Hemolytic anemia historical perspective
|
Hemolytic anemia Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Hemolytic anemia historical perspective On the Web |
|
American Roentgen Ray Society Images of Hemolytic anemia historical perspective |
|
Risk calculators and risk factors for Hemolytic anemia historical perspective |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Shyam Patel [2]
Overview
The history of hemolytic anemia dates back to the 16th century, when the initial experiments were conducted on transfusion of blood. Soon after, the development of the simple microscope revolutionized the study of red blood cells, as red blood cells could be directly observed. After multiple patients began to present with jaundice and splenomegaly, it was observed that there was an association between these symptoms and the destruction of red blood cells. Eventually, it was determined that hemolytic anemia was largely due to immune-mediated mechanisms leading to destruction of red blood cells. Since the 1980s, various immunosuppressive medications have been developed to help treat hemolytic anemia.
Historical Perspective
- In the mid-1500s, seminal experiments were conducted by Richard Lower and Jean-Baptiste Denis on transfusion of blood.[1]
- In 1661, Malpighi observed red blood cells using a microscope and noted that red blood cells were within capillaries.[1]
- In 1673, van Leeuwenhoek described red blood cells in detail.[1]
- In 1769, Morgagni described the case of a priest who developed hemolytic anemia symptoms, which included red urine, pallor, and splenomegaly. However, since simple microscopes could not show red blood cells in detail, further perspective about hemolytic anemia could not be gained.[1]
- In 1843, Andral proposed the idea that anemia was due to possible destruction of blood, which we now know as hemolysis.[1]
- In 1854, Dressler described the case of a 10-year-old child who developed hemolytic anemia upon exposure to cold weather. The boy developed red urine, and exam of his urine under the microscope showed a brown pigment with no red blood cells.
- In 1871, Vanlair and Masius describes a patient who had anemia, splenomegaly, and red urine. They showed that jaundice as a clinical symptoms was due to destruction of red blood cells.[1] They noted microcytes (small cells) in the blood.
- In 1890, Wilson described hemolytic anemia from hereditary spherocytosis. The patient had splenomegaly and quick onset of anemia.
- In 1891, Paul Ehrlich discovered that methylene blue had activity against malaria.[2]
- In 1900, Minkowski showed that jaundice could be from either hemolytic anemia or liver disease.[1]
- In 1920, it was noted that primaquine was an effective anti-malarial medication.
- In 1940, Dameshek and Schwartz described acquired hemolytic anemia. They noted that red blood cells had increased fragility and that hemolysins could be released into the circulation.
- In 1944, Race and Weiner showed that Rhesus antigen antibodies could bind to red blood cell surfaces and trigger hemolysis.
- In 1945, the Coombs test, or direct antiglobulin test, was described. This test assesses for antibodies bound to a patient's cells.
- In 1948, Wagley showed that removal of the spleen could alleviate the destruction of red blood cells, suggesting the spleen was the anatomic location of hemolysis.[3]
- In 1951, Young and colleagues created the term "autoimmune hemolytic anemia". Glucocorticoids were used to treat warm autoimmune hemolytic anemia.
- In 1953, there was large-scale use of primaquine for troops in the army in order to protect against malaria, and it was soon noted that soldiers developed abdominal discomfort, anemia, and jaundice.[2]
- In 1956, Carson's group showed that people who experienced hemolysis from primaquine had decreased level of G6PD.[2]
- In 1962, Alving's group showed that acute hemolytic anemia could be triggered by primaquine.[2]
- In 1962, Iafusco and Biffa described a case of warm autoimmune hemolytic anemia in a newborn.[4]
- In 1971, Dacie proposed that hemolytic anemia was due to a failure of immune surveillance, ultimately leading to red blood cell destruction.
- After the 1980s, a variety of immunosuppressive medications were used to treat hemolytic anemias on the basis that this was an immune-mediated phenomenon.
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Freedman J (2015). "Autoimmune Hemolysis: A Journey through Time". Transfus Med Hemother. 42 (5): 278–85. doi:10.1159/000437195. PMC 4678316. PMID 26696795.
- ↑ 2.0 2.1 2.2 2.3 Luzzatto L, Seneca E (2014). "G6PD deficiency: a classic example of pharmacogenetics with on-going clinical implications". Br J Haematol. 164 (4): 469–80. doi:10.1111/bjh.12665. PMC 4153881. PMID 24372186.
- ↑ WAGLEY PF, SHEN SC (1948). "The spleen as a source of a substance causing agglutination of the red blood cells of certain patients with acquired hemolytic jaundice by an antihuman serum rabbit serum (Coombs' serum)". J Lab Clin Med. 33 (10): