Clinical Pathology : Systemic Lupus Erythematosus

Hypo-vitaminosis D in Patients with Rheumatoid Arthritis, Systemic Lupus Erythematosus and Ankylosing Spondylitis Mohamed Ismail Abdel Kareem1, Reem Hamdy A Mohammed2*, Hanan Sayed M Abozaid3, Mohamed Moneer Rayanv4, Abeer Mohamed Mohamed5 and Nihal Ahmad Fathi6 1Rheumatology and Rehabiltation, Al-Azhar Faculty of Medicine Assuit Egypt 2Rheumatology and Rehabilitation, Kasr Alaini School of Medicine Cairo University Hospital, Cairo Egypt 3Rheumatology and Rehabilitation, Faculty of Medicine

Pathogenesis, prevalence, and affected individuals. In general, the term “lupus” is used to describe a multi-systemic inflammation that results from an abnormal immunological function. It includes four main types: neonatal and pediatric lupus erythematosus (NLE); discoid lupus erythematosus (DLE); drug-induced lupus (DIL); and systemic lupus erythematosus (SLE). The latter is the most common type, and it is referred to simply as “lupus”. SLE is a complex rheumatic disease of an autoimmune origin, with an

are threatening to the mankind. Systemic lupus erythematosus (SLE) is a classic example of such a disease. SLE is a chronic, often life-long, autoimmune condition, ranging from mild to severe in severity. SLE may affect many organs in the body, including but not limited to kidneys, skin, joints, respiratory and nervous systems. The name of this disease describes it; word systemic indicates the widespread involvement of various tissues and organs of the body. Lupus is a word derived from Latin language

diverse proteins that constitute the FAS/FASL apoptotic pathway. This brief synopsis will focus on the ALPS attributed mutation of the FAS gene, classified as ALPS 1A, which constitutes 75% proportion of ALPS cases (Bleesing et al. 2005). Pathology ALPS is

Gene therapy was first proposed as a method of manipulating cells at the molecular level through the transfer of defined genetic material into a genome for the ultimate purpose of preventing or altering rare genetic disease states. Viruses have the natural ability to deliver genetic material to cells, which makes them excellent vectors for gene delivery (Waehler, Russell, & Curiel, 2007). Lentivirus, Herpes Simplex Virus, Adenovirus and Adeno-Associated viruses (AAV) are among the most prominently

(5)tension pneumothorax and (6)pericardial tamponade (Butler and Swencki, 2006). I-Pathology of Pulmonary embolism (PE): As the third most common reason of cardiovascular death after myocardial ischemia and stroke, pulmonary embolism (PE) is a conceivably fatal condition connected with significant morbidity and mortality (Araoz et al., 2007). PE and DVT are two clinical presentations of venous thrombo-embolism and offer the same predisposing factors. In many cases

Congenital heart disease’s incidence depends on how the population is studied. With better diagnosis through the introduction of echocardiography the incidence figures of congenital heart diseases has raised from the range of 5-8 per 1000 live births to 8-12 per 1000 live births (Hoffman JIE, 2013). All the countries have similar incidence of congenital heart disease. Some minor differences in types of congenital heart disease by country are there. China and Japan for example have a higher

ABSTRACT There is now compelling evidence from animal models autoimmune hemolytic anemia (AIHA) that naturally occurring regulatory T cells (n-Tregs) play an important role in immunologic tolerance and control of immune-mediated pathology. However their study in human AIHA is still ill defined. Aim: To measure the peripheral blood proportions of n-Treg cells and the levels of IL10 and IL12 in basal and mitogen-induced (Lipopolysaccharide, LPS) cultures of PBMCs in patients with idiopathic warm

diagnosis techniques, pharmacological management, physical therapeutics and surgical treatment interventions. I shall explore the expected prognosis and the key developments we can expect in the future. Aetiology and Prevalence RA is a chronic, systemic and inflammatory disease that progressively impacts peripheral joints (Panayi 2011).The damage that occurs is predominantly symmetrical and polyarthropathic (Rindfleisch & Muller 2005). It affects the host’s joint synovial membranes, tendon sheaths

TERMINOLOGY CLINICAL CLARIFICATION • Heart failure is a clinical syndrome characterized by structural or functional impairment of ventricular filling or ejection of blood resulting in insufficient perfusion to meet metabolic demands; most commonly results from impaired left ventricular myocardial function; cardinal manifestations include edema, dyspnea, and Fatigue4•5 CLASSIFICATION • Classification by American College of Cardiology Foundation/American Heart Association {based on structure and progression