China
Africa
Explore chapters and articles related to this topic
Biosimilars in the EU
Published in Laszlo Endrenyi, Paul Jules Declerck, Shein-Chung Chow, Biosimilar Drug Product Development, 2017
Advances in molecular biology and genetic engineering allowed a large and reliable source of these medicines from microbial cell cultures (bacteria, yeast) or mammalian cell lines. Modified versions of these proteins (e.g., pegylated interferon, B-domain deleted factor VIII, insulin glargine) or fusion proteins (e.g., etanercept, abatacept) also became available. Recombinant enzymes and certain monoclonal antibodies are currently the standard of care for many diseases and have also allowed the treatment of rare disorders (e.g., alglucosidase alfa, human C1-inhibitor, eculizumab). Biotechnology drugs have a clearly established efficacy and safety profile as they are the treatment option for many chronic conditions and no transmission of infectious disease has ever been reported even when materials from biological origin are used in their production. More biotechnology-derived medicines are becoming available, and monoclonal antibodies are used in many different therapeutic areas, some providing an entirely novel approach to the treatment of their respective indications (e.g., rheumatoid arthritis, oncology, macular degeneration, or lupus), including rare orphan diseases (e.g., eculizumab for paroxysmal nocturnal hemoglobinuria).
Hieh-Dose Immunosuppressive Chemotherapy with Autologous Stem Cell Support for Chronic Autoimmune Thrombocytopenia
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Richard D. Huhn, Patrick F. Fogarty, Ryotaro Nakamura, Cynthia E. Dunbar
Recently developed molecular techniques using polymorphisms in the beta-variable region of the T cell receptor DNA could be used to study T cell repertoires in patients with AITP. Limited TCR diversity has been demonstrated in patients with various diseases involving autoimmunity (e.g., rheumatoid arthritis, renal allograft rejection, graft-vs.-host disease and alloimmune thrombocytopenia) and immune dysregulation (e.g., paroxysmal nocturnal hemoglobinuria and aplastic anemia).53-60 The T cell repertoire tended to normalize in aplastic anemia patients who achieved unmaintained remission after immunosuppressive treatment with cyclosporine, suggesting that the establishment and propogation of T cell clones contribute to the pathogenesis of that disease.60
List of Chemical Substances
Published in T.S.S. Dikshith, and Safety, 2016
Arsine is a highly toxic gas. It primarily targets the erythrocyte (red blood cell) and rapidly induces intravascular hemolysis. Secondary effects resulting from hemolysis include hemolytic anemia, hepatic and renal damage. The exact mechanism by which arsenic causes erythrocytes to rupture is unknown, but it is believed to be due to either oxidative damage or a reaction with sulfydryl. As stated, arsine is a potent hemolytic agent and causes acute intravascular hemolysis, rapid red blood cell destruction, and renal failure. Arsine is highly soluble in body fat and hence, can easily cross the alveolo-capillary membrane and into the red blood cell. Arsine causes chemical burns. Exposures to arsine cause headaches, malaise, weakness, dizziness, dyspnea; abdomen and back pain; nausea, vomiting, diarrhea, bronze skin; hematuria (hemoglobin in urine), jaundice, liver enlargement, fever, anxiety, disorientation, delirium, shivering, muscular cramps, tachypnea, tachycardia, anemia, hyperkalemia, electro-cardiographic changes, burning sensations, peripheral neuropathy (focal anesthesia and paresthesia), agitation, disori-entation, and hallucinations. The exposed individual and/or the occupational worker soon develops a sensation of cold and paresis in the limbs, hemoglobinuria, a garlic-like odor to the breath, multi-organ failure, and massive hemolysis and kidney failure. Toxic pulmonary edema or acute circulatory failure has been reported as the cause of death in some cases of arsine poisoning. Studies have indicated that occupational exposures to arsine cause increased rates of miscarriage among women associated with the semiconductor industry.
Hemolysis during short-term mechanical circulatory support: from pathophysiology to diagnosis and treatment
Published in Expert Review of Medical Devices, 2022
Tim Balthazar, Johan Bennett, Tom Adriaenssens
Hemoglobinuria occurs only in the setting of severe and rapid intravascular hemolysis. It occurs when the binding capacity of haptoglobin for free plasma hemoglobin is exceeded. Serum haptoglobin plays an important role as a circulating buffer protecting the kidney when free hemoglobin level starts to increase. The molecular size of the haptoglobin-hemoglobin complex is too large to be filtered by the kidney [21]. Dimers of alpha-beta globin that are not bound by haptoglobin are small enough to be filtered by the glomerulus. When the capacity of the proximal renal tubule to reabsorb the hemoglobin from the lumen is exceeded, the hemoglobin is freely excreted into the urine, and hemoglobinuria ensues.