.

    Epidemiology: Bullous reactions can occur often in people with various hematological malignancies and chronic lymphocytic leukemia (2).

    Signs: Plaques or erythematous papules that develop into tight, fluid filled bullae (1,2). Lesions may be encircled by erythema or edema and frequently appear at the site of an insect attack (1).

    Symptoms: At the location of the blisters, patients may experience itching, burning, or pain (1,2). Scratching the blisters increases the risk of bacterial infection (1).

    Differentials: Bullous pemphigoid, dermatitis herpetiformis, contact dermatitis, insect sting hypersensitivity (1,3).

    Diagnosis: Diagnosis is clinical and based on the patient’s history of insect exposure and characteristics of the lesions. 

    Treatment: Due to the increased risk of bacterial infection, appropriate wound care is necessary using soap and water (1). Antihistamines and topical or oral corticosteroids can be used to relieve symptoms(2). The use of insect repellant and protective clothing is the best way to prevent bites.

    References: (AMA)

    1.      B Koyani B, D Pathak R, H Thacker D. Bullous arthropod bite reaction. International Journal of Case Reports and Images. 2022;13(2):164-167. doi:10.5348/101352z01bk2022cr 

    1. Collins P, Sepede J. Bullous arthropod bite reaction. BMJ Case Reports. 2018;11(1). doi:10.1136/bcr-2018-228079 
    2. Kim JE, Kim S-C. Insect bite-like reaction with bullous lesions mimicking bullous pemphigoid in a patient with chronic lymphocytic leukemia. Annals of Dermatology. 2018;30(4):468. doi:10.5021/ad.2018.30.4.468 
  • Bites, Arthropod

    Bites, Arthropod

    Bites, Arthropod

    Definition: Arthropod bites are skin reactions caused by the bite or sting of different arthropods such as arachnids (spiders,ticks), insects (mosquitoes, fleas, and bedbugs), Chilopods (centipedes) and Diplopods (millipedes)(1).

    Etiology: The skin reaction is brought on by the entry of venom, saliva, or other compounds from arthropods into the skin, which triggers an inflammatory reaction ( ).

    Epidemiology: Arthropod bites are prevalent across the world, especially in warmer climates (1,2). The incidence is higher in those that participate in outdoor activities (1,2).

    Signs: At the site of the bite there may be erythematous papules, weals, or vesicles along with surrounding erythema and edema (3). 

    Symptoms: Burning, local redness discomfort, or localized itching at the bite site (1). Systemic symptoms including fever, headaches, or allergic reactions (i.e. anaphylaxis) can occur in certain people (1).

    Differentials: Urticaria, cellulitis, contact dermatitis, drug eruption, mastocytosis bullous disease, dermatitis herpetiformis, tinea, eczema, vasculitis, pityriasis, erythema multiforme, viral exanthem (1).

    Diagnosis: Diagnosis is clinical, based on history and clinical findings. A thorough history may be useful to determine the exact arthropod. Diagnostic tests (labs, biopsy and imaging are rarely needed but in some cases may help confirm diagnosis (1). 

    Treatment: For arthropod stings the stinger should be removed followed by a cold compress, topical steroid cream or calamine lotion (2). Oral antihistamine can be used to reduce the itching sensation and weals (2). Epinephrine for anaphylaxis may be necessary in severe cases (2). Wearing protective clothes and applying insect repellent are the best preventive actions (2).

    References: (AMA)

    1.     Domino FJ, Baldor RA, Golding J, Grimes JA. The 5-Minute Clinical Consult Premium 2015. Wolters Kluwer Health; 2014. 

    2.     Arthropod bites and stings. DermNet®. May 23, 2024. Accessed August 24, 2024. https://dermnetnz.org/topics/arthropod-bites-and-stings. 

    3.     Powers J. Insect bites. StatPearls [Internet]. August 8, 2023. Accessed August 24, 2024. https://www.ncbi.nlm.nih.gov/books/NBK537235/#:~:text=There%20is%20usually%20a%20pruritic,bacterial%20infection%20may%20be%20present.

  • Atopic Dermatitis

    Atopic Dermatitis

    Atopic Dermatitis 

    Definition: Atopic Dermatitis (AD) is a chronic inflammatory skin disorder marked by scaly, erythematous, and itchy skin lesions that are frequently seen in the body’s flexural surfaces (1).

