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Skin Type: 3

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

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 

Porphyria Cutanea Tarda

Porphyria Cutanea Tarda

Condition Name: Porphyria Cutanea Tarda (PCT)

Definition: PCT is a disorder characterized by blistering lesions on sun-exposed skin due to a deficiency of the enzyme uroporphyrinogen decarboxylase (UROD).

Etiology: PCT can be inherited or acquired. Acquired PCT is often linked to liver disease, such as hepatitis C, alcohol abuse, or hemochromatosis, while familial PCT involves a genetic mutation in the UROD gene.

Epidemiology: PCT is the most common type of porphyria, typically presenting in adults in their 40s or 50s. Familial cases tend to present earlier in life, while sporadic cases often appear in the fourth or fifth decades.

Signs: Blistering, fragile skin on sun-exposed areas like the hands and face, with potential hyperpigmentation, scarring, and milia.

Symptoms: Skin sensitivity to sunlight, pain and discomfort in affected areas, and dark urine due to elevated porphyrins.

Differentials: Variegate porphyria, bullous pemphigoid, lupus erythematosus.

Diagnosis: Confirmed through porphyrin level testing in blood, urine, and stool, with a Wood’s lamp examination revealing fluorescence in urine.

Treatment: Therapeutic phlebotomy to reduce iron levels, low-dose antimalarials like hydroxychloroquine, and strict sun protection.

References:

1.     Singal AK. Porphyria cutanea tarda: Recent update. Mol Genet Metab. 2019;128(3):271-281. doi:10.1016/j.ymgme.2019.01.004

2.     Frank J, Poblete-Gutiérrez P. Porphyria cutanea tarda–when skin meets liver. Best Pract Res Clin Gastroenterol. 2010;24(5):735-745. doi:10.1016/j.bpg.2010.07.002

Impetigo

Impetigo

Definition: Impetigo is a common infection of the superficial layers of the epidermis that is very contagious and most often caused by gram-positive bacteria. This condition is characterized by pustules and honey-coloured crusted erosions. It can be classified into non-bullous and bullous impetigo. 

Etiology: Impetigo is caused by Staphylococcus aureus and less commonly, Streptococcus pyogenes. Nonbullous impetigo can be caused by either bacteria or a conjoint infection. Disruption in skin integrity allows for the invasion and colonization of bacteria on the surface. Bullous impetigo is caused by Staphylococcus aureus, which produces exfoliative toxins that target intracellular adhesion molecules of the epidermal granular layer. This results in the dissociation of epidermal cells, leading to blister formation.

Epidemiology: Impetigo accounts for approximately 10% of skin ailments in the pediatric population, most prevalent in children aged 2-5. The male-to-female ratio of incidence is approximately 1:1. Men are more commonly affected. Bullous impetigo is more common in children younger than two. Non-bullous impetigo caused by S. aureus accounts for approximately 80% of cases. Group A beta-hemolytic Strep (GABHS) accounts for 10% of cases. Methicillin-resistant S aureus (MRSA) has become more prevalent in hospitalized patients. 

Signs: Non-bullous impetigo can occur on the face, extremities or other body parts. It begins with a single erythematous macule that evolves into a pustule. This may be erythematous on lighter skin tones, and violaceous or brown on deeper skin tones. When this pustule or vesicle ruptures, it releases serous contents which dry to leave a typical honey-coloured crust.

Bullous impetigo is typically found on the face, trunk, extremities, buttocks and perianal regions. Autoinoculation may cause distal spread of lesions. Bullous impetigo appears as superficial small or large, thin-roofed bullae which spontaneously rupture to leave collarette.

Ecthyma is a deep ulcerated infection that can develop as a complication of bullous impetigo.

Symptoms: Individuals with non-bullous impetigo may experience some itching and regional lymphadenopathy. Individuals with bullous impetigo may experience systemic symptoms of fever, malaise and lymphadenopathy.

