A case of histiocytoid angiosarcoma mimicking Rosai-Dorfman disease histopathologically.

There are very few documented cases of histiocytoid angiosarcoma in the literature. We report a rare case of histiocytoid angiosarcoma demonstrating emperipolesis, a histopathologic finding that mimics Rosai-Dorfman disease (RDD). A 77-year-old male presented with a subcutaneous nodule on his left forehead.

The Use of Real-World Data to Evaluate the Association Between Atopic Dermatitis and Cardiovascular Disease: A Retrospective Claims Analysis.

Introduction: Atopic dermatitis (AD) is a systemic inflammatory condition that may increase the risk of cardiovascular disease (CVD); however, ongoing debate exists surrounding its direct association. We aimed to elucidate whether AD contributes to a higher incidence of CVD and major adverse cardiovascular events (MACE) in adult patients with AD, independent of metabolic disorders.

Methods: We retrospectively analyzed a large US-based population of patients with AD (≥ 18 years of age).

Clinical improvement of a patient with both amyopathic dermatomyositis and psoriasis following treatment with cyclosporine.

Clinically amyopathic dermatomyositis (CADM) is an uncommon subtype of dermatomyositis that rarely presents simultaneously with psoriasis. There are subsequently few reports discussing the management of concurrent CADM and psoriasis. Furthermore, skin lesions of CADM are often recalcitrant to first line dermatomyositis interventions.

A systematic review of active comparator controlled clinical trials in patients with moderate-to-severe psoriasis.

Purpose: Interleukin (IL)-17 and IL-23 inhibitors are the newest biologic agents used in the management of moderate-to-severe psoriasis. Active comparator studies allow for direct comparison of different biologic agents. We sought to systematically investigate the efficacy of newer biologic agents compared to earlier biologics.

Choosing First-Line Biologic Treatment for Moderate-to-Severe Psoriasis: What Does the Evidence Say?

An advanced understanding of the pathogenesis of psoriasis has led to the development of multiple therapeutic options for moderate-to-severe psoriasis. Tumor necrosis factor inhibitors, ustekinumab, interleukin-17 inhibitors, and guselkumab (an interleukin-23 inhibitor recently approved for psoriasis) are commercially available biologic agents for psoriasis. Evidence from clinical trials provides pertinent information regarding the safety and efficacy of biologic agents for psoriasis, which should be integrated into clinical decision making.

Drug survival of biologic treatments in psoriasis: a systematic review.

Drug survival measures the length of time until discontinuation of a drug. The length of time a patient remains on a biologic drug is impacted by several factors such as tolerability, side effects, safety profile and effectiveness. To evaluate the long-term drug survival, data of the most commonly prescribed biologic medications used in the treatment of psoriasis, a systematic review was conducted.

Review of IL-17 inhibitors for psoriasis.

The development of biologic agents directed against distinct cytokines and receptors has advanced the therapeutic options available for psoriasis patients. Evidence from preclinical studies suggests that IL-17 may contribute to the pathogenesis of psoriasis. The objective was to review the safety and efficacy profile for each IL-17 inhibitor by evaluating phase III clinical trial data.

Atopic dermatitis 2017: where we were 10-15 years ago in psoriasis.

Novel and innovative treatment options for atopic dermatitis (AD) are underway. The recent advancements in understanding AD are reminiscent of the progress made in psoriasis research over a decade ago.

Review of U.S. registries for psoriasis.

Background: Patient registries are databases comprised of standardized clinical data for a specific population of patients with a particular disease or medical condition. Information from patient registries allows clinicians to assess long-lasting outcomes in patients with a specific disease, such as psoriasis.

Objective: Our primary objective was to identify available psoriasis registries in the United States (U.

Intestinal microbiome analyses identify melanoma patients at risk for checkpoint-blockade-induced colitis.

The composition of the intestinal microbiota influences the development of inflammatory disorders. However, associating inflammatory diseases with specific microbial members of the microbiota is challenging, because clinically detectable inflammation and its treatment can alter the microbiota's composition. Immunologic checkpoint blockade with ipilimumab, a monoclonal antibody that blocks cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) signalling, is associated with new-onset, immune-mediated colitis.

Precision microbiome reconstitution restores bile acid mediated resistance to Clostridium difficile.

