Selective immunoglobulin A deficiency (SIgAD) is a primary immunodeficiency disease and is the most common of the primary antibody deficiencies.[1] Total immunoglobulin A deficiency (IgAD) is defined as an undetectable serum immunoglobulin A (IgA) level at a value < 5 mg/dL (0.05 g/L) in humans. Partial IgAD refers to detectable but decreased IgA levels that are more than 2 standard deviations below normal age-adjusted means.[2, 3] IgAD is commonly associated with normal B lymphocytes in peripheral blood, normal CD4+ and CD8+ T cells, and, usually, normal neutrophil and lymphocyte counts. Anti-IgA autoantibodies of the IgG and/or IgE isotype may be present. Peripheral blood may also be affected by autoimmune cytopenias, eg, autoimmune thrombocytopenia,[4, 5] and patients may have other autoimmune phenomena. IgA was first identified by Graber and Williams in 1952; ten years later, the first patients with IgAD were described. IgAD is a heterogeneous disorder, and the results of intensive study are beginning to elucidate genetic loci and molecular pathogenesis that contribute to various subtypes of this disorder. Several lines of evidence suggest that, in many cases, IgAD and common variable immunodeficiency (CVID) have a common pathogenesis, which is discussed further in Pathophysiology. Other data indicate different genetic risk factors. Family studies show variable inheritance patterns. Familial inheritance of IgAD occurs in approximately 20% of cases,[6] and, within families, IgAD and CVID are associated.[7, 8] Many IgAD patients are asymptomatic (ie, "normal" blood donors) and are identified by finding a laboratory abnormality, without any apparent associated clinical disease. Some patients with IgAD may have the following associated conditions: (1) deficits in one or more immunoglobulin G (IgG) subclasses (this accounts for 20-30% of IgA-deficient patients, many of whom may have total IgG levels within the normal range) or (2) a deficient antibody response to pneumococcal immunization (specific polysaccharide antibody deficiency [SPAD]). Some patients with IgAD later develop CVID, and family members of patients with CVID may have only selective IgAD. Characterization of the receptor for the transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI), encoded by the gene TNFRSF13B ( tumor necrosis factor receptor superfamily member 13B), suggests that people with the C104, A181E, and ins204A variants may be at risk for IgAD that progresses to CVID.[9] Primary IgAD is permanent, and below-normal levels have been noted to remain static and persist after 20 years of observation.[10] A recent report documents a rare case of reversion.[11] Environmental factors such as drugs or infections can cause IgAD, but this form is reversible in more than half the cases (see Causes). Although individuals with IgAD have largely been considered healthy, recent studies indicate a higher rate of symptoms. A 20-year follow-up study that compared 204 healthy blood donors with incidentally identified IgAD to 237 healthy subjects with normal IgA levels demonstrated that 80% of IgAD donors and 50% of control subjects had episodes of infections, drug allergy, or autoimmune or atopic disease. Severe respiratory tract infections occurred in 26% of IgAD subjects, in 24% of subjects with decreased IgA levels, and in 8% of control subjects; however, the incidence of life-threatening infections was not increased. IgAD is more common in adult patients with chronic lung disease than in healthy age-matched control subjects.[12] Patients with IgAD are at some increased risk of developing severe reactions after receiving blood products.[13, 14, 15] IgG anti-IgA antibodies may cause severe transfusion reactions if patients with IgAD are given whole blood; therefore, IgA-poor blood or washed red cells are preferred for those patients. IgA-deficient patients with immunoglobulin E (IgE)–class anti-IgA antibodies are at risk for anaphylaxis if they receive blood or intravenous immunoglobulin, but this situation is extremely rare. Individuals with such an unusual profile should receive only low IgA intravenous immunoglobulin preparations. However, caution must be used when administering IGIV to patients with IgAD if their anti-IgA status is unknown. A history devoid of previous blood product administration does not exclude the possibility of anti-IgA antibodies or adverse reactions. Fortunately, appropriate precautions can significantly reduce morbidity (see Treatment). Blood banks can use a simple ELISA screening approach to establish an IgAD blood donor poo

Orchidectomy and Orchidopexy in Testicular Torsion

Anatomy of Love

NURSING VIDEO ACTUAL CATHETERIZATION PROCEDURE OF MALE. FULL LENGTH VERSION Clear quality photography. This video provides an excellant clinical view of the entire procedure.

Visualization of the larynx by direct or indirect means is referred to as laryngoscopy and is the principal aim during airway management for passage of a tracheal tube. This paper presents a brief background regarding the development and practice of laryngoscopy and examines the equipment and techniques for both direct and indirect methods. Patient evaluation during the airway examination is discussed, as are predictors for difficult intubation. Laryngoscope blade design, newer intubating techniques, and a variety of indirect laryngoscopic technologies are reviewed, as is the learning curve for these techniques and devices.

Paronychia Fingernail Abscess Infection Treatment

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An animation of blood flow inside the Hemodialysis circuit.

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Dr. Ahmad Oussama Rifai is certified by the American Board of Internal Medicine (ABIM) in the specialty of Internal Medicine and the sub-specialty of Nephrology.

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Insertion of a Palindrome TDC in the right internal jugular vein under ultrasound and fluoroscopic guidance at a restructured hospital in Singapore

The Valsalva Maneuver is any attempt to exhale with the mouth and nose closed. Named after the Italian physician and anatomist, Antonio Maria Valsalva (1666-1723), it is also known as Valsalva's Test and Valsalva's Method.

Watch that Female to Male Gender Changing Surgery

Demonstration of vertical mattress suturing technique for laceration repair or wound closure in the operating room.

Plantar warts are hard, grainy growths that usually appear on the heels or balls of your feet, areas that feel the most pressure. This pressure also may cause plantar warts to grow inward beneath a hard, thick layer of skin (callus). Plantar warts are caused by the human papillomavirus (HPV). The virus enters your body through tiny cuts, breaks or other weak spots on the bottom of your feet. Most plantar warts aren't a serious health concern and may not require treatment. But plantar warts can cause discomfort or pain. If self-care treatments for plantar warts don't work, you may want to see your doctor to have them removed.

This is an educational medical video for Medical Students showing how to examine a hernia swelling

Watch that Cutting Inside Human Fat Body video

Watch that Human Baby Medical Abortion Surgery

Watch that video to know the Types of Female Genital discharge

Doctor makes magic - Doctor hace magia (Sorprendente) - Doctor Magic