Differentials: scabies, atopic dermatitis, contact dermatitis, candidiasis, herpes simplex

Diagnosis: diagnosis of impetigo begins with a thorough history and physical examination. Bacterial cultures may be in the confirmation of diagnosis if MRSA is suspected or if there is an impetigo outbreak. Skin biopsy may be used in refractory cases. Human immunodeficiency virus testing should be considered when a previously healthy adult develops bullous impetigo.

Treatment: Specific measures in treating impetigo include topical or oral antibiotics, proper hand hygiene and avoiding close contact with confirmed cases.

References:

1.     Nardi NM, Schaefer TJ. Impetigo. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 31, 2023.

2.     Quirke K. Impetigo | DermNet NZ. dermnetnz.org. Published March 2022. https://dermnetnz.org/topics/impetigo

Impetigo

Impetigo

Definition: Impetigo is a common infection of the superficial layers of the epidermis that is very contagious and most often caused by gram-positive bacteria. This condition is characterized by pustules and honey-coloured crusted erosions. It can be classified into non-bullous and bullous impetigo. 

Etiology: Impetigo is caused by Staphylococcus aureus and less commonly, Streptococcus pyogenes. Nonbullous impetigo can be caused by either bacteria or a conjoint infection. Disruption in skin integrity allows for the invasion and colonization of bacteria on the surface. Bullous impetigo is caused by Staphylococcus aureus, which produces exfoliative toxins that target intracellular adhesion molecules of the epidermal granular layer. This results in the dissociation of epidermal cells, leading to blister formation.

Epidemiology: Impetigo accounts for approximately 10% of skin ailments in the pediatric population, most prevalent in children aged 2-5. The male-to-female ratio of incidence is approximately 1:1. Men are more commonly affected. Bullous impetigo is more common in children younger than two. Non-bullous impetigo caused by S. aureus accounts for approximately 80% of cases. Group A beta-hemolytic Strep (GABHS) accounts for 10% of cases. Methicillin-resistant S aureus (MRSA) has become more prevalent in hospitalized patients. 

Signs: Non-bullous impetigo can occur on the face, extremities or other body parts. It begins with a single erythematous macule that evolves into a pustule. This may be erythematous on lighter skin tones, and violaceous or brown on deeper skin tones. When this pustule or vesicle ruptures, it releases serous contents which dry to leave a typical honey-coloured crust.

Bullous impetigo is typically found on the face, trunk, extremities, buttocks and perianal regions. Autoinoculation may cause distal spread of lesions. Bullous impetigo appears as superficial small or large, thin-roofed bullae which spontaneously rupture to leave collarette.

Ecthyma is a deep ulcerated infection that can develop as a complication of bullous impetigo.

Symptoms: Individuals with non-bullous impetigo may experience some itching and regional lymphadenopathy. Individuals with bullous impetigo may experience systemic symptoms of fever, malaise and lymphadenopathy.

Differentials: scabies, atopic dermatitis, contact dermatitis, candidiasis, herpes simplex

Diagnosis: diagnosis of impetigo begins with a thorough history and physical examination. Bacterial cultures may be in the confirmation of diagnosis if MRSA is suspected or if there is an impetigo outbreak. Skin biopsy may be used in refractory cases. Human immunodeficiency virus testing should be considered when a previously healthy adult develops bullous impetigo.

Treatment: Specific measures in treating impetigo include topical or oral antibiotics, proper hand hygiene and avoiding close contact with confirmed cases.

References:

1.     Nardi NM, Schaefer TJ. Impetigo. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 31, 2023.

2.     Quirke K. Impetigo | DermNet NZ. dermnetnz.org. Published March 2022. https://dermnetnz.org/topics/impetigo

Impetigo

Impetigo

Definition: Impetigo is a common infection of the superficial layers of the epidermis that is very contagious and most often caused by gram-positive bacteria. This condition is characterized by pustules and honey-coloured crusted erosions. It can be classified into non-bullous and bullous impetigo. 

