Emerging Therapies in Treating Psoriasis


Psoriasis is being treated with a variety of medicines that are currently being researched. These treatments are intended to treat psoriasis through a number of methods, including:


Therapies targeting the Th17 pathway – Interleukins (ILs) from the T helper type 17 (Th17) pathway (IL-23 and IL-17) play a key role in psoriasis pathogenesis and have become therapeutic targets:

Bimekizumab – Bimekizumab, a monoclonal IgG1 antibody that suppresses IL-17A and IL-17F, has been shown to be effective in phase III randomized studies. Adults with moderate to severe plaque psoriasis were randomly randomized to receive bimekizumab (320 mg every four weeks) or placebo in a 4:1 ratio in the BE READY study (n = 435). At week 16, 317 of 349 bimekizumab patients (91%) had a 90 percent improvement in the Psoriasis Area and Severity Index (PASI 90), compared to only 1 of 86 patients (1%) in the placebo group. Over the next 40 weeks, patients in the bimekizumab group who attained PASI 90 were randomly assigned (1:1:1) to receive bimekizumab 320 mg every four weeks, bimekizumab 320 mg every eight weeks, or placebo. Patients who received bimekizumab every four or eight weeks were more likely than those in the placebo group to reach PASI 90 at week 56. (87, 91, and 16 percent, respectively). Nasopharyngitis, oral candidiasis, and upper respiratory tract infections were the most prevalent treatment-emergent adverse events for bimekizumab.

Bimekizumab, ustekinumab, and placebo were tested in the BE VIVID study (n = 567) for effectiveness and safety. For 16 weeks, adults with moderate to severe plaque psoriasis were given bimekizumab (320 mg every four weeks), ustekinumab (weight-based dosage of 45 or 90 mg at weeks 0 and 4, then every 12 weeks), or placebo (every four weeks). Patients in the placebo group switched to bimekizumab at week 16, while those in the active treatment groups stayed on it until week 52. Patients in the bimekizumab (n = 321) group were more likely than those in the ustekinumab (n = 163) and placebo (n = 83) groups to attain PASI 90 at week 16. (PASI 90 achieved in 85, 50, and 5 percent of patients, respectively). Nasopharyngitis, oral candidiasis, and upper respiratory tract infection were the most prevalent treatment-emergent adverse events for bimekizumab, with candidiasis occurring more often in the bimekizumab group than in the ustekinumab group. Over the course of 52 weeks, five serious cardiac adverse events occurred in bimekizumab-treated individuals with pre-existing cardiovascular risk factors, but none happened in the ustekinumab-treated group.Oral candidiasis was more common than with other IL-17 pathway inhibitors, and one instance of inflammatory bowel illness was reported. Additional research might help to clarify the issue of safety.

Trials comparing bimekizumab to adalimumab or secukinumab show that bimekizumab is more effective. Adults with moderate to severe plaque psoriasis were randomly allocated to bimekizumab (320 mg every four weeks for 56 weeks), bimekizumab (320 mg every four weeks for 16 weeks and then every eight weeks until week 56), or adalimumab in a 56-week phase III study (BE SURE trial) (80 mg followed by 40 mg one week later and then 40 mg every two weeks until week 24).

Patients who received adalimumab were then given bimekizumab (320 mg every four weeks from week 24 to 56). At week 16, 275 of 319 patients (86%) who received bimekizumab had a PASI of 90, compared to 75 of 159 patients (47%) who received adalimumab (adjusted risk difference 28.2 percentage points, 95 percent CI 19.7-36.7). With both bimekizumab dose regimens, responses were sustained until week 56.

Adults with moderate to severe plaque psoriasis were randomly allocated to bimekizumab (320 mg every four weeks) or secukinumab in a 48-week phase III study (BE RADIANT trial) (300 mg weekly to week 4 and then once every four weeks). Bimekizumab patients were rerandomized at week 16 to receive bimekizumab once every four weeks or once every eight weeks. At week 16, 230 of 373 bimekizumab patients (62%) had complete eradication of skin disease on the Psoriasis Area and Severity Index (PASI 100), compared to 181 of 370 patients (49%) in the secukinumab group (adjusted risk difference 12.7 percentage points, 95 percent CI 5.8-19.6). Bimekizumab’s effectiveness remained better after 48 weeks (PASI 100 in 67 versus 46 percent of patients). The study’s power to identify differences between the two bimekizumab maintenance therapy groups was insufficient.


