Short term efficacy of biological treatment for moderate-to-severe plaque psoriasis: a systematic review and network meta-analysis.

Psoriasis is a chronic inflammatory disease that is debilitating, particularly in its more severe forms. Multiple systemic therapies are used in moderate-to-severe psoriasis, but the development of biological interventions has revolutionized its management and improved its outcomes. To compare the effectiveness and safety of the different biological interventions approved for use in moderate-to-severe plaque psoriasis.

Idiopathic acquired true leukonychia: a unique entity.

Idiopathic acquired true leukonychia is a rare benign acquired disorder that typically affects adults. Diagnosis is made clinically, with investigations required to exclude any underlying cause. The cause of this condition is largely unknown, yet it understandably causes significant anxiety to patients due to concerns about underlying systemic disease.

Investigating the prevalence of body dysmorphic disorder among Jordanian adults with dermatologic and cosmetic concerns: a case-control study.

Body Dysmorphic Disorder (BDD) is an underexplored psychiatric condition in Middle Eastern countries, particularly in patients with dermatologic concerns, where alterations in appearance may elevate the risk of BDD. We studied patients at Jordan University Hospital's general dermatology and cosmetic clinics from July to September 2022, comparing them to healthy controls. Patients with dermatologic conditions were evaluated per the International Classification of Diseases (ICD-10) criteria by trained dermatologists.

Incidence Trends of Melanoma and Nonmelanoma Skin Cancers in Jordan From 2000 to 2016.

Purpose: Skin cancers are among the commonest cancers worldwide, and the incidence of melanoma and non-melanoma skin cancer (NMSC) continues to rise worldwide. However, there are no comprehensive reports on skin cancer incidence in Jordan during the past two decades. This report investigates the incidence of skin cancers in Jordan, in particular their time trends for the period 2000-2016.

Immunohistochemical Expression Patterns of CD45RO, p105/p50, JAK3, TOX, and IL-17 in Early-Stage Mycosis Fungoides.

The morphologic changes in early-stage mycosis fungoides (MF) might overlap with benign inflammatory dermatitis (BID). Previous studies have described altered expression patterns of several proteins in MF, but their diagnostic significance is uncertain. This study aims at examining the frequency of expression of CD45RO, NFkB-p105/p50, JAK3, TOX, and IL-17 proteins by immunohistochemistry.

Epidermolysis bullosa pruriginosa masquerading as psychogenic pruritus.

Background: Epidermolysis bullosa pruriginosa is a rare clinical subtype of dystrophic epidermolysis bullosa characterized by intense pruritus, secondary scratching-induced lesions, and pronounced scarring.

Observations: We describe a patient with epidermolysis bullosa pruriginosa who was misdiagnosed as having psychogenic pruritus for several years. Except for nail (toenail) dystrophy, no features of the disease were evident among his immediate family members.

Identical glycine substitution mutations in type VII collagen may underlie both dominant and recessive forms of dystrophic epidermolysis bullosa.

Autosomal dominant and recessive forms of dystrophic epidermolysis bullosa (DEB) result from mutations in the type VII collagen gene (COL7A1). Although paradigms have emerged for genotype/phenotype correlation in DEB, some pathogenic mutations in COL7A1, notably glycine substitutions within the type VII collagen triple helix, may lead to diagnostic difficulties, since certain glycine substitutions can result in either dominant or recessive mutant alleles. Delineation of glycine substitution mutations into two discrete groups, however, is made difficult by observations that, for some particular glycine substitutions in type VII collagen, the same mutation can result in both dominant and recessive disease.

The molecular skin pathology of familial primary localized cutaneous amyloidosis.

Familial primary localized cutaneous amyloidosis (FPLCA) is an autosomal dominant disorder associated with chronic itching and skin lichenification. In lesional skin, there are apoptotic basal keratinocytes and deposits of amyloid material on degenerate keratin filaments in the upper dermis. The genetic basis of FPLCA involves mutations in the OSMR and IL31RA genes but the disease pathophysiology is not fully understood.

Genitourinary tract involvement in epidermolysis bullosa.

Involvement of the genitourinary tract has been described in many different types of epidermolysis bullosa (EB). Pathology may be broadly divided into problems resulting in obstruction, that may in turn lead to hydroureter or hydronephrosis, or disease primarily affecting the renal parenchyma. Left unrecognized and untreated, renal tract disease may lead to chronic renal failure, and consequent problems associated with providing renal replacement therapy.

Loss-of-function FERMT1 mutations in kindler syndrome implicate a role for fermitin family homolog-1 in integrin activation.

Kindler syndrome is an autosomal recessive disorder characterized by skin atrophy and blistering. It results from loss-of-function mutations in the FERMT1 gene encoding the focal adhesion protein, fermitin family homolog-1. How and why deficiency of fermitin family homolog-1 results in skin atrophy and blistering are unclear.

New glycine substitution mutations in type VII collagen underlying epidermolysis bullosa pruriginosa but the phenotype is not explained by a common polymorphism in the matrix metalloproteinase-1 gene promoter.

Epidermolysis bullosa (EB) pruriginosa is an unusual variant of dystrophic EB in which intense itching can lead to striking skin changes resembling acquired skin disorders such as nodular prurigo or hypertrophic lichen planus. The molecular pathology involves mutations in the COL7A1 gene, but the nature of the mutations is similar to those seen in other non-pruritic forms of dystrophic EB. The mechanism of the dramatic phenotypic differences is currently unknown.