Etiology: Impetigo is caused by Staphylococcus aureus and less commonly, Streptococcus pyogenes. Nonbullous impetigo can be caused by either bacteria or a conjoint infection. Disruption in skin integrity allows for the invasion and colonization of bacteria on the surface. Bullous impetigo is caused by Staphylococcus aureus, which produces exfoliative toxins that target intracellular adhesion molecules of the epidermal granular layer. This results in the dissociation of epidermal cells, leading to blister formation.

Epidemiology: Impetigo accounts for approximately 10% of skin ailments in the pediatric population, most prevalent in children aged 2-5. The male-to-female ratio of incidence is approximately 1:1. Men are more commonly affected. Bullous impetigo is more common in children younger than two. Non-bullous impetigo caused by S. aureus accounts for approximately 80% of cases. Group A beta-hemolytic Strep (GABHS) accounts for 10% of cases. Methicillin-resistant S aureus (MRSA) has become more prevalent in hospitalized patients. 

Signs: Non-bullous impetigo can occur on the face, extremities or other body parts. It begins with a single erythematous macule that evolves into a pustule. This may be erythematous on lighter skin tones, and violaceous or brown on deeper skin tones. When this pustule or vesicle ruptures, it releases serous contents which dry to leave a typical honey-coloured crust.

Bullous impetigo is typically found on the face, trunk, extremities, buttocks and perianal regions. Autoinoculation may cause distal spread of lesions. Bullous impetigo appears as superficial small or large, thin-roofed bullae which spontaneously rupture to leave collarette.

Ecthyma is a deep ulcerated infection that can develop as a complication of bullous impetigo.

Symptoms: Individuals with non-bullous impetigo may experience some itching and regional lymphadenopathy. Individuals with bullous impetigo may experience systemic symptoms of fever, malaise and lymphadenopathy.

Differentials: scabies, atopic dermatitis, contact dermatitis, candidiasis, herpes simplex

Diagnosis: diagnosis of impetigo begins with a thorough history and physical examination. Bacterial cultures may be in the confirmation of diagnosis if MRSA is suspected or if there is an impetigo outbreak. Skin biopsy may be used in refractory cases. Human immunodeficiency virus testing should be considered when a previously healthy adult develops bullous impetigo.

Treatment: Specific measures in treating impetigo include topical or oral antibiotics, proper hand hygiene and avoiding close contact with confirmed cases.

References:

1.     Nardi NM, Schaefer TJ. Impetigo. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 31, 2023.

2.     Quirke K. Impetigo | DermNet NZ. dermnetnz.org. Published March 2022. https://dermnetnz.org/topics/impetigo

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

Basal Cell Carcinoma

Basal Cell Carcinoma (BCC)

Definition: BCC is a slow-growing nonmelanocytic skin cancer arising from basal cells in the epidermis that rarely metastasizes but can invade locally and be destructive (1,4,5).

Etiology:  Ultraviolet exposure is a major risk factor and explains why BCC typically grows on sun-exposed areas of the skin (1). Other factors that influence the development of BCC include fairer skin colour, light-coloured eyes, Northern European ancestry, red hair and a history of sunburns (5). Pathobiologicallt, most BCCs are caused by activation of the Hedgehog signaling system, which is also a target for therapeutic intervention (5).

Epidemiology: The incidence of BCC varies depending on geographic location and race (5). Australia is reported to have one of the highest incidences of 1000/100,000 (5). BCC is one of the most common skin cancers in fair-skinned individuals and is increasing in incidence globally (1). It is usually seen after the age of 50 with an incidence ratio of 2:1 in females and males respectively (1).

Signs: BCC manifests as a translucent or pearly nodule accompanied by telangiectasia on sun-exposed regions such as the neck, ears, and face (2).

Symptoms: Typically asymptomatic but with time may crust, bleed or develop ulcers (2,3).

Differentials: Squamous cell carcinoma, adnexal tumors, seborrheic keratosis(1).

Diagnosis: Diagnosis requires a biopsy and is recommended before undergoing surgery or systemic treatment (1). Diagnosis also involves historical examination and direct inspection of the lesion (5). 

Treatment: The standard treatment for BCC is typically surgery (surgical excision, Mohs micrographic surgery and curettage and electrodesiccation) but non-surgical treatments options are also available including: freezing or light therapy, topical medications and radiation treatments (1).