Tapinarof – Tapinarof is a topical aryl hydrocarbon receptor-modifying drug that may help with psoriasis by modulating Th17 cytokines including IL-17A and IL-17F, as well as normalizing the skin barrier and providing antioxidant action. A total of 1025 persons with chronic plaque psoriasis encompassing 3 to 20% of total body surface area were randomly allocated in a 2:1 ratio to either tapinarof 1 percent cream or vehicle used once daily in two similar phase III studies (PSOARING 1 and PSOARING 2). Patients in the tapinarof groups were more likely than patients in the placebo group to achieve the primary endpoint of a PGA score of 0 (clear) or 1 (almost clear) and a two-point decrease in the five-point PGA scale at week 12. (35.4 versus 6 percent [adjusted difference 29.4 percentage points; relative rate 5.8, 95 percent CI 2.9-11.5] in PSOARING 1 and 40.2 versus 6.3 percent [adjusted difference 33.9 percentage points; relative rate 6.1, 95 percent CI 3.3-11.4] in PSOARING 2). The tapinarof groups improved 75% more than the vehicle groups in terms of the Psoriasis Area and Severity Index (PASI 75) and PASI 90 rates. In the tapinarof groups, foliculitis, contact dermatitis, and headache were more common than in the other groups. In the tapinarof groups, folliculitis, contact dermatitis, and headache were more common than in the vehicle groups.


Small molecules – Other possible treatments include a variety of tiny compounds that aim to disrupt cellular signaling, which is crucial for the propagation of the inflammatory response. Small compounds that block Janus kinases (JAKs), lipids, a protein kinase C inhibitor, a selective tyrosine kinase 2 (TYK2) inhibitor, and crisaborole, a topical phosphodiesterase 4 inhibitor are some of the small molecules being researched for the treatment of psoriasis:


  • In randomized studies, oral tofacitinib, a small molecule JAK inhibitor licensed for the treatment of psoriatic arthritis, was beneficial for moderate to severe plaque psoriasis. Tofacitinib 10 mg twice daily was superior to placebo and noninferior to etanercept in a phase III trial that randomly assigned 1106 adults with moderate to severe plaque psoriasis to treatment with tofacitinib 10 mg twice daily, tofacitinib 5 mg twice daily, etanercept (50 mg twice weekly), or placebo.By week 12, 64, 40, 59, and 6% of patients receiving tofacitinib 10 mg twice daily, tofacitinib 5 mg twice daily, etanercept, and placebo, respectively, had met this objective. Other phase III studies found tofacitinib 10 mg twice daily and tofacitinib 5 mg twice daily to be helpful for chronic plaque psoriasis. The finest outcomes come from taking 10 mg twice a day. Tofacitinib has a quick beginning of action, with responses visible by week 4, and there is evidence of tofacitinib’s effectiveness for up to two years. In most cases, the treatment is well tolerated. Tofacitinib may make you more susceptible to infection. Cholesterol and creatine phosphokinase levels may also rise during treatment. A phase II randomized study also indicated that a topical formulation of tofacitinib was more efficacious than vehicle for plaque psoriasis.
  • In a phase II, dose-ranging, randomized study, baricitinib, another oral reversible inhibitor of JAK1/JAK2 tyrosine kinases, was examined for the treatment of moderate to severe psoriasis. 271 participants were randomly randomized to receive daily dosages of baricitinib 2, 4, 8, or 10 mg, or a placebo, in this trial. More patients in the baricitinib 8 and 10 mg groups attained PASI 75 at 12 weeks than those in the placebo group (43, 54, and 17 percent, respectively). Infections, lymphopenia, neutropenia, anemia, and an increase in creatine phosphokinase were more prevalent among patients receiving the highest baricitinib dosages.
  • Selective inhibition of TYK2, an intracellular signaling enzyme implicated in psoriasis pathogenesis, using the experimental drug BMS-986165 was related with clinical improvement in people with moderate to severe psoriasis in a phase II study (n = 268) [237]. Participants were allocated to one of five BMS-986165 dosage regimens or a placebo. More patients receiving 3 mg daily, 3 mg twice daily, 6 mg twice daily, or 12 mg daily of BMS-986165 attained PASI 75 after 12 weeks than patients receiving placebo (39, 69, 67, 75, and 7 percent, respectively). A three-milligram dosage given every other day did not outperform the placebo. In the active therapy groups, adverse events were more prevalent. Nasopharyngitis, headache, diarrhea, nausea, and upper respiratory infection were the most prevalent side effects. Mild to severe acne was more common in the active treatment groups, and one melanoma diagnosis was made in the 3 mg daily group.
  • Sphingosine 1-phosphate receptor 1 (S1PR1), a receptor involved in lymphocyte migration from secondary lymphoid tissues into the bloodstream, might be another viable treatment for psoriasis. Ponesimod, a selective S1PR1 modulator also being explored for the treatment of multiple sclerosis, causes S1PR1 internalization, preventing lymphocyte egress triggered by sphingosine 1-phosphate (S1P). Individuals treated with ponesimod were considerably more likely than patients treated with placebo to attain PASI 75 after 16 weeks in a phase II randomized study including 326 patients with moderate to severe chronic plaque psoriasis.
  • Treatment with a glucagon-like peptide 1 (GLP-1) analog (exenatide or liraglutide) seems to induce moderate improvement in psoriasis in people with both psoriasis and type 2 diabetes in small, uncontrolled studies. Liraglutide, on the other hand, was shown to be ineffective for plaque psoriasis in a placebo-controlled randomized study (n = 20).
  • Treatment with topical crisaborole, a phosphodiesterase 4 inhibitor, has been linked to improvements in facial psoriasis, intertriginous psoriasis, and palmoplantar psoriasis, all of which manifest as erythematous plaques, papules, and deep-seated pustules on the palms and soles, according to case reports.


