Cutaneous Squamous Cell Carcinoma

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Cutaneous squamous cell carcinoma (cSCC) is a malignant skin tumor that arises from the epidermal keratinocytes. They can develop on any cutaneous surface, including the head, neck, trunk, extremities, oral mucosa, periungual skin, and anogenital areas. In individuals with fair-skin, it mainly arises in sun-exposed areas. On the other hand, in individuals with darker skin tones, it primarily develops in non-sun exposed areas, such as the lower legs, anogenital region, and areas of chronic inflammation or scarring. The latter accounts for 20-40% of cSCC in black patients.

More than 90% of cases of SCC are associated with countless DNA mutations in various somatic genes. For example, mutations in the p53 tumor suppressor gene are caused by exposure to ultraviolet radiation (UV), especially UVB (signature 7). Other signature mutations are related to cigarette smoking, aging, immunosuppression.

 

Clinical features:

Cutaneous SCC presents with a wide variety of cutaneous lesions, including papules, plaques, or nodules, that can be smooth, hyperkeratotic, firm/indurated (more with well-differentiated), or ulcerated, fleshy, granulomatous, +/- area of hemorrhage or necrosis (poorly differentiated). Cutaneous SCC in situ (Bowen’s disease) mainly presents as an erythematous, well-demarcated, scaly patch or plaque located in sun-exposed areas. Lesions of invasive cSCC are often asymptomatic but may be painful or pruritic or have local neurologic symptoms (e.g., numbness, stinging, burning, paresthesias, paralysis, or visual changes).

 

Diagnosis: 

SCC is diagnosed based on clinical features and confirmed pathologically by diagnostic biopsy or following excision. Staging investigations may also be carried out in high-risk SCC to determine whether it has spread to lymph nodes or elsewhere.

Cutaneous SCC is catigorized as low-risk or high-risk, depending on the chance of tumor recurrence and metastasis. Characteristics of high-risk SCC are shown in this Figure. Metastatic SCC is found in regional lymph nodes (80%), lungs, liver, brain, bones, and skin.

 

Management:

Cutaneous SCC is almost always treated surgically, and most cases are excised with a 3–10 mm margin of normal tissue around the tumor. Reconstruction using a flap or skin graft may be needed to repair the defect. Other methods of removal include:

  • Shave, curettage, and electrocautery: for low-risk tumors on trunk and limbs
  • Aggressive cryotherapy: for tiny, thin, low-risk tumors
  • Mohs micrographic surgery: for large facial tumors with indistinct margins or recurrent tumors
  • Radiotherapy: for an inoperable tumor, patients unsuitable for surgery, or as adjuvant

 

For advanced/or metastatic SCC?

Locally advanced primary, recurrent or metastatic SCC requires multidisciplinary team (MDT) consultation. Usually, a combination of treatments is used, including surgery, radiotherapy, cemiplimab, and experimental targeted therapy using epidermal growth factor receptor (EGFR) inhibitors.

 

Written By: Dr. Iman Nazer,  Dermatology resident.

References:

Uptodate 

Dermnetnz.org

BAD guidelines 

Cutaneous Leishmaniasis

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Leishmaniasis is a parasitic disease transmitted by the bite of infected female sandflies. It is caused by more than 20 species of Leishmania which is a flagellated protozoa.

Epidemiology:
– Worldwide, there are approximately 2 million new cases of leishmaniasis annually.
– Cutaneous or mucocutaneous disease presents 75% of the affected individuals
– Over 90% of cutaneous infections with Leishmania occur in the Middle East (Afghanistan, Algeria, Iran, Iraq, Saudi Arabia, Syria) and South America (Brazil, Peru, Colombia)

The incubation period of Cutaneous leishmaniasis is usually several weeks to 2 months. The clinical manifestations of leishmaniasis depend on the species of Leishmania, the host’s cell-mediated response, and the ability of the parasite to evade host defense mechanisms. Cutaneous leishmaniasis is divided into two subsets: Old World and New World. Old World cutaneous leishmaniasis caused by L. major or L tropica, and less often L.infantum (Europe) or L. aethiopica (Ethiopia and Kenya). In the New World, cutaneous leishmaniasis is caused primarily by L. mexicana and the L. braziliensis complex. Both Old World and New World cutaneous leishmaniasis usually begin as a small, well-circumscribed papule at the inoculation site (usually involve the exposed sites of the skin—arms, face, legs). This lesion may slowly enlarge over several weeks into a nodule or plaque and then become ulcerated.

