In this rare disease, the immune system (the bodys defence system) works abnormally and destroys the protective covering over the nerves.It is indicated for replacement therapy in adults and children in primary immunodeficiency syndromes such as:

congenital agammaglobulinaemia and hypogammaglobulinaemia (low levels of antibodies);
common variable immunodeficiency;
severe combined immunodeficiency;
immunoglobulin-G-subclass deficiencies with recurrent infections;
replacement therapy in myeloma or chronic lymphocytic leukaemia with severe secondary hypogammaglobulinaemia and recurrent infections.Flebogamma DIF is indicated for the replacement therapy in adults, children and adolescents (0–18 years) in:

primary immunodeficiency syndromes with impaired antibody production;
hypogammaglobulinaemia (low levels of antibodies) and recurrent bacterial infections in patients with chronic lymphocytic leukaemia (a cancer of a type of white blood cell), in whom prophylactic antibiotics have failed;
hypogammaglobulinaemia (low levels of antibodies) and recurrent bacterial infections in plateau-phase-multiple-myeloma (another cancer of a type of white blood cell) patients who failed to respond to pneumococcal immunisation;
hypogammaglobulinaemia (low levels of antibodies) in patients after allogenic haematopoietic-stem-cell transplantation (HSCT) (when the patient receives stem cells from a matched donor to help restore the bone marrow);
congenital acquired immune deficiency syndrome (AIDS) with recurrent bacterial infections.and for the immunomodulation in adults, children and adolescents (0–18 years) in:

primary immune thrombocytopenia (ITP), in patients at high risk of bleeding or prior to surgery to correct the platelet count;
Guillain–Barré syndrome, which causes multiple inflammations of the nerves in the body;
Kawasaki disease, which causes multiple inflammation of several organs in the body.
Respiratory depression is a common side effect, but is subject to a ceiling effect, such that at a certain dose the degree of respiratory depression will no longer increase with dose increases. Likewise rarely it has been associated with agranulocytosis, erythema multiforme and toxic epidermal necrolysis. Tissue damage at injection sites
Severe injection site necrosis and sepsis has occurred (sometimes requiring amputation of limb) with multiple injection of pentazocine lactate. In addition, animal studies have demonstrated that Pentazocine is tolerated less well subcutaneously than intramuscularly. History
Pentazocine was developed by the Sterling Drug Company, Sterling-Winthrop Research Institute, of Rensselaer, New York. The analgesic compound was first made at Sterling in 1958. U.S. testing was conducted between 1961 and 1967.It was approved by the Food and Drug Administration in June 1967 after being favorably reviewed following testing on 12,000 patients in the United States. By mid 1967 Pentazocine was already being sold in Mexico, England, and Argentina, under different trade names. Society and culture
Legal status
Pentazocine was originally unclassified under the Controlled Substances Act. A petition was filed with the Drug Enforcement Administration on October 1, 1971, to shift it to Schedule III. The petition was filed by Joseph L. Fink III, a pharmacist and law student at Georgetown University Law Center as part of the course Lawyering in the Public Interest. That petition was accepted for review on November 10, 1971. D.E.A. published a Final Rule transferring it to schedule IV on January 10, 1979, with an effective date of February 9, 1979.