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Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor,...
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Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features...
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Hypersensitivity Reactions: Cytolytic Reactions01:01

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Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
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Regulation of Hematopoietic Stem Cells01:01

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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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Graves' Disease I: Introduction01:28

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Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence...
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Isolating Human Peripheral Blood Mononuclear Cells and CD4+ T cells from Sézary Syndrome Patients for Transcriptomic Profiling
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Updates on histiocytic disorders.

Sarah R Vaiselbuh1, Yenan T Bryceson, Carl E Allen

  • 1Children's Cancer Center, Staten Island University Hospital, Staten Island, New York.

Pediatric Blood & Cancer
|March 11, 2014
PubMed
Summary
This summary is machine-generated.

Rare histiocytic disorders, including Langerhans cell histiocytosis (LCH) and hemophagocytic lymphohistiocytosis (HLH), are increasingly recognized. This review covers new insights into their pathogenesis, diagnosis, and treatment from a 2013 symposium.

Keywords:
Langerhans cell histiocytosisRosai Dorfman diseasehemophagocytic lymphohistiocytosistargeted therapies

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Area of Science:

  • Pediatric Hematology/Oncology
  • Rare Diseases
  • Immunology

Background:

  • Histiocytic disorders are rare but increasingly recognized clinical entities.
  • Advances in understanding molecular pathogenesis are driving novel diagnostic and therapeutic strategies.
  • A symposium at the American Society of Pediatric Hematology/Oncology (ASPHO) 2013 Annual Meeting focused on recent developments.

Purpose of the Study:

  • To review key insights presented at the ASPHO 2013 symposium on histiocytic disorders.
  • To highlight advancements in the understanding of Langerhans cell histiocytosis (LCH), hemophagocytic lymphohistiocytosis (HLH), and Rosai Dorfman disease (RDD).
  • To discuss novel approaches to pathogenesis, clinical diagnosis, and treatment for these conditions.

Main Methods:

  • Review of presentations from the ASPHO 2013 Annual Meeting symposium.
  • Synthesis of information on pathogenesis, clinical diagnostic criteria, and novel treatment insights.
  • Focus on LCH, HLH, and RDD, with exclusion of other histiocytic disorders and standard guidelines.

Main Results:

  • New insights into the molecular pathogenesis of LCH, HLH, and RDD were discussed.
  • Updated clinical diagnostic criteria for these histiocytic disorders were presented.
  • Novel therapeutic strategies and treatment advancements were highlighted.

Conclusions:

  • Understanding the molecular basis of histiocytic disorders is crucial for developing targeted therapies.
  • The symposium provided valuable updates on the diagnosis and management of LCH, HLH, and RDD.
  • Continued research and collaboration are essential for improving outcomes in rare histiocytic disorders.