    Etiology: Atopic dermatitis can often present as part of an atopic/allergic triad presenting with asthma and allergic rhinitis (1). Most individuals with AD will have a personal or family history and/or an increased production of immunoglobulin (Ig) E antibodies (4).

    Epidemiology: The onset is typically before the age of two with a reported 10% of cases presenting after the age of five (1). The prevalence in children is approximately 20% and in adults it ranges from 7% to 14% (2).

    Signs: Scaly, erythematous plaques usually accompanied by lichenification (4). 

    Symptoms: Patients present with dry skin and an itchy rash which can lead to infection and substantial reduction of quality of life (2).

    Differentials: Candidiasis, conditions that cause generalized pruritus, contact dermatitis, dermatitis herpetiformis, impetigo, lichen simplex chronicus, nummular eczema, psoriasis, scabies, seborrheic dermatitis, urticaria and xerosis (1).

    Diagnosis: Diagnosis is based on a comprehensive history and physical exam (1). If needed a biopsy or patch can be performed (3).

    Treatment: The goal of treatment is to relieve symptoms and increase the period in between flare-ups (1). Emollients are recommended as treatment with topical corticosteroids being first line treatment for flare-ups of atopic dermatitis (1).

    References: (AMA)

    1.      1. Berke R, Singh A, Guralnick M. Atopic dermatitis: An overview. American Family Physician. July 1, 2012. Accessed August 18, 2024. https://www.aafp.org/pubs/afp/issues/2012/0701/p35.html#clinical-presentation-and-differential-diagnosis.

    2.     Bylund S, Kobyletzki L, Svalstedt M, Svensson. Prevalence and incidence of atopic dermatitis: A systematic review. Acta Dermato Venereologica. 2020;100(12). doi:10.2340/00015555-3510 

    3.     Sidbury R, Alikhan A, Bercovitch L, et al. Guidelines of care for the management of atopic dermatitis in adults with topical therapies. Journal of the American Academy of Dermatology. 2023;89(1). doi:10.1016/j.jaad.2022.12.029

    4.     Saeki H, Ohya Y, Furuta J, et al. English version of Clinical Practice Guidelines for the management of atopic dermatitis 2021. The Journal of Dermatology. 2022;49(10). doi:10.1111/1346-8138.16527 

  • 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. 
  • Familial Lipomatosis/Lipomas

    Familial Lipomatosis/Lipomas

    Familial Lipomatosis/Lipomas

    Condition Name: Familial lipomatosis/lipomas

    Definition: Familial lipomatosis/lipomas is a hereditary condition characterized by the development of multiple lipomas, which are benign tumours composed of mature fat cells. These soft, mobile, and usually painless nodules can occur anywhere on the body but are most commonly found on the trunk, forearms, and thighs.

    Etiology: The condition is inherited in an autosomal dominant pattern.

    Epidemiology: Familial multiple lipomatosis affects both men and women, with lipomas typically appearing in adulthood.

    Signs: The presence of multiple subcutaneous lipomas, which can vary in size from small (a few millimetres) to large (several centimetres).

    Symptoms: Although the lipomas are generally asymptomatic, they can become painful if they compress nerves or other structures.

    Differentials: Other conditions causing subcutaneous nodules or tumours, such as neurofibromas, cysts, or liposarcomas, may be considered.

    Diagnosis: Diagnosis is based on clinical examination, family history, and, if necessary, imaging or biopsy to rule out other conditions.

    Treatment: Treatment is usually not necessary unless the lipomas cause discomfort, restrict movement, or are cosmetically concerning. Management options include surgical excision, liposuction, and, in some cases, injection lipolysis. Regular monitoring is recommended to manage potential complications and assess the need for intervention.

    References:

    • Brodland, D. G., & Thomas, J. R. (2005). Lipomas and liposuction. In Cummings Otolaryngology-Head and Neck Surgery (4th ed., pp. 2914-2922). Elsevier.
    • Meier, D. E., & Patel, R. J. (2008). Lipoma. In StatPearls [Internet]. StatPearls Publishing. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537086/
    • Billing, V. J., & Resnick, S. D. (2020). Lipomas and lipomatosis: Clinical considerations and management. Dermatologic Surgery, 46(8), 1032-1039.
  • 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
  • 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