Topical calcineurin inhibitor – Treatment with topical crisaborole, a phosphodiesterase 4 inhibitor, has been linked to improvements in facial psoriasis, intertriginous psoriasis, and palmoplantar psoriasis, all of which manifest as erythematous plaques, papules, and deep-seated pustules on the palms and soles, according to case reports.



written by: Lama Altamimi, medical intern




Airborne contact dermatitis


Airborne contact dermatitis refers to acute and chronic dermatitis of exposed parts of the body, especially the face, caused by particles suspended in the air. These particles may include fibers, dust, vapors, sprays, gasses, and plant materials.Airborne contact dermatitis can affect anyone; it is seen commonly in occupations associated with exposure to known allergens.

Clinical presentation

The distribution of airborne contact dermatitis is usually symmetrical. The exposed areas are most commonly affected, including the face, dorsal hands, neck, upper chest, and forearms.

Eyelid contact dermatitis is common and can be the only affected site.Occasionally, covered areas can also be affected due to the accumulation of airborne particles under the garments.Common symptoms of airborne contact dermatitis include itching, burning, and stinging.

Airborne contact dermatitis usually presents with diffuse scaly erythematous macules but plaques may also occur. Sometimes a pustular rash can occur as a result of secondary bacterial infection


The diagnosis of airborne contact dermatitis can be difficult. The diagnosis relies on taking a comprehensive clinical history, the timeline of the symptoms, consideration of occupational and non-occupational exposures, and finding the characteristic distribution and morphology of the rash on physical examination.Tests that can be considered are patch test & photopatch test.


There are many differential diagnoses to consider and airborne contact dermatitis should be distinguished from the following; Non-airborne irritant contact dermatitis and allergic contact dermatitis, Non-airborne photocontact dermatitis, Systemic contact dermatitis and Ectopic contact dermatitis.

Treatment & Management

The treatment for airborne contact dermatitis depends on the specific cause. After identifying the specific substance causing airborne contact dermatitis, every effort should be made to reduce the exposure to it. A change of job or residence is sometimes necessary to reduce exposure.

Other measures include Emollients and topical corticosteroids.For severe cases treatment can include Systemic steroids, Azathioprine, Mycophenolate, Methotrexate and Cyclosporine.

Airborne contact dermatitis can have a significant impact on patients’ quality of life. Complete recovery can often be achieved with avoidance of further exposure, but in severe cases such as Parthenium dermatitis, immunosuppression is often required . Some patients may progress to chronic actinic dermatitis

Written by: Khalid Nagshabandi, medical student




Open dermatology journal

Mycosis Fungoides

Mycosis Fungoides (MF) is a form of non-Hodgkin lymphoma that is considered the most common type of primary cutaneous T-cell lymphoma (CTCL).MF is a neoplasia of malignant monoclonal T lymphocytes that generally invades the skin and causes cutaneous signs and symptoms.It is characterized clinically during early stages as erythematous scaly patches and plaques, or during advanced stages as tumors or erythroderma, with lymph node and/or visceral involvement.And histologically presents as an epidermotropic infiltrate of small-medium sized CD4+ T lymphocytes with cerebriform nuclei. Mycosis Fungoides (MF) is the most prevalent cutaneous T-cell lymphoma, accounting for 50-65% of cases. Typically seen in men [1.6-2:1] ratio and appears in late adulthood with 55-60 years as a median age of diagnosis. Even so, MF is a rare and uncommon condition, the incidence of MF in the United States is approximately 0.3-1.02 new cases per 100.000/year. MF follows an indolent clinical course over years, with an estimated 5-year survival rate of 87% and a median survival of 11.4 years. Also patients who present with involvement of lymph nodes or viscera have a median survival of <1.5%.
MF natural history is a classical slow progression from patches to plaques to tumors stage typically on unexposed areas such as the trunk, buttocks and thighs. Due to MF manifesting a variety of clinical and pathological presentations, atypical presentations of MF may be difficult to diagnose. Within this broad spectrum of clinical presentations, the World Health Organization (WHO) classified MF into 3 main variants or subtypes; folliculotropic MF, pagetoid reticulosis, and granulomatous slack skin.