References: (AMA)

1.      Basset-Seguin N, Herms F. Update in the management of basal cell carcinoma. Acta Dermato Venereologica. 2020;100(11). doi:10.2340/00015555-3495 

2.     1. McDaniel B. Basal cell carcinoma. StatPearls [Internet]. March 13, 2024. Accessed August 18, 2024. https://www.ncbi.nlm.nih.gov/books/NBK482439/#:~:text=BCC%20typically%20presents%20as%20a,rolled%20or%20rodent%20ulcer%20appearance.

3.     Oakley A. Basal cell carcinoma: Symptoms, causes, and treatment – dermnet. DermNet®. July 3, 2024. Accessed August 18, 2024. https://dermnetnz.org/topics/basal-cell-carcinoma. 

4.     Robert S Bader M. Basal cell carcinoma. Practice Essentials, Background, Pathophysiology. April 3, 2024. Accessed August 18, 2024. https://emedicine.medscape.com/article/276624-overview?gad_source=1&gbraid=0AAAAADoSQiUCwFng3uMBdxWlXHVuNMVrw&gclid=Cj0KCQjwt4a2BhD6ARIsALgH7Dqhf-P79uzm848PdW5k8auVX_QjoRGo38V0m2dFrNN42l3MpFCbyS0aAm4_EALw_wcB&form=fpf#a2.

5.     Tanese K. Diagnosis and management of basal cell carcinoma. Current Treatment Options in Oncology. 2019;20(2). doi:10.1007/s11864-019-0610-0 

Basal Cell Carcinoma

Basal Cell Carcinoma (BCC)

Definition: BCC is a slow-growing nonmelanocytic skin cancer arising from basal cells in the epidermis that rarely metastasizes but can invade locally and be destructive (1,4,5).

Etiology:  Ultraviolet exposure is a major risk factor and explains why BCC typically grows on sun-exposed areas of the skin (1). Other factors that influence the development of BCC include fairer skin colour, light-coloured eyes, Northern European ancestry, red hair and a history of sunburns (5). Pathobiologicallt, most BCCs are caused by activation of the Hedgehog signaling system, which is also a target for therapeutic intervention (5).

Epidemiology: The incidence of BCC varies depending on geographic location and race (5). Australia is reported to have one of the highest incidences of 1000/100,000 (5). BCC is one of the most common skin cancers in fair-skinned individuals and is increasing in incidence globally (1). It is usually seen after the age of 50 with an incidence ratio of 2:1 in females and males respectively (1).

Signs: BCC manifests as a translucent or pearly nodule accompanied by telangiectasia on sun-exposed regions such as the neck, ears, and face (2).

Symptoms: Typically asymptomatic but with time may crust, bleed or develop ulcers (2,3).

Differentials: Squamous cell carcinoma, adnexal tumors, seborrheic keratosis(1).

Diagnosis: Diagnosis requires a biopsy and is recommended before undergoing surgery or systemic treatment (1). Diagnosis also involves historical examination and direct inspection of the lesion (5). 

Treatment: The standard treatment for BCC is typically surgery (surgical excision, Mohs micrographic surgery and curettage and electrodesiccation) but non-surgical treatments options are also available including: freezing or light therapy, topical medications and radiation treatments (1).

References: (AMA)

1.      Basset-Seguin N, Herms F. Update in the management of basal cell carcinoma. Acta Dermato Venereologica. 2020;100(11). doi:10.2340/00015555-3495 

2.     1. McDaniel B. Basal cell carcinoma. StatPearls [Internet]. March 13, 2024. Accessed August 18, 2024. https://www.ncbi.nlm.nih.gov/books/NBK482439/#:~:text=BCC%20typically%20presents%20as%20a,rolled%20or%20rodent%20ulcer%20appearance.

3.     Oakley A. Basal cell carcinoma: Symptoms, causes, and treatment – dermnet. DermNet®. July 3, 2024. Accessed August 18, 2024. https://dermnetnz.org/topics/basal-cell-carcinoma. 

