As IgM and IgA-enriched preparations are needed to complete the immunotherapeutic spectrum, a simple procedure is described for the preparation of IgM and IgA enriched IMMUNOGLOBULINs. Fraction ill which was prepared by cold ethanol fractionation was treated by octanoic acid followed by ethanol precipitation and ion-exchange chromatography using Sephadex DEAE A-50 and 0.1 M tris-0.35M NaCl buffer, pH 8.1, resulting in recovery of 85% IgM, 84% IgA and 33% IgG. The comparison of our results with IMMUNOGLOBULINs" percentage in plasma indicates that IgM and IgA-enrichment was obtained by three times.

Myocarditis is an inflammatory disease of the myocardium with lymphocyte infiltration and myocyte necrosis leading to a wide range of clinical presentations including heart failure, arrhythmia, and cardiogenic shock. Infectious and noninfectious agents may trigger the disease. The fact that immunosuppressive drugs are useful in several kinds of autoimmune myocarditis is proof of the autoimmune mechanisms involved in the development of myocarditis. Pathogenic mechanisms in myocardial inflammation are including inflammasome activation followed by myocyte destruction, myocarditis, and pericarditis. Intravenous IMMUNOGLOBULIN (IVIG) is a serum product made up of IMMUNOGLOBULINs, widely used in a variety of diseases. This product is effective in several immune-mediated pathologies. As well as the determined usage of IVIG in Kawasaki disease, IVIG may be useful in several kinds of heart failure including fulminant myocarditis, acute inflammatory cardiomyopathy, Giant Cell Myocarditis, and peripartum cardiomyopathy. Generally, IVIG is used in two different doses of low dose (200 to 400 mg/kg) and high dose (2 g/kg) regimen. The exact therapeutic effects of IVIG are not clear, however over the last decades, our knowledge about its mechanism of function has greatly enhanced. IVIG administration should be based on the accepted protocols of its transfusion. In this review article, we try to provide an overview of the different kinds of myocarditis, pathologic mechanisms and their common treatments and evaluation of the administration of IVIG in these diseases. Furthermore, we will review current protocols using IVIG in each disease individually.

Human plasma proteins are important for therapy or prophylaxis of human diseases. Due to the preparation of human plasma proteins from human plasma pools and risk of contamination with human viruses, different viral reduction treatments such as: pasteurization, solvent/detergent, dry heat treatment, steam treatment, beta-propiolactone/UV and nanofiltration have been implemented. As pasteurization can be performed for liquid protein, this method (a 10-hour heat treatment of the aqueous solutions at 60°C) was introduced into the manufacturing procedure of IgM-enriched IMMUNOGLOBULIN, to improve its safety further. The efficiency of this method for inactivation of viruses was evaluated by the use of Foot-and-Mouth Disease Virus (a non-enveloped virus) and Infectious Bovine Rhinotracheitis (IBR) Virus (a lipid-enveloped virus). Pasteurization inactivated Foot-and-Mouth Disease Virus by 7 log10 and for IBR Virus by 5log10. These findings show a significant added measure of virus safety associated with pasteurization of IgM-enriched IMMUNOGLOBULIN preparation.

Kawasaki disease is a systemic vasculitis that mainly affects younger children. Although the definite cause still remains unknown but the clinical and epidemiologic findings discuss an infectious cause. The prevalence of incomplete Kawasaki disease reported 15 to 36.2%, and it is more frequent in the extremes of the age spectrum. Non delayed treatment of disease should be initiated because of critical cardiac vascular complications. Up to 15%-25% of patients with Kawasaki disease who remain febrile after administration of first dose of intravenous immunoglobin plus aspirin are classified as refractory disease. These intravenous immunoglobin resistant cases are at increasing risk for coronary artery complications. The strategy on prediction of potentially non responder and treatment of intravenous immunoglobin resistant patients is now controversial but some useful points were recommended.

Intravenous IMMUNOGLOBULIN (IVIG) is a safe biological product used in many cases, such as primary and secondary immune deficiency, infectious diseases, critically ill patients and autoimmune disorders. IVIG has many advantages compared with intramuscular IMMUNOGLOBULIN and is obtained from pooled plasma of 10.000-60.000 donors. Today, IVIG use in clinical settings has increased. Despite its use in many diseases, FDA only has approved its use in patients suffering from ITP, primary immunodeficiency, pediatric HIV, Kawasaki disease, bone marrow transplantation and B-cells chronic lymphocytic leukemia. But, it has been used for other cases like Guillain–Barré syndrome, premature infants, critically ill patients admitted to ICU, severe asthma and uncontrolled seizures which FDA had not approved yet.This biological product affects immune deficiency and autoimmune diseases in different ways. Despite the relative safety of this product, the patient may experience mild but acute complications.In most cases acute reaction is due to high speed infusion rate which is mild but systemic side effects in the form of allergic and non-allergic anaphylaxis are seen, especially in patients with CVID and IgA selective deficiency. The patient should be under medical supervision during infusion and to deal with anaphylaxis shock, facilities should be available.Today, the subcutaneous type of IMMUNOGLOBULIN is used at home under supervision of a nurse and the patient satisfaction is high, because of its lower cost and also it does not need hospital admission.

Hereditary spherocytosis is a familial hemolytic anemia. IMMUNOGLOBULIN A (IgA) nephropathy associated with hereditary spherocytosis has not been reported in children. Here, we report a case of a 17-year-old boy with IgA nephropathy and hereditary spherocytosis. The patient was diagnosed with hereditary spherocytosis at the age of 12 years and splenectomy was done at the age of 15 years. Later, the patient presented with macroscopic hematuria and proteinuria. Kidney biopsy of the boy was consistent with IgA nephropathy. Treatment with angiotensin-converting enzyme inhibitor was started. The patient became free of proteinuria after the 6th month of therapy.