Patch stage:
● Poorly defined, irregular, finely scaling, red patches of variable size often with atrophic (thin, wrinkled) skin
● Occurs mainly on sun-protected sites particularly the lower trunk, thighs and, in women, the breasts
● Often asymptomatic
● Hypopigmented variant: pale, finely scaly patches without atrophy in children and Fitzpatrick skin types
● Poikiloderma atrophicans vasculare is atrophic patch stage MF presenting with skin thinning, pigment
changes, and dilation of capillaries (telangiectasia)
Plaque stage:
● Well-demarcated annular or arciform itchy thickened lesions
● Color often red, violaceous, or brown, sometimes scaly
Tumor stage:
● Large irregular lumps (>1 cm) developing from plaques
● Deep red to violaceous color, often shiny surface

The diagnosis of mycosis fungoides requires careful clinicopathological correlation. Dermoscopy can help to distinguish MF from inflammatory dermatosis.

Mycosis fungoides is treatable, not curable. There are no globally accepted treatment guidelines. Treatment should be guided by the patient’s wishes, stage of disease, availability of options, and local expertise.

Topical treatment:
● Topical steroids
● Topical chemotherapy eg, nitrogen mustard, carmustine
● Topical bexarotene
Procedural treatment:
● Phototherapy — PUVA, narrowband UVB
● Radiotherapy and whole-body total skin electron beam therapy
● Extracorporeal photopheresis
Systemic treatment:
● Chemotherapy — mycosis fungoides is relatively chemoresistant
● Immunotherapy — interferon-alpha
● Oral retinoids and rexinoids (eg, bexarotene)
Only brentuximab vedotin (for CD30+ MF) and allogeneic haematopoietic stem cell transplant alter the natural history of the disease.


Written by: Khalid Nagshabandi, medical student

Reference: DermNet

Poikiloderma of Civatte



Poikiloderma of civatte is a chronic benign skin condition. It is characterised by a triad of skin atrophy, hyper\hypopigmentation and telangiectasia. It is most commonly seen in middle aged fair-skinned people, especially postmenopausal ladies.


The main etiology behind this skin condition is unknown. However, there are some factors that contribute to its occurrence. Among these factors, sun exposure is thought to be the most significant. Other factors include: Hormonal changes (low estrogen levels), genetic predisposition and being repeatedly exposed to photosensitizing components of cosmetics and perfumes.

Clinical presentation:

Clinically, poikiloderma presents as a rash that affects mainly the sun-exposed areas, such as the neck and the lateral aspects of the cheeks, usually sparing the shaded area under the chin. It is characterised by confluent reddish-brown patches with atrophy of the involved area. Poikiloderma is mostly asymptomatic, but patients could present with mild burning, itching, or episodes of flushing.


Poikiloderma is a chronic, irreversible skin condition. It responds poorly to available treatments. Most importantly, the patient should be educated regarding the importance of avoiding sun exposure, and should be encouraged to apply sunscreen. They should also avoid all perfumes on or near the affected site, including scented soaps. Treatment options that could help improve the condition include: 

  • Hydroquinone
  • Hydrocortisone cream 
  • Topical retinoids can be of benefit if used for about a year.
  • Alpha hydroxy-acids may help reduce pigmentation.
  • Pulsed dye laser treatment and intense pulsed light (IPL) used to reduce the telangiectasia and pigmentation
  • Fractional nonablative laser treatment could improve the vascular, pigmented and textural components of poikiloderma of Civatte. 


Written by: Rema Aldihan, medical intern.




Clinical Presentation of Sézary Syndrome


Sézary syndrome (SS) is a leukemic type of cutaneous T cell lymphoma (CTCL) in which the peripheral blood contains a large number of circulating malignant (Sézary) cells. SS is assumed to be made up of mature epidermotropic skin homing CD4+ T cells or central memory T cells. The goal of this discussion is to go over the clinical characteristics of SS.


Skin lesions — SS patients typically have extensive erythema that is finely scaled, indurated, or resembles livedo reticularis. The severity of erythema and the amount of body surface area (BSA) involved may fluctuate, but at some point during the disease’s course, the skin involvement must cover >80% of the BSA to meet the SS definition from The International Society for Cutaneous Lymphoma (ISCL), European Organization for Research and Treatment of Cancer (EORTC), and United States Cutaneous Lymphoma Consortium (USCLC).