4.     Robert S Bader M. Basal cell carcinoma. Practice Essentials, Background, Pathophysiology. April 3, 2024. Accessed August 18, 2024. https://emedicine.medscape.com/article/276624-overview?gad_source=1&gbraid=0AAAAADoSQiUCwFng3uMBdxWlXHVuNMVrw&gclid=Cj0KCQjwt4a2BhD6ARIsALgH7Dqhf-P79uzm848PdW5k8auVX_QjoRGo38V0m2dFrNN42l3MpFCbyS0aAm4_EALw_wcB&form=fpf#a2.

5.     Tanese K. Diagnosis and management of basal cell carcinoma. Current Treatment Options in Oncology. 2019;20(2). doi:10.1007/s11864-019-0610-0 

Basal Cell Carcinoma

Basal Cell Carcinoma (BCC)

Definition: BCC is a slow-growing nonmelanocytic skin cancer arising from basal cells in the epidermis that rarely metastasizes but can invade locally and be destructive (1,4,5).

Etiology:  Ultraviolet exposure is a major risk factor and explains why BCC typically grows on sun-exposed areas of the skin (1). Other factors that influence the development of BCC include fairer skin colour, light-coloured eyes, Northern European ancestry, red hair and a history of sunburns (5). Pathobiologicallt, most BCCs are caused by activation of the Hedgehog signaling system, which is also a target for therapeutic intervention (5).

Epidemiology: The incidence of BCC varies depending on geographic location and race (5). Australia is reported to have one of the highest incidences of 1000/100,000 (5). BCC is one of the most common skin cancers in fair-skinned individuals and is increasing in incidence globally (1). It is usually seen after the age of 50 with an incidence ratio of 2:1 in females and males respectively (1).

Signs: BCC manifests as a translucent or pearly nodule accompanied by telangiectasia on sun-exposed regions such as the neck, ears, and face (2).

Symptoms: Typically asymptomatic but with time may crust, bleed or develop ulcers (2,3).

Differentials: Squamous cell carcinoma, adnexal tumors, seborrheic keratosis(1).

Diagnosis: Diagnosis requires a biopsy and is recommended before undergoing surgery or systemic treatment (1). Diagnosis also involves historical examination and direct inspection of the lesion (5). 

Treatment: The standard treatment for BCC is typically surgery (surgical excision, Mohs micrographic surgery and curettage and electrodesiccation) but non-surgical treatments options are also available including: freezing or light therapy, topical medications and radiation treatments (1).

References: (AMA)

1.      Basset-Seguin N, Herms F. Update in the management of basal cell carcinoma. Acta Dermato Venereologica. 2020;100(11). doi:10.2340/00015555-3495 

2.     1. McDaniel B. Basal cell carcinoma. StatPearls [Internet]. March 13, 2024. Accessed August 18, 2024. https://www.ncbi.nlm.nih.gov/books/NBK482439/#:~:text=BCC%20typically%20presents%20as%20a,rolled%20or%20rodent%20ulcer%20appearance.

3.     Oakley A. Basal cell carcinoma: Symptoms, causes, and treatment – dermnet. DermNet®. July 3, 2024. Accessed August 18, 2024. https://dermnetnz.org/topics/basal-cell-carcinoma. 

4.     Robert S Bader M. Basal cell carcinoma. Practice Essentials, Background, Pathophysiology. April 3, 2024. Accessed August 18, 2024. https://emedicine.medscape.com/article/276624-overview?gad_source=1&gbraid=0AAAAADoSQiUCwFng3uMBdxWlXHVuNMVrw&gclid=Cj0KCQjwt4a2BhD6ARIsALgH7Dqhf-P79uzm848PdW5k8auVX_QjoRGo38V0m2dFrNN42l3MpFCbyS0aAm4_EALw_wcB&form=fpf#a2.

5.     Tanese K. Diagnosis and management of basal cell carcinoma. Current Treatment Options in Oncology. 2019;20(2). doi:10.1007/s11864-019-0610-0