The gastrointestinal tracts of mammals are colonized by hundreds of microbial species that contribute to health, including colonization resistance against intestinal pathogens. Many antibiotics destroy intestinal microbial communities and increase susceptibility to intestinal pathogens. Among these, Clostridium difficile, a major cause of antibiotic-induced diarrhoea, greatly increases morbidity and mortality in hospitalized patients.

The effects of intestinal tract bacterial diversity on mortality following allogeneic hematopoietic stem cell transplantation.

Highly diverse bacterial populations inhabit the gastrointestinal tract and modulate host inflammation and promote immune tolerance. In allogeneic hematopoietic stem cell transplantation (allo-HSCT), the gastrointestinal mucosa is damaged, and colonizing bacteria are impacted, leading to an impaired intestinal microbiota with reduced diversity. We examined the impact of intestinal diversity on subsequent mortality outcomes following transplantation.

Early Clostridium difficile infection during allogeneic hematopoietic stem cell transplantation.

Clostridium difficile infection (CDI) is frequently diagnosed in recipients of allogeneic hematopoietic stem cell transplantation (allo-HSCT). We characterized early-transplant CDI and its associations, and analyzed serially-collected feces to determine intestinal carriage of toxigenic C. difficile.

Novel GNE mutations in autosomal recessive hereditary inclusion body myopathy patients.

Hereditary Inclusion Body Myopathy (HIBM, IBM2, MIM:600737) is an autosomal recessive adult onset progressive muscle wasting disorder. It is associated with the degeneration of distal and proximal muscles, while often sparing the quadriceps. The bifunctional enzyme UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE/MNK), encoded by the GNE gene, catalyzes the first two committed, rate-limiting steps in the biosynthesis of N-acetylneunaminic acid (sialic acid).

Intestinal microbiota containing Barnesiella species cures vancomycin-resistant Enterococcus faecium colonization.

Bacteria causing infections in hospitalized patients are increasingly antibiotic resistant. Classical infection control practices are only partially effective at preventing spread of antibiotic-resistant bacteria within hospitals. Because the density of intestinal colonization by the highly antibiotic-resistant bacterium vancomycin-resistant Enterococcus (VRE) can exceed 10(9) organisms per gram of feces, even optimally implemented hygiene protocols often fail.

Rapid evolution of HIV-1 to functional CD8⁺ T cell responses in humanized BLT mice.

The development of mouse/human chimeras through the engraftment of human immune cells and tissues into immunodeficient mice, including the recently described humanized BLT (bone marrow, liver, thymus) mouse model, holds great promise to facilitate the in vivo study of human immune responses. However, little data exist regarding the extent to which cellular immune responses in humanized mice accurately reflect those seen in humans. We infected humanized BLT mice with HIV-1 as a model pathogen and characterized HIV-1-specific immune responses and viral evolution during the acute phase of infection.

Serum neural cell adhesion molecule is hyposialylated in hereditary inclusion body myopathy.

Hereditary inclusion body myopathy (HIBM) is a young-adult onset autosomal recessive disorder caused by a hypomorphic rate limiting enzyme of sialic acid biosynthesis. The enzyme is UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase, and is encoded by the GNE gene. HIBM causes slowly progressive muscle weakness and atrophy.

Wolman disease (LIPA p.G87V) genotype frequency in people of Iranian-Jewish ancestry.

Wolman disease (WD) is a rare inherited condition caused by lysosomal acid lipase (LAL) deficiency first described in Iranian-Jewish (IJ) children. Newborns with WD are healthy and active, but soon the infant develops symptoms of severe malnutrition in the first few months of life, and often dies before the age of 1 year. Harmful amounts of lipids accumulate in the spleen, liver, bone marrow, intestine, adrenal glands, and lymph nodes.

Novel GNE mutations in hereditary inclusion body myopathy patients of non-Middle Eastern descent.

Autosomal recessive hereditary inclusion body myopathy (HIBM or IBM2) is a progressive adult onset muscle wasting disorder characterized by sparing of the quadriceps. IBM2 is also known as distal myopathy with rimmed vacuoles or nonaka myopathy. IBM2 is associated with mutations in the UDP-GlcNAc 2-Epimerase/ManNAc Kinase gene (GNE).