The following is an overview of the skin lesions:


  • Keratosis pilaris-like lesions –Follicular involvement may be characterized by inflamed follicular-based papules or scale.
  • Alopecia – Alopecia is common and manifests as a loss of hair density all over the scalp and body, or as patches of alopecia.
  • Ectropion – Because of the tautness and induration in the skin, an outward tilting of the lower eyelid with increased exposure of the ocular surface and sensitive mucous membranes of the inner lid might develop, which may be related with disruption of normal tear drainage pattern.
  • Keratoderma – Keratoderma, or thicker keratin retention on the palms and soles, is a typical feature that can help distinguish SS from other causes of erythroderma, but it can also make the diagnosis between SS and pityriasis rubra pilaris difficult.
  • Hypertrophic nails – Because of the involvement of the posterior nail fold, the nails may become hypertrophic.
  • Erosions and superinfection –Patients are frequently colonized with Staphylococcus aureus, and persistent scratching causes erosions and superinfection.
  • Focal areas of scaling – Tinea corporis is prevalent, and if scaly areas are present, a potassium hydroxide preparation should be conducted.
  • Lichenification – Long-term disease, chronic pruritus, and scratching can cause diffuse lichenification, which is defined as thickening skin with enlarged skin lines. Fissures are a regular occurrence.


Lymphadenopathy — Peripheral lymphadenopathy is common, and a biopsy usually reveals either dermatopathic changes or lymphoma-like alterations, both of which are linked to the underlying cutaneous lymphoma.


Viscera — The prevalence of visceral involvement in SS patients is unknown. Because bone marrow examination is not frequently conducted, unless in the case of unexplained hematologic abnormalities, the prevalence of bone marrow involvement is unknown.


Pruritus — The most common and debilitating symptom of SS sufferers is pruritus. The length and depth of erythema, as well as the degree of blood involvement, are not always connected to the degree of pruritus. Pruritus can make sleep problems, anxiety, and depression worse.



Written by: Lama Altamimi, medical intern.

Reference: UptToDate



Dermatofibroma, aka cutaneous fibrous histiocytoma, is a benign fibrous nodule composed of fibroblasts and histiocytes. It mainly occurs on the lower extremities. Dermatofibromas are mostly seen in females —although some histological variants are more common among males. Moreover, developing multiple dermatofibromas is usually associated with immunosuppression and autoimmune diseases.


It is unclear whether dermatofibroma arises as a result of a reactive process or a true neoplasm. There still isn’t a well-established cause for this condition. However, minor traumas, such as insect bites and injections are believed to trigger the development of these nodules. 

Clinical presentation:

Dermatofibroma characteristically presents as a firm papule/nodule. The size of the nodule varies, it ranges from 5 mm to about 1.5 cm in diameter. The nodule is usually tethered to the skin above it —the skin dimples when pinching the lesion— and mobile over subcutaneous tissue beneath it. The color of the nodule is usually pink or light brown in fair-skinned individuals, and dark brown or black in those with darker skin tones; some nodules may appear paler in the center. Furthermore, dermatofibromas are mainly asymptomatic, but could sometimes be painful, tender, or itchy. 


The diagnosis is made clinically, and is supported by dermoscopy. The most common finding on dermoscopy is a central white area surrounded by a faint pigmented network. A diagnostic skin biopsy is only required if there are atypical features; whether clinically or on dermoscopy. These features include a recent enlargement, ulceration, or asymmetrical structures and colors on dermoscopy. 


These lesions are benign and harmless, and therefore don’t require any intervention. However, it can be removed surgically if the patient is concerned. Patients should be informed that recurrence is common, as the lesion usually extend beyond the clinical margins. Other modalities, such as cryotherapy and laser rarely showed complete success.

Written by: Rema Aldihan, medical intern.




Ultraviolet radiation exposure causes deleterious effects on the skin, contributing to skin aging, cancer and photosensitivity. To prevent its impact, sunscreen application is imperative in protecting the skin against these harmful radiation. 


The sun emits three main UV radiation at different wavelengths:

  • Ultraviolet A (UVA) comprises 95% of the UV radiation. Its intensity is consistent throughout the day and from season to another. 
  • Ultraviolet B (UVB) makes up the remaining 5% UV radiation detected on the earth’s surface. The intensity of UVB is highest during summer and from 10 a.m to 4 p.m during the day. 
  • Ultraviolet C (UVC) is absorbed by earth’s atmosphere and is of little concern.  