Treatment:
· For an isolated lesion, conservative therapy (e.g. observation, heat, cryotherapy) or topical paromycin can be used
· For more extensive disease, IV or IM pentavalent antimony (sodium stibogluconate, meglumine antimonate) or oral miltefosine

Written by: Dr. Arwa Alsubhi, dermatology resident.

References:
-Bolognia textbook of dermatology
-Dermatology Essentials

Morphea

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Morphea is an autoimmune connective tissue disorder, which is characterized by the hardening of the skin. It is a relatively uncommon disorder as the annual incidence rate is estimated to be 27 per million; however, the prevalence increases with age. In addition, the disease is more prevalent in females. Although the etiology of morphea is poorly understood, It is thought to be due to several factors, namely genetics such as HLADRB1 ∗ 04:04 and HLA-B37 that increase the susceptibility. Moreover, environmental triggers play a significant role in pathogenesis. All of this will result in T-cell activation, vascular damage, and deposit of fibroblast.

There are three recognized types of the disorder: plaque, linear, and generalized, as shown in the table below.

 

Subtype

 page1image5822704

Location

 page1image5824576

Symptoms

 page1image5062496

Picture

Plaque

 page1image1696000

Plaque

Trunk and proximal Extremities

Erythematous to violaceous patches

Guttate

Upper half of trunk
  • Multiple small chalk
  • White
  • Flat

Atrophoderma of pasini and pierini

Trunk Upper arms

page1image5780272
  • Large (20cm)
  • Brownish-gray
  • hyperpigmented oval atrophic well demarcated plaques
  • Sharp sloping border

Deep

 Involving subcutaneous tissue

Nodular/ Keloidal

 page1image3791488 

Hyperpigmented sclerotic nodules that mimic keloids

Linear

En coupe de sabre

Frontal, frontoparietal, parasaggital forehead or scalp

Indented appearance

Parry- Romberg syndrome

Unilateral atrophy of faceà epilepsy, trigeminal neuralgia, and cerebral atrophy

Generalized

Entire trunk and extremities

page1image3702048

Widespread indurated plaquesà muscle atrophy and difficulty breathing

page1image3703088

Morphea is primarily diagnosed clinically, and no further tests are needed to confirm. Blood tests, imaging, and biopsy are used to exclude other diseases. The most prominent biopsy findings of morphea are:

  • Overall square punch.
  • Epidermal atrophy or loss.
  • Dense dermal collagen.
  • Lymphocytes and plasma in the subcutaneous layer.
Morphea is an incurable disorder; nonetheless, certain medications can help control the disease. These treatments can be divided into topical and systemic. Topical medications include steroids, calcineurin inhibitors, imiquimod, and vitamin A/D analogue. Systemic are corticosteroids, methotrexate, mycophenolate mofetil. For superficial morphea, topical therapies are commonly used. Furthermore, the treatment of choice for moderate to severe morphea is methotrexate, in addition to systemic corticosteroids.

Written By: Dr. Alanoud Hakami, dermatology resident.

References:

Dermatology 4th edition, by Jean L. Bolognia, Julie V. Schaffer, and Lorenzo Cerroni

Fitzpatrick’s Dermatology, Ninth Edition

https://dermnetnz.org

 

Cutaneous T-Cell Lymphoma

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CTCL is a type of non-Hodgkin’s lymphoma. It is a group of lymphoproliferative disorders characterized by the localization of neoplastic T cells to the skin. CTCL tends to affect older individuals with a mean onset at 50 to 60 years of age. It primarily affects males with a male-to-female ratio of 2:1. The two main subtypes of CTCL are Mycosis Fungoides (MF) and Sézary Syndrome (SS). MF is the most common subtype of CTCL, and it is mainly localized to the skin with an indolent course. SS is the second most common subtype that follows a more aggressive course where neoplastic T cells are found in the skin and bloodstream.

CTCL arises due to the malignant transformation of epidermal T-cells. The exact underlying pathophysiologic mechanism is not fully established. It has been linked to multiple factors, including viral infections (HTLV-1, EBV), medications (hydrochlorothiazide), immunosuppression (HIV, organ transplantation), environmental factors (exposure to chemicals, ionizing radiation or UV rays), and certain HLA subtypes.

