scholarly journals Hidradenitis Suppurativa: Where We Are and Where We Are Going

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2094
Author(s):  
Emanuele Scala ◽  
Sara Cacciapuoti ◽  
Natalie Garzorz-Stark ◽  
Matteo Megna ◽  
Claudio Marasca ◽  
...  
Keyword(s):  
Hidradenitis Suppurativa ◽  
Plasma Cells ◽  
Current Knowledge ◽  
The Body ◽  
Tissue Destruction ◽  
Primary Defect ◽  
Surgical Interventions ◽  
Th22 Cells ◽  
Valid Animal Model ◽  
Genetic And Environmental Factors

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease primarily affecting apocrine gland-rich areas of the body. It is a multifactorial disease in which genetic and environmental factors play a key role. The primary defect in HS pathophysiology involves follicular occlusion of the folliculopilosebaceous unit, followed by follicular rupture and immune responses. Innate pro-inflammatory cytokines (e.g., IL-1β, and TNF-α); mediators of activated T helper (Th)1 and Th17 cells (e.g., IFN-γ, and IL-17); and effector mechanisms of neutrophilic granulocytes, macrophages, and plasma cells are involved. On the other hand, HS lesions contain anti-inflammatory mediators (e.g., IL-10) and show limited activity of Th22 cells. The inflammatory vicious circle finally results in pain, purulence, tissue destruction, and scarring. HS pathogenesis is still enigmatic, and a valid animal model for HS is currently not available. All these aspects represent a challenge for the development of therapeutic approaches, which are urgently needed for this debilitating disease. Available treatments are limited, mostly off-label, and surgical interventions are often required to achieve remission. In this paper, we provide an overview of the current knowledge surrounding HS, including the diagnosis, pathogenesis, treatments, and existing translational studies.

scholarly journals Dynamic Leukocyte Populations Are Associated With Early- and Late-stage Lesions in Hidradenitis Suppurativa

2020 ◽  
pp. 002215542097853
Author(s):  
Savanna R. Altman ◽  
Sheila L. Criswell
Keyword(s):  
Late Stage ◽  
Hidradenitis Suppurativa ◽  
Inflammatory Cell ◽  
Plasma Cells ◽  
Early Stage ◽  
Skin Condition ◽  
The Body ◽  
Inflammatory Cell Infiltrate ◽  
Cell Counts ◽  
Cell Fractions

Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition typically targeting the axillary and anogenital regions of the body. The massive inflammatory cell infiltrate produced in this cryptogenic condition has led investigators in the attempt to link particular inflammatory cell fractions and cytokines to disease development, and ultimately to disease treatment. This study qualitatively and quantitatively analyzes the white blood cell fractions of macrophages, B-lymphocytes, T-lymphocytes, plasma cells, and granulocytes in 104 HS lesions on formalin-fixed paraffin-embedded tissues using immunohistochemistry (IHC). Four dermis-associated epithelial categories were investigated from persons with HS: 15 unaffected HS skin (US), 19 distended but unruptured follicle epithelium (UF), 62 migrating stratified squamous epithelium (MSSE) from ruptured follicles, and 35 degraded migrating epithelial sheets (DMES). In addition, 27 control skin (CS) from persons without HS were evaluated. Analysis of cell counts indicated that non-migratory dermal epithelium (CS, US, and UF) stimulated very little inflammatory response. However, contrary to previous studies which indicated macrophages to be the chief inflammatory cell in HS, this study showed that plasma cells were the primary cell type present in early-stage HS lesions (MSSE), whereas granulocytes were the major cell population seen in late-stage HS lesions (DMES):

scholarly journals Assessment of Risk Factors in the Causation & Outcomes of Diabetic Foot

2021 ◽  
pp. 264-270
Author(s):  
Chava Aravind Kumar ◽  
Chandrashekhar Mahakalkar ◽  
Meenakshi Yeola (Pate)
Keyword(s):  
Risk Factors ◽  
Diabetic Foot ◽  
The Body ◽  
Treatment Modalities ◽  
Foot Ulcers ◽  
Tissue Destruction ◽  
Metabolic Complications ◽  
Surgical Interventions ◽  
Peripheral Arterial Diseases ◽  
Peripheral Arterial

Background: Diabetic foot identifies   a Diabetic patient foot that has a potential risk of pathological risk effects that includes inflammation, ulceration and deep tissue destruction consistent with neurological   disorders, differing degrees of Peripheral arterial disease , and lower limb with  metabolic complications. An ulcer is a breach of the continuity of skin, epithelium of mucous membrane in the body which is caused by removal of necrotic tissue . Foot ulcers may be caused by numerous medical conditions. The key to treatment is daily sterile dressing till the formation of healthy granulation tissue, infection control by appropriate use of antibiotics, surgical interventions such as debridement or amputation if needed. Methods: It will be a observational study, done on the patients with Diabetic foot . It will be conducted at Dept. of General Surgery, J.N.M.C. and AVBRH, Sawangi (Meghe), Wardha of DMIMS (DU). The study will be conducted on patients of foot ulcers. Objectives: To evaluate the microbiological and clinical characteristics of diabetic foot infection To analyze the outcomes of a patient with diabetic foot with underlying risk factors HBA1c, Hypertension, Smoking, Diabetic Neuropathy, Recurrence, Obesity, Peripheral arterial diseases. To analyze the association of Risk factors in the causation of Diabetic foot. To predict outcome parameters based on Risk factors and its treatment modalities. Results: The results will be analyzed after data collection in SPSS software. Conclusion: Conclusion will be drawn on findings of study.

scholarly journals A teenage girl with extensive form of Hidradenitis suppurativa of sternal, submammary region and both axilla

1970 ◽  
Vol 1 (2) ◽  
pp. 30-37
Author(s):  
MA Kalam ◽  
SA Rahman ◽  
F Ahmad ◽  
SMQ Akhter
Keyword(s):  
Hidradenitis Suppurativa ◽  
Early Stage ◽  
Advancement Flap ◽  
The Body ◽  
Sweat Glands ◽  
Histopathological Study ◽  
Incision And Drainage ◽  
Surgical Interventions ◽  
Key Word

Hidradenitis suppurativa is a rare non-contagious, chronic, relapsing suppurativa cicatrizing skin disease that most commonly affects areas of the body bearing apocrine sweat glands or sebaceous glands, such as the underarms,  breasts, inner thighs, groin and buttocks, which manifests itself as a clusters of chronic abscesses, sinus, fistulas  or multilocalised infections. This physically, psychologically, and socially disabling disease is extremely painful  to touch and may persist for years with occasional to frequent periods of inflammation, culminating in drainage,  often leaving open wounds that will not heal. As it is considered as a rare disease the incidence rate is not well known, but estimated in a range between 1:24(4.1%) and 1:600(0.2%) in which the post-pubertal females are more affected than males. The exact cause of hidradenitis suppurativa remains unclear. What is understood is  that the condition is a disorder of follicular occlusion. With genetic predisposition, obesity, hormonal influences  etc contribute to the causation of the disease .There is no cure for hidradenitis suppurativa. But early treatment can help to manage the symptoms and to prevent new lesions from developing. Long term antibiotics are the treatment of choice in early stage, but relapsing and recurrent cases may need surgical interventions. Here we present an 18 year old girl suffering from this disabling disease in both axillas, sternal and submammary region for six years. She was treated inadequately with oral antibiotics and surgical intervention in the form of incision and drainage done previously. We treated her with wide excision of the diseased skin and defect reconstructed with  local advancement flap. Histopathological study of the excised skin revealed Hidradenitis suppurativa.   Key word : Epidermis/surgery; vitiligo/therapy; transplantation alutologous DOI: http://dx.doi.org/10.3329/bdjps.v1i2.8803 BDJPS 2010; 1(2): 30-37

Immunotherapy and potential predictive biomarkers in the treatment of neuroendocrine neoplasia

2020 ◽  
Author(s):  
Guanghui Xu ◽  
Yuhao Wang ◽  
Hushan Zhang ◽  
Xueke She ◽  
Jianjun Yang
Keyword(s):  
Current Knowledge ◽  
Checkpoint Inhibitors ◽  
Treatment Options ◽  
Predictive Biomarkers ◽  
The Body ◽  
Low Grade ◽  
Ablative Therapies ◽  
Cancer Types ◽  
New Treatment ◽  
Well Differentiated

Neuroendocrine neoplasias (NENs) are a heterogeneous group of rare tumors scattered throughout the body. Surgery, locoregional or ablative therapies as well as maintenance treatments are applied in well-differentiated, low-grade NENs, whereas cytotoxic chemotherapy is usually applied in high-grade neuroendocrine carcinomas. However, treatment options for patients with advanced or metastatic NENs are limited. Immunotherapy has provided new treatment approaches for many cancer types, including neuroendocrine tumors, but predictive biomarkers of immune checkpoint inhibitors (ICIs) in the treatment of NENs have not been fully reported. By reviewing the literature and international congress abstracts, we summarize the current knowledge of ICIs, potential predicative biomarkers in the treatment of NENs, implications and efficacy of ICIs as well as biomarkers for NENs of gastroenteropancreatic system, lung NENs and Merkel cell carcinoma in clinical practice.

scholarly journals Glucocorticoid Receptor β (GRβ): Beyond Its Dominant-Negative Function

2021 ◽  
Vol 22 (7) ◽  
pp. 3649
Author(s):  
Patricia Ramos-Ramírez ◽  
Omar Tliba
Keyword(s):  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Cell Communication ◽  
Cell Types ◽  
The Body ◽  
Dominant Negative ◽  
Negative Effects ◽  
Independent Manner ◽  
Distinct Cell ◽  
Induced Apoptosis

Glucocorticoids (GCs) act via the GC receptor (GR), a receptor ubiquitously expressed in the body where it drives a broad spectrum of responses within distinct cell types and tissues, which vary in strength and specificity. The variability of GR-mediated cell responses is further extended by the existence of GR isoforms, such as GRα and GRβ, generated through alternative splicing mechanisms. While GRα is the classic receptor responsible for GC actions, GRβ has been implicated in the impairment of GRα-mediated activities. Interestingly, in contrast to the popular belief that GRβ actions are restricted to its dominant-negative effects on GRα-mediated responses, GRβ has been shown to have intrinsic activities and “directly” regulates a plethora of genes related to inflammatory process, cell communication, migration, and malignancy, each in a GRα-independent manner. Furthermore, GRβ has been associated with increased cell migration, growth, and reduced sensitivity to GC-induced apoptosis. We will summarize the current knowledge of GRβ-mediated responses, with a focus on the GRα-independent/intrinsic effects of GRβ and the associated non-canonical signaling pathways. Where appropriate, potential links to airway inflammatory diseases will be highlighted.

scholarly journals Anti-PD-1-Induced Hidradenitis Suppurativa

2021 ◽  
Vol 8 (1) ◽  
pp. 37-39
Author(s):  
Alexia Maillard ◽  
Damien Pastor ◽  
Rastine Merat
Keyword(s):  
Adverse Events ◽  
Hidradenitis Suppurativa ◽  
Checkpoint Inhibitors ◽  
Latency Period ◽  
The Body ◽  
Skin Reactions ◽  
Zinc Gluconate ◽  
Severe Acne ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Mucocutaneous adverse events are commonly observed under immune checkpoint inhibitors (ICIs) therapy. Here, we report the case of a 43-year-old male patient with a stage IIIC melanoma disease who developed hidradenitis suppurativa (HS) three months after the beginning of an anti-PD-1 (nivolumab) adjuvant therapy. The patient had no comorbidities other than obesity and severe acne during adolescence. After an unsuccessful course of lymecycline while he was still treated with nivolumab, he gradually improved under zinc gluconate therapy and, more importantly, after nivolumab cessation. HS is a recurrent follicular inflammatory disease in the apocrine gland-bearing areas of the body often associated with obesity, metabolic syndrome, tobacco smoking, inflammatory bowel diseases, psoriasis, and arthritis. In our patient, the latency period between drug initiation and onset of HS symptoms and the improvement after immunotherapy discontinuation, argued strongly in favor of an anti-PD-1-induced HS. Anti-PD-1 therapies often trigger T cells-mediated adverse events that mimic Th17-mediated inflammatory and neutrophilic diseases. We suggest that HS, as other pustular skin reactions and ICIs-induced neutrophilic colitis, can be part of the anti-PD-1 mucocutaneous adverse event spectrum.

scholarly journals Vascular endothelial cell specification in health and disease

Angiogenesis ◽  
2021 ◽  
Author(s):  
Corina Marziano ◽  
Gael Genet ◽  
Karen K. Hirschi
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Current Knowledge ◽  
Vascular Malformations ◽  
Immune Surveillance ◽  
Vascular Endothelial Cell ◽  
Lymphatic Vessels ◽  
Lymphatic Endothelial Cell ◽  
The Body ◽  
Vascular Networks

AbstractThere are two vascular networks in mammals that coordinately function as the main supply and drainage systems of the body. The blood vasculature carries oxygen, nutrients, circulating cells, and soluble factors to and from every tissue. The lymphatic vasculature maintains interstitial fluid homeostasis, transports hematopoietic cells for immune surveillance, and absorbs fat from the gastrointestinal tract. These vascular systems consist of highly organized networks of specialized vessels including arteries, veins, capillaries, and lymphatic vessels that exhibit different structures and cellular composition enabling distinct functions. All vessels are composed of an inner layer of endothelial cells that are in direct contact with the circulating fluid; therefore, they are the first responders to circulating factors. However, endothelial cells are not homogenous; rather, they are a heterogenous population of specialized cells perfectly designed for the physiological demands of the vessel they constitute. This review provides an overview of the current knowledge of the specification of arterial, venous, capillary, and lymphatic endothelial cell identities during vascular development. We also discuss how the dysregulation of these processes can lead to vascular malformations, and therapeutic approaches that have been developed for their treatment.

scholarly journals Semen quality as a potential susceptibility indicator to SARS-CoV-2 insults in polluted areas

2021 ◽  
Author(s):  
Luigi Montano ◽  
Francesco Donato ◽  
Pietro Massimiliano Bianco ◽  
Gennaro Lettieri ◽  
Antonino Guglielmino ◽  
...  
Keyword(s):  
Semen Quality ◽  
Current Knowledge ◽  
Environmental Pollutants ◽  
Virus Transmission ◽  
Specific Area ◽  
The Body ◽  
Atmospheric Pollutants ◽  
Pollution Levels ◽  
Potential Indicator ◽  
Harmful Effects

AbstractThe epidemic of the new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has impacted worldwide with its infectious spread and mortality rate. Thousands of articles have been published to tackle this crisis and many of these have indicated that high air pollution levels may be a contributing factor to high outbreak rates of COVID-19. Atmospheric pollutants, indeed, producing oxidative stress, inflammation, immuno-unbalance, and systemic coagulation, may be a possible significant co-factor of further damage, rendering the body prone to infections by a variety of pathogens, including viruses. Spermatozoa are extremely responsive to prooxidative effects produced by environmental pollutants and may serve as a powerful alert that signals the extent that environmental pressure, in a specific area, is doing damage to humans. In order to improve our current knowledge on this topic, this review article summarizes the relevant current observations emphasizing the weight that environmental pollution has on the sensitivity of a given population to several diseases and how semen quality, may be a potential indicator of sensitivity for virus insults (including SARS-CoV-2) in high polluted areas, and help to predict the risk for harmful effects of the SARS-CoV-2 epidemic. In addition, this review focused on the potential routes of virus transmission that may represent a population health risk and also identified the areas of critical importance that require urgent research to assess and manage the COVID-19 outbreak.

scholarly journals Immunological Aspects of SARS-CoV-2 Infection and the Putative Beneficial Role of Vitamin-D

2021 ◽  
Vol 22 (10) ◽  
pp. 5251
Author(s):  
Ming-Yieh Peng ◽  
Wen-Chih Liu ◽  
Jing-Quan Zheng ◽  
Chien-Lin Lu ◽  
Yi-Chou Hou ◽  
...  
Keyword(s):  
Vitamin D ◽  
Innate Immunity ◽  
T Cells ◽  
Adaptive Immunity ◽  
Cd4 T Cells ◽  
Vitamin D Supplementation ◽  
The Body ◽  
Alveolar Type ◽  
Tissue Destruction ◽  
Health Crisis