Sunscreen works by absorbing or scattering UV radiation, primarily UVA and UVB, minimizing the effect on the skin. There are two categories of sunscreen agents with different mechanisms: Chemical (organic) and physical (inorganic). 


Chemical (organic) filters 

It acts by absorbing high energy light. They are further classified into UVA filters and UVB filters but companies use a combination of both filters to yield higher sun protection factor (SPF), stability and broad-spectrum absorption. In addition, organic filters have outstanding safety and aesthetic properties with minimal phototoxicity, photosensitivity and staining on skin. 


Physical (inorganic) filters

Inorganic filters reflect and scatter light. Most common agents are metal oxides titanium dioxide and zinc oxide, it’s chemically inert and protects against the full UV spectrum. However the inorganic leaves a whitecast that raises cosmetic concerns. 


There are other measures for protection that can be implemented alongside sunscreen application, like choosing long sleeves and trousers, wearing broad hats and adequately applying/reapplying sunscreen. 

The use of sunscreen is beneficial in mitigating the risks of skin cancer and disorders from UV radiation. Both chemical and physical sunscreens generally have an excellent safety profile, but chemical sunscreens are systemically absorbed. There are no harms, but further studies are required to confirm that.


Written by: Naif Alalshaikh, medical student.



“Topical Sunscreen Agents.” Sunscreens, Sunblocks | DermNet NZ, https://dermnetnz.org/topics/topical-sunscreen-agents. 

Gasparro, Francis P., et al. “A Review of Sunscreen Safety and Efficacy.” Photochemistry and Photobiology, vol. 68, no. 3, 1998, pp. 243–256., https://doi.org/10.1111/j.1751-1097.1998.tb09677.x. 


Ngoc, et al. “Recent Trends of Sunscreen Cosmetic: An Update Review.” Cosmetics, vol. 6, no. 4, 2019, p. 64., https://doi.org/10.3390/cosmetics6040064. 

Female Pattern Hair Loss

Female pattern hair loss (FPHL) is a type of nonscarring hair loss that affects mostly adult women. The disorder is marked by the loss of terminal hairs in the frontal and vertex regions of the scalp, resulting in an apparent loss of hair density. In contrast to many cases of androgenetic alopecia in males (male pattern hair loss), the loss of terminal hairs in afflicted areas is generally partial, and the frontal hairline is frequently preserved. This article will go through the pathophysiology, clinical symptoms, and diagnosis of FPHL.

The phrase “androgenetic alopecia” was once the most popular word used to describe the emergence of common, progressive hair loss on the frontal scalp and/or vertex of the scalp in both men and women. The terms “andro” and “genetic” denoted a hormonal etiology and a component of inheritance to the clinical presentation, respectively. As more research on hair loss was published throughout time, the phrase “female pattern hair loss” evolved to be the favored word for this kind of hair loss in women. This updated name reflects the absence of evidence to support a hormonal impact in all cases of the illness and helps to separate the distinct clinical aspects of this process in women vs males.

Hair loss across the frontal scalp and vertex of the scalp in FPHL is caused by a gradual decrease in the ratio of terminal hairs to shorter, thinner vellus hairs in the afflicted regions, a process known as follicular shrinkage. The duration of the anagen (growth) phase of hair follicles is reduced from a few years to weeks or months as a result of this process. Although hormonal variables and genetic predisposition are thought to have a role in FPHL, the mechanism by which these factors cause FPHL is unknown. The majority of women with FPHL do not have high amounts of androgens in their blood.

FPHL is a non-scarring type of hair loss that manifests as a gradual decrease in the density of terminal scalp hairs in a specific pattern. The principal areas of involvement are the frontal scalp and the vertex of the scalp. Although widespread involvement does occur from time to time, the occipital scalp is typically avoided.

The trend of hair loss differs from woman to woman. Frontal scalp thinning is the most apparent characteristic in some individuals, resulting in a “Christmas-tree” pattern when the hair is separated at the midline, but diffuse center thinning is the most prominent feature in others. Although women commonly have modest bitemporal thinning, the frontal hairline is typically preserved. It’s uncommon to observe a combination pattern that looks like male androgenetic alopecia (frontotemporal recession and vertex loss).

FPHL is not characterized by scarring, inflammation, or scaling. If these characteristics are present in a patient with hair loss, another scalp condition may be present alongside FPHL or may be the only cause of the clinical symptoms. FPHL is generally diagnosed clinically, depending on the patient’s medical history and physical examination. The presence of a reduction in hair density in the typical distribution, as well as an increasing incidence of miniaturized hairs, suggests the diagnosis. Biopsies of the skin are seldom done, although they might be useful when the diagnosis is unclear or a concurrent scalp condition is suspected. Several types of non scarring and scarring hair loss are included in the differential diagnosis of FPHL. Telogen effluvium, central centrifugal cicatricial alopecia, and traction alopecia are among of the more frequent illnesses having FPHL-like characteristics.


Written by:  Lama Altamimi, medical intern.







Monkeypox virus belongs to the orthopoxvirus genus. Orthopoxvirus is a genus of viruses in the family Poxviridae –the same family as cowpox and smallpox. Monkeypox is endemic in several African countries. Since 13 May 2022, several cases of monkeypox have been reported outside the endemic countries. Surprisingly, there hasn’t been any established travel links to endemic areas in those cases. Moreover, the current outbreak of monkeypox is evolving, as the number of cases is changing rapidly.


Monkeypox virus is transmitted from person to person through contact with body fluids or lesion material, contact with fomites, or exposure to respiratory secretions. Fortunately, monkeypox is not easily transmitted.


The diagnosis of monkeypox virus requires a 2-step process to be done on the specimen. First is the OPX DNA testing to confirm the presence of orthopox virus –CDC is currently treating all orthopox virus cases as monkeypox until proven otherwise. The second step is a PCR test (only available at CDC) which confirms monkeypox virus. 

Clinical features: 

Monkeypox initially begins as a flu-like illness with fever and lymphadenopathy –lymphadenopathy is a key clinical feature that helps differentiate monkeypox from smallpox. Then a centrifugal rash erupts; rash starts as macules>papules>vesicles>pustules>scabs. Lesions usually appears simultaneously and evolve together at any part of the body, eg. pustules on the face and vesicles on the arm. Lesions are well circumscribed, deep seated and are occasionally umbilicated. Lesions could be pruritic or painful. 


 All specimens reported outside of endemic countries, to date, are from the West African clade of monkeypox. This variant is associated with milder illness, therefore, supportive treatment is usually sufficient. Nevertheless, there are 2 CDC-approved therapies to be used in severe cases of monkeypox: tecovirimat and Vaccinia Immune Globulin Intravenous (VIGIV). 


Written by: Rema Aldihan, Medical student.





Basal Cell Carcinoma

Basal cell carcinoma is by far the most common cutaneous malignancy. Basal cell carcinoma is a tumor that grows slowly and rarely metastasizes.  BCC is more common among males living in geographic locations with greater UV exposure. Furthermore, previous history of SCC or BCC is the most common predictor of BCC development. 


It is believed that BCC originates from pluripotent cells in the basal layer of the epidermis or the pilosebaceous unit. This might explain the rare occurrence of BCC in the hand despite it being a frequently sun exposed area. As the dorsum of the hand lacks the presence of sebaceous structures. 

Moreover, it is well-established that the single most important risk factor for developing BCC is UV light exposure –particularly UVB light. Lighter skin phototypes, ionizing radiation exposure, immunosuppression, and genetic predisposition are all associated with increased risk of BCC. 

Clinical Features: 

BCC presents as a slowly growing skin colored/pink plaque or nodule, that could bleed or ulcerate spontaneously. Occasionally BCC could metastasise to lymph nodes. 

 BCC subtypes: 

1.Nodular BCC:

It presents as a pearly nodule with a smooth surface, rolled edges, and may have central depression, ulceration, and telangiectasia . Cystic variant is soft, with jelly-like consistency. 

2. Superficial BCC:

It presents as a scaly, irregular plaque with thin rolled edges. It may present with multiple micro-erosions.

3.Morphoeic BCC:

It presents as a waxy, scar-like plaque with irregular borders. It may present with deep extensions, sometimes infiltrating cutaneous nerves. 

4. Basosquamous carcinoma:

It is a mix between basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). it has an infiltrative growth pattern and could potentially be more aggressive than other subtypes of BCC

5. Pigmented BCC:

The rarest type of BCC, which comprises 6% of total BCC. This type can occasionally mimic melanoma. 

Diagnosis and Treatment: 

A histological diagnosis of BCC is a must, either through a biopsy or following excision. Furthermore, there are multiple treatment modalities used for BCC, which include both surgical and non-surgical therapies. Surgical treatment include: excision biopsy, mohs micrographically controlled excision, and superficial skin surgery.  Non-surgical modalities include: cryotherapy, Imiquimod cream, radiotherapy, photodynamic therapy and Fluorouracil cream.


Written by: Rema Aldihan, medical student. 


  1. https://www.ncbi.nlm.nih.gov/books/NBK482439/
  2. dermnet


What is melanoma?

Melanoma is a serious type of skin cancer that affects melanocytes, which are pigment-producing cells that give skin its color. Melanoma is more likely to spread and invade other organs in the body, making it more dangerous and malignant than other forms of skin cancers.

How does melanoma develop?

Transformation of melanocytes to melanoma requires a complex interaction of various factors. The cells undergo histological changes and ultimately progress to malignant melanoma. The first change that occurs is the development of benign nevi, comprising mainly of neval melanocytes, a variant of normal melanocytes but slightly larger. Nevi can remain dormant and static for decades but with certain endogenous and exogenous factors, like genetic mutations in CDKN2A and BRAF, it can progress to malignancy.

Who gets melanoma and what are the risk factors?

The strongest risk factors for melanoma are UV light exposure, family history of melanoma, previous melanoma and sun sensitivity. It affects mainly white population with fair skin, and the highest reported rate are in Australia and New Zealand. Melanoma occurs most commonly between the age of 40 to 60 years, however there has been an increase in incidence in young adults around the age of 20. The occurrence is extremely rare in children. 

What are the clinical features of melanoma?

Melanocytes are found throughout the body, thereby melanoma can be present anywhere on the body, not necessarily in areas with a lot of sun exposure. It begins as a mole or freckle, frequently on the back in males and lower extremities in females, but clinical presentation varies depending on the type.

Melanoma subtypes

There are four main types of melanoma that are associated with the same growth pattern, i.e horizontal, and anatomical site predilection.

Superficial spreading melanoma

Most common type, associated with intermittent UV exposure. It can appear on an existing mole or a new mole. It is likely found on the torso in men and legs of women.

Lentigo malinga

Occurs in chronically sun-exposed individuals and it is easily detected by simple visual inspection.

Nodular melanoma

This type is rapid growing and aggressive.

Acral and mucosal melanoma

Most common type of melanoma in Asian and African population. This type is not associated with UV radiation. 

Melanoma comes in many shapes, sizes and colors. Clinical diagnosis is primarily based on patient history total-body skin examination. Early detection and prevention are key in curing and preventing melanoma; applying sunscreen and UV radiation avoidance (staying indoor, avoiding tanning bed) may prevent the development of melanoma.

Written by: Naif Alalshaikh, Medical student. 


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Pachyonychia congenita

Pachyonychia congenita is a rare inherited disorder of keratinization that primarily affects the nails and skin. Affected people develop thickened skin on the soles and palms, white patches on the tongue and mouth, and bumps around the elbow and knees. 

What is the cause of pachyonychia congenita?

The disorder is caused by a genetic mutation but features vary depending on the affected gene. Five keratin specific genes are involved: K6a, K6b, K6c, K16, and K17. These genes provide instructions for the synthesis of keratin; a protein found in the skin, hair and nails. The frequent pathogenic variant is in K6a.


Pachyonychia congenita is inherited in an autosomal dominant manner. It is found in ethnic groups and occurence is equal in both sexes.

What are the clinical features of pachyonychia congenita?

Clinical features vary based on the involved keratin gene and specific genetic mutation but it is usually characterized by:

  • Calloused palms and soles with plantar pain in most of the patients. Sometimes underlying blisters are present 
  • Thickened nails often with brown discoloration. 
  • Certain types of sebaceous gland cysts, steatocystoma and pilosebaceous, are found in PC patients.
  • White patches affecting the tongue and inside of the mouth. 


Diagnosis is based on the presence of clinical signs and appearance. There is a clinical diagnostic criteria that includes the triad of the commonest features of toenail thickening, plantar keratoderma and plantar pain of pachyonychia congenita (PC) In addition, detection of a mutation in only one of the aforementioned genes confirms PC diagnosis. 

What is the treatment of pachyonychia congenita?

Limiting certain physical activity like walking, maintaining ideal body weight, and wearing ventilated shoes with moisture-wicking socks. Regular trimming of nails and calluses when necessary, and if needed, appropriate treatment of infections. Topical therapy to remove hyperkeratosis includes emollients and retinoids.

Pachyonychia congenita is an extremely rare disease that does affect the lifespan of the affected person, however it can negatively impact the quality of life. The pain and appearance of this condition can interfere with day-to-day activities and social life. 

Written by: Naif Alalshaikh, Medical student.


  1. “Pachyonychia Congenita.” Pachyonychia Congenita | DermNet NZ, https://dermnetnz.org/topics/pachyonychia-congenita
  2. “Pachyonychia Congenita.” Genetic and Rare Diseases Information Center, U.S. Department of Health and Human Services, https://rarediseases.info.nih.gov/diseases/10753/pachyonychia-congenita. 
  3.  PMC, Europe. Europe PMC, https://europepmc.org/article/nbk/nbk1280#free-full-text