CTCL can present in various ways that can progress depending on the stage of the disease. The lesions range from patches, plaques, tumors, or erythroderma. Lymph nodes and internal organs may be involved as well.

Diagnosis of CTCL is based on a combination of clinical, histological, immunophenotypical, radiological, and genetic data. Appropriate clinical staging should be carried out to determine the extent of the disease and the appropriate therapeutic option.

 There is no current cure for CTCL. Management is aimed at reducing tumor burden, delaying progression, and preserving the quality of life. Current approaches are based on the underlying type and stage of the disease. Available options include:

  • Topical treatment (steroids, nitrogen mustard, bexarotene).
  • Phototherapy (UVB, NBUVB, UVA, PUVA).
  • Radiation (localized, external beam).
  • Systemic treatment (Retinoids, immunotherapy, biologics, histone deacetylate inhibitors, chemotherapy, allogeneic stem cell transplantation).

Written By: Dr. Jumana Aldhalaan, dermatology resident

Reference: 

https://dermnetnz.org

Leprosy

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Leprosy or “Hansen’s disease” is a contagious disease caused by mycobacterium leprae complex. In 2000, leprosy was eliminated as a cause of public health concern. Yet, cases still occur, especially in resource-limited countries such as India, Nepal, and Bangladesh. The reservoirs of M.leprae are the armadillos and red squirrels. Moreover, the primary mode of transmission is thought to be respiratory droplets. Risk factors include contact with active cases, especially with the lepromatous type of leprosy, exposure to armadillos, immunosuppression, and age.

Leprosy can be classified into a mild tuberculoid form and a more severe lepromatous form, with intermediate stages in-between. Signs include red or hypopigmented skin patches and loss of sensation in the same skin patches. The lepromatous form presents with more generalized symptoms with erythematous skin nodules, thickening of earlobes, and loss of body hair. Complications include painful neuropathy, corneal ulceration, and abrasion. Late diagnosis and incomplete treatment of leprosy are associated with an increased burden of the disease, deformities, and stigma. The diagnosis is based on clinical presentation supported by the presence of acid-fast bacilli on full-thickness skin biopsy from the most active skin lesion. PCR for M. leprae DNA can also be used for diagnosis.

Leprosy is treated with multi-drug therapy (rifampicin, dapsone, and clofazimine). The duration ranges from 6 months for tuberculoid form and 12 months for lepromatous form. Drug resistance has been reported in some countries in which second-line drugs can be used, such as clarithromycin, minocycline, and fluoroquinolones.

Skin lesions usually start to resolve after few months to years if the patient is compliant with the drug regimen. Although rare, leprosy might relapse mostly 5 to 10 years after stopping the treatment. In areas with a high prevalence of leprosy, a single dose of BCG vaccine can give 50 percent protection. For contacts with active cases of leprosy, chemoprophylaxis with single-dose rifampicin can be given for adults and children more than two years.

 

Written by: Dr. Tammam Alanazi, Dermatology resident.

References:
1- WHO Guidelines for the Diagnosis, Treatment, and Prevention of Leprosy
2- UptoDate

 

Onychomycosis

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Onychomycosis is a fungal infection of the nail caused by dermatophytes, non-dermatophyte molds, and yeasts (mainly Candida species). Incidence increases with age, and it rarely occurs in children. Dermatophytes (Trichophyton rubrum) account for 80% of toenail infections. Onychomycosis is categorized clinically as distal and lateral subungual onychomycosis (DLSO), superficial white onychomycosis (SWO), proximal subungual onychomycosis (PSO), candida onychomycosis, and total dystrophic onychomycosis. Diagnosis of onychomycosis involves physical, microscopic examination and culture. Histologic evaluation using PAS staining is a sensitive method for detecting onychomycosis. Moreover, eradication of the infection is important to improving the cosmetical appearance and avoiding complications. However, it is not simply accomplished because nails are made of hard keratin, which is avascular and resistant to many agents. Thus, creams and other topical medications are commonly not effective against nail fungus. Treatment results take up to a year to appear because nails have poor drug delivery. Treatment differs depending on the severity of nail changes, the involved organism, and adverse effects. Clinical cure refers to improvement in the nail’s appearance, often described as a normal appearance in 80% to 100% of the nail. Usually, effective treatment is achieved by systemic antifungal therapy. Antifungals from the allylamine and azole classes are the most widely used oral medications to treat onychomycosis. The azole class includes itraconazole, fluconazole, and ketoconazole; however, ketoconazole is seldom prescribed because of hepatotoxicity and drug interactions. Itraconazole is prescribed in “pulse doses” one week per month for 2 or 3 months. It can interact with erythromycin or asthma medications. Furthermore, itraconazole’s most frequent side effects include gastrointestinal side effects, transaminitis, high lipids, and skin rash. The allylamine class is represented by terbinafine. Terbinafine is taken daily for eight weeks for fingernail fungus and 12 weeks for toenail fungus. The most frequent side effects are gastrointestinal disturbance, headache, and transaminitis.