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is still an ongoing global health crisis. Immediately after the inhalation of SARS-CoV-2 viral particles, alveolar type II epithelial cells harbor and initiate local innate immunity. These particles can infect circulating macrophages, which then present the coronavirus antigens to T cells. Subsequently, the activation and differentiation of various types of T cells, as well as uncontrollable cytokine release (also known as cytokine storms), result in tissue destruction and amplification of the immune response. Vitamin D enhances the innate immunity required for combating COVID-19 by activating toll-like receptor 2. It also enhances antimicrobial peptide synthesis, such as through the promotion of the expression and secretion of cathelicidin and β-defensin; promotes autophagy through autophagosome formation; and increases the synthesis of lysosomal degradation enzymes within macrophages. Regarding adaptive immunity, vitamin D enhances CD4+ T cells, suppresses T helper 17 cells, and promotes the production of virus-specific antibodies by activating T cell-dependent B cells. Moreover, vitamin D attenuates the release of pro-inflammatory cytokines by CD4+ T cells through nuclear factor κB signaling, thereby inhibiting the development of a cytokine storm. SARS-CoV-2 enters cells after its spike proteins are bound to angiotensin-converting enzyme 2 (ACE2) receptors. Vitamin D increases the bioavailability and expression of ACE2, which may be responsible for trapping and inactivating the virus. Activation of the renin–angiotensin–aldosterone system (RAS) is responsible for tissue destruction, inflammation, and organ failure related to SARS-CoV-2. Vitamin D inhibits renin expression and serves as a negative RAS regulator. In conclusion, vitamin D defends the body against SARS-CoV-2 through a novel complex mechanism that operates through interactions between the activation of both innate and adaptive immunity, ACE2 expression, and inhibition of the RAS system. Multiple observation studies have shown that serum concentrations of 25 hydroxyvitamin D are inversely correlated with the incidence or severity of COVID-19. The evidence gathered thus far, generally meets Hill’s causality criteria in a biological system, although experimental verification is not sufficient. We speculated that adequate vitamin D supplementation may be essential for mitigating the progression and severity of COVID-19. Future studies are warranted to determine the dosage and effectiveness of vitamin D supplementation among different populations of individuals with COVID-19.

scholarly journals Morphometric analysis of collagen and inflammatory cells in periodontal disease

2015 ◽  
Vol 72 (3) ◽  
pp. 219-224 ◽  
Author(s):  
Ranko Golijanin ◽  
Bojan Kujundzic ◽  
Zoran Milosavljevic ◽  
Dragan Milovanovic ◽  
Zlatibor Andjelkovic ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Morphometric Analysis ◽  
Plasma Cells ◽  
Relative Proportion ◽  
Inflammatory Cells ◽  
Test System ◽  
Clinical Staging ◽  
Gingival Tissue ◽  
Tissue Destruction ◽  
Immunochemical Method

Background/Aim. Periodontal disease affects gingival tissue and supporting apparatus of the teeth leading to its decay. The aim of this study was to highlight and precisely determine histological changes in the gum tissue. Methods. Gingival biopsy samples from 53 healthy and parodontopathy-affected patients were used. Clinical staging of the disease was performed. Tissue specimens were fixed and routinely processed. Sections, 5 ?m thin, were stained with hematoxylin and eosin, histochemical Van-Gieson for the collagen content, Spicer method for mast-cells and immunochemical method with anti-CD68 and anti-CD38 for the labelling of the macrophages and plasma-cells. Morphometric analysis was performed by a M42 test system. Results. While the disease advanced, collagen and fibroblast volume density decreased almost twice in the severe cases compared to the control ones, but a significant variation was observed within the investigated groups. The mast-cell number increased nearly two times, while the macrophage content was up to three times higher in severe parodontopathy than in healthy gingival tissue. However, the relative proportion of these cells stayed around 6% in all cases. Plasma-cells had the most prominent increase in the number (over 8 times) compared to the control, but again, a variation within investigated groups was very high. Conclusion. Gingival tissue destruction caused by inflammatory process leads to significant changes in collagen density and population of resident connective tissue cells. Although inflammatory cells dominated with the disease advancing, a high variation within the same investigated groups suggests fluctuation of the pathological process. <br><br><font color="red"><b> This article has been corrected. Link to the correction <u><a href="http://dx.doi.org/10.2298/VSP1704391E">10.2298/VSP1704391E</a><u></b></font>

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