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Leiomyosarcoma

Leiomyosarcoma

Definition: Leiomyosarcoma is an aggressive mesenchymal malignancy and one of the most common subtypes of sarcoma. Leiomyosarcoma typically occurs in the retroperitoneum, uterus and extremities.

Etiology: Leiomyosarcoma is a heterogeneous disease primarily associated with RB1 and PTEN tumor suppressor gene mutations. The definitive cause for leiomyosarcoma is unknown, but risk factors have been associated with developing other soft tissue sarcomas. Radiation exposure, radiotherapy, genetic syndromes such as retinoblastoma and Li- Frarumeni syndrome have been highlighted as risk factors.

Epidemiology: Leiomyosarcoma accounts for 10- 20% of newly diagnosed soft tissue sarcomas and 80% of uterine sarcomas. The incidence of leiomyosarcoma increases with age, peaking at the 7th decade of life. Uterine leiomyosarcoma most commonly occurs in perimenopausal women. Retroperitoneal leiomyosarcoma is more common in women. Studies have reported that the incidence rates of leiomyosarcoma are substantially higher (IRR > 1.60) in Non- Hispanic Black people.

Signs: Clinical presentation of leiomyosarcoma is variable and depends on the location. 

Symptoms: Symptoms associated with leiomyosarcoma are associated with the compression of surrounding organs. These include unexplained weight loss, changes in bowel habits and pain and discomfort.

Differentials: Meningioma, GIST, leiomyoma, Spindle cell squamous cell carcinoma, malignant peripheral nerve sheath tumor

Diagnosis: Initial imaging involves computed tomography or magnetic resonance imaging scans. An image- guided core needle biopsy is required for diagnosis. Morphological diagnosis based on microscopic examination is the gold standard. Histology of leiomyosarcoma will show a poorly circumscribed nodule that may be dermal based, or in the subcutaneous form. Leiomyosarcoma consists of spindle cell proliferation, with “cigar- shaped nuclei”, which form rough bundles and fascicles.

Treatment: Treatment is dependent on the size, grade and location of the lesion. Surgery is regarded as the curative therapy, in conjunction with radiation and/ or chemotherapy.

References:

  1. Menon G, Mangla A, Yadav U. Leiomyosarcoma. In: StatPearls. Treasure Island (FL): StatPearls Publishing; February 28, 2024.
  2. Leiomyosarcoma pathology | DermNet. dermnetnz.org. https://dermnetnz.org/topics/leiomyosarcoma-pathology
  3. Diessner BJ, Weigel BJ, Murugan P, Zhang L, Poynter JN, Spector LG. Racial and Ethnic Differences in Sarcoma Incidence Are Independent of Census-Tract Socioeconomic Status. Cancer Epidemiol Biomarkers Prev. 2020;29(11):2141-2148. doi:10.1158/1055-9965.EPI-20-0520

Leiomyosarcoma

Leiomyosarcoma

Definition: Leiomyosarcoma is an aggressive mesenchymal malignancy and one of the most common subtypes of sarcoma. Leiomyosarcoma typically occurs in the retroperitoneum, uterus and extremities.

Etiology: Leiomyosarcoma is a heterogeneous disease primarily associated with RB1 and PTEN tumor suppressor gene mutations. The definitive cause for leiomyosarcoma is unknown, but risk factors have been associated with developing other soft tissue sarcomas. Radiation exposure, radiotherapy, genetic syndromes such as retinoblastoma and Li- Frarumeni syndrome have been highlighted as risk factors.

Epidemiology: Leiomyosarcoma accounts for 10- 20% of newly diagnosed soft tissue sarcomas and 80% of uterine sarcomas. The incidence of leiomyosarcoma increases with age, peaking at the 7th decade of life. Uterine leiomyosarcoma most commonly occurs in perimenopausal women. Retroperitoneal leiomyosarcoma is more common in women. Studies have reported that the incidence rates of leiomyosarcoma are substantially higher (IRR > 1.60) in Non- Hispanic Black people.

Signs: Clinical presentation of leiomyosarcoma is variable and depends on the location. 

Symptoms: Symptoms associated with leiomyosarcoma are associated with the compression of surrounding organs. These include unexplained weight loss, changes in bowel habits and pain and discomfort.

Differentials: Meningioma, GIST, leiomyoma, Spindle cell squamous cell carcinoma, malignant peripheral nerve sheath tumor

Diagnosis: Initial imaging involves computed tomography or magnetic resonance imaging scans. An image- guided core needle biopsy is required for diagnosis. Morphological diagnosis based on microscopic examination is the gold standard. Histology of leiomyosarcoma will show a poorly circumscribed nodule that may be dermal based, or in the subcutaneous form. Leiomyosarcoma consists of spindle cell proliferation, with “cigar- shaped nuclei”, which form rough bundles and fascicles.

Treatment: Treatment is dependent on the size, grade and location of the lesion. Surgery is regarded as the curative therapy, in conjunction with radiation and/ or chemotherapy.

References:

  1. Menon G, Mangla A, Yadav U. Leiomyosarcoma. In: StatPearls. Treasure Island (FL): StatPearls Publishing; February 28, 2024.
  2. Leiomyosarcoma pathology | DermNet. dermnetnz.org. https://dermnetnz.org/topics/leiomyosarcoma-pathology
  3. Diessner BJ, Weigel BJ, Murugan P, Zhang L, Poynter JN, Spector LG. Racial and Ethnic Differences in Sarcoma Incidence Are Independent of Census-Tract Socioeconomic Status. Cancer Epidemiol Biomarkers Prev. 2020;29(11):2141-2148. doi:10.1158/1055-9965.EPI-20-0520

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.

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

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

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 

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.

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

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