Written By: Dr. Fatimah Alowirdi, Dermatology Resident

References:

https://dermnetnz.org/topics/fungal-nail-infections/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC88888/

 

Dermatomyositis

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Dermatomyositis is a rare disease that causes muscle inflammation and skin rash.

It can occur at any age, but it most often affects adults over the age of 50, the exact cause is not known but is thought to be an autoimmune disorders, with genetic predisposition and environmental factors that might play a role.

 

symptoms are caused by swelling and inflammation in the blood vessels that supply the skin and muscle scan appear suddenly or develop gradually over time most commonly a violet-colored or dusky red rash develops on the face and eyelids(heliotrope rash), knuckles (guttron’s sign), elbows, knees, chest and back(shawl sign). The rash can be itchy and painful.Muscle changes usually develops after the rash ,muscles are stiff and tender which make it difficult to do things like brushing hair ,walking upstairs and lifting legs.

 

Dermatomyositis might cause other conditions including Raynaud’s phenomenonwhen  fingersturn pale when exposed to cold temperature,cardiovascular diseases, lung diseases and increased likelihood of developing cancer.

 

Diagnosis of dermatomyositis is based on person’s medical history and a physical exam, also by ordering blood tests to look for autoantibodies. muscle biopsy, Electromyography, and imaging screening for underlying cancer.

 

There’s no cure for dermatomyositis, but treatment aim is to improveskin rash and muscle strength and functionwith medications like corticosteroid and steroid sparing agents, also general measures including sun protection and regular exercises.

 

 

Written by:

Yasmeen Alanazi, Dermatology resident, King Fahad Medical City.

 

References:

bad.org.uk

dermnetnz.org

Vitiligo: classification ,severity scoring system and psychosocial impact

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The Vitiligo European Taskforce came to a consensus about the classification of vitiligo in 2007.

They decided on four main categories with subtypes. Classification  Subtype  Comments 
Nonsegmental vitiligo   Focal 

 Mucosal 

 Acrofacial 

 Generalised 

 Universal 

 bilateral and symmetrical in distribution. 

Stable or unstable 
Segmental vitiligo   Focal 

 Mucosal 

 Unisegmental, bi- or multisegmental 

 Single white patch in 90% 

Border often irregular 

Affects young people 

Stable 

Cutaneous mosaicism 
Mixed vitiligo   Nonsegmental combined with segmental vitiligo  Rare 
Unclassified vitiligo   Focal at onset 

 Multifocal asymmetrical non-segmental 

 Unifocal mucosal 

 Early disease 

 At least two scoring systems have been devised for vitiligo and are used in clinical trials. 

 Vitiligo Area Scoring Index (VASI) 

 Vitiligo European Task Force (VETF) system 

 

VASI : It measures the extent and degree of depigmentation in 6 sites: hands, upper extremities, trunk, lower extremities and feet, head/neck. 

VETF: The VETF assesses the extent, staging and spreading/progression in 5 sites: head/neck, trunk, arms, legs and hands/feet. It grades from 0 (normal pigmentation) to 4 (complete hair whitening). Spreading is assessed using the following scores: 0 (stable disease), -1 (regressive disease) and +1 (progressive disease) 

 

Because vitiligo affects a person’s physical appearance, there are various associated psychological and social impacts. Higher levels of depression and social anxiety have been reported in patients with vitiligo. Patients may also experience low self-esteem, social stigmatization, shame, avoidance of intimacy, adjustment disorder, fear, suicidal ideation, and other psychiatric morbidities .Family support, counselling and cognitive behavioural treatment can be of benefit. 

 

 

Written by: Abdul Aziz Al-mufadhi, PGY1 Dermatology Resident 

 

Resources: 

www.DermNetNZ.org 

https://www.medscape.com/ 

bolognia dermatology 4th edition 

Sunscreen Awareness Month

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Introduction: 

According to the American Academy of Dermatology Association, May is Skin Cancer Awareness Month, and May 28 is National Sunscreen Day, by the early 20-century sunscreen started to manufacture and by the mid-1970s that sunscreens gained a degree of consumer acceptance, which help and prevent a variety of dermatological conditions. 

How to have optimal sun protection 

To have good sunscreen: 

Broad-spectrum sunscreen= UVA + UVB protection 

Water resistance = maintenance of SPF after 40 or 80 minutes in water. 

SPF ≥ 15 or 30 recommended. 

Re-apply1-2 hours during outdoor activates 

Other measures: 

Staying in the shade especially from 10 AM – 2 PM 

Wide brim hats 

Sunglasses 

Protective clothing 

Types of sunscreens: Chemical  Physical 
works like a sponge on the surface of your skin, absorbing the sun’s rays.  works like a shield on the surface of your skin, deflecting the sun’s rays. 
Optimal if you have sensitive skin  Easier to rub in the skin without leaving residue 
Example: zinc oxide, titanium dioxide  oxybenzone, avobenzone, and ecamsule 

 Concentrations as are utilized in SPF testing is: 2 mg/cm2 to achieve 2 mg/cm2 of density: 

1 teaspoon of sunscreen to the face/head/neck 

1 teaspoon to each upper extremity 

2 teaspoons to the front and back torso 

2 teaspoons to each lower extremity 

Benefits of sunscreen: 

Reduce the onset of Photoaging 

Photo immune Suppression 

Non-melanoma Skin cancer 

Photosensitivity Disorders 

 

Written by: Abdullah Nasser Al-Omair, Dermatology Resident

Reference: UpToDate

Psoriasis Awareness Month

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August is National Psoriasis Awareness Month, which gives us the opportunity to educate the public about it. The below article elicits some information about psoriasis definition, causes, presentation, and treatment.

 

Psoriasis is a dermatologic condition that makes the skin red, thick, and flaky. It is usually pink/salmon colored skin areas covered with silver or white scales. However, in darker skin tones, the psoriasis spots are purple, dark brown, or dark grey. It is mainly an adult disease, but it can develop in both children and adolescents. Both males and females are equally affected. It is not a contagious disease, because it is not an infection.

 

The exact cause behind psoriasis is yet to be identified. One of the important players in developing psoriasis is the immune system. The skin is made up of several layers; the top layer is the epidermis, and it has cells that divide rapidly and eventually die forming a layer of dead cells called the stratum corneum. In skin affected by psoriasis, immune cells enter the skin through blood vessels and cause the epidermis to grow very rapidly and to stop shedding properly.

 

The second player behind developing psoriasis is genetics. About 40% of people with psoriasis have family members with the disorder. Several genes have been identified to make people more susceptible to psoriasis. Some specific environmental and behavioral factors have been identified to be linked to psoriasis. Bacterial and viral infections, alcohol consumption, and some medications may affect the person’s risk of developing psoriasis or worsen the symptoms.

 

The symptoms of psoriasis include dry, red, or dark areas covered with white or silvery flakes. It can be on the scalp, elbows, genitals, or skin folds. It can be itchy or associated with skin pain. Joint swelling, pain, or stiffness. Nails can be affected too, and look pitted crumbly, or different in color. There are multiple types of psoriasis, however, the most common form is plaque psoriasis. It mainly affects young and middle-aged adults. Each skin plaque or spot is usually between 1-10 cm. It can appear on the scalp, elbows, knees, and back.  

 

The disease course is usually lifelong as it is currently not curable. However, the severity of the disease can improve or worsen over time, and it is controllable by treatment.

 

Patients with psoriasis are affected emotionally as well. As people with the condition might feel embarrassed of their skin. They might get depressed or anxious. Working with a psychologist is often helpful.

 

The diagnosis is usually made by examining the skin, only occasionally a skin biopsy or scraping is required. The treatment is mainly to control the symptoms. It varies based on the severity of the psoriasis. It includes various topical, oral, or injectable medications.

 

 

Written by: Ghada Alhayaza, PGY-1 Dermatology Resident

 

Resources:

Uptodate

Vitamin D in Acne

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  Vitamin D is a fat-soluble hormone found in the body that serves many purposes, most famously bone formation. Although vitamin D is most important for bone health, it also plays a key role in many of the body’s other functions including but not limited to; antimicrobial, antiproliferative, anti comedogenic, and antioxidative processes. Vitamin D is gained through diet, supplements, and exposure to sunlight. In regards to dermatologic diseases, and more specifically in the treatment of acne vulgaris, the antimicrobial properties of vitamin D have been an interesting area of research in recent years.

 

  It has been established that acne vulgaris patients were more likely to have deficient vitamin D levels than controls. Variable associations have been made between the severity of acne lesions and deficient vitamin D levels, although some studies have shown improvement in inflammatory acne lesions when patients were given vitamin D supplementation. This improvement is restricted to inflammatory lesions, while non-inflammatory lesions showed no improvement. This could be due to vitamin D’s antimicrobial properties, as inflammation caused by propionibacterium acnes is significant to the pathogenesis of acne vulgaris. Another association between vitamin D levels and acne vulgaris is linked to sebaceous gland activity, in which it was found that lower levels of vitamin D stimulate lipogenesis in sebaceous glands. The increased lipogenesis promotes inflammatory lesions in acne vulgaris.

 

 These findings open the door to the possibility of using topical vitamin D analogues in the treatment of acne, as well as screening acne vulgaris patients for Vitamin D deficiency. As of today, using vitamin D in the treatment of acne is grade B recommendation with IIb level of evidence.

 

 

 

 

Written by: Hadeel Awartani, Medical Student

 

 

Resources:

1-Amal Ahmed Mohamed, Eman Mohamed Salah Ahmed, Rasha T.A. Abdel-Aziz, Halaa H. Eldeeb Abdallah, Hadeel El-Hanafi, Ghada Hussein, Maggie M. Abbassi & Radwa El Borolossy (2020) The impact of active vitamin D administration on the clinical outcomes of acne vulgaris, Journal of Dermatological Treatment, DOI: 10.1080/09546634.2019.1708852

2-Navarro-Triviño FJ, Arias-Santiago S, Gilaberte-Calzada Y. Vitamin D and the Skin: A Review for Dermatologists [Internet]. Actas Dermo-Sifiliográficas (English Edition). Elsevier Doyma; 2019 [cited 2021Apr23]. Available from: https://www.sciencedirect.com/science/article/pii/S157821901930112X

3-Mostafa WZ, Hegazy RA. Vitamin D and the skin: Focus on a complex relationship: A review [Internet]. Journal of advanced research. Elsevier; 2015 [cited 2021Apr23]. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4642156/

4-Study links vitamin D deficiency with acne [Internet]. Dermatology Times. [cited 2021Apr23]. Available from: https://www.dermatologytimes.com/view/study-links-vitamin-d-deficiency-with-acne

5-Vitamin D for Acne: Benefits, Uses, & Effects of Vitamin D Deficiency [Internet]. Healthline. 2021 [cited 23 April 2021]. Available from: https://www.healthline.com/health/vitamin-d-for-acne

Occupational skin manifestations

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It is possible for some skin manifestations to arise due to an individual’s occupation, some of those occupations include hairdressers, food industry, health care, farmers, construction. Parts affected depend on exposure, mostly hands.

 

An individual’s likelihood of developing occupational skin manifestations includes an individual’s predisposition, hygiene, and exposure. These conditions arise due to exposure to chemicals such as rubber additives, hair dyes, cement, arsenic. Furthermore, biological exposure plays a role as well some of which include contact with an infected human, plants, and animals. In addition to the above, physical exposure may contribute which consist of mechanical trauma, heat, humidity, cold, and radiation. The most common conditions in these individuals are hand dermatitis, mechanical injury, and infections. Some precautions should be taken to prevent such skin manifestations by identifying, minimizing, and eliminating the causes. Moreover, monitoring the workers with relation to the exposure and appropriate treatment when indicated.

 

Occupational skin manifestations are common in wet working environments, for example, hairdressers, food industry, health care workers, and farmers. Steps should be taken to avoid such skin manifestations and injuries.

 

 

 

Written by: Khalid Al Dakheel, Medical Student 

 

Resources:

www.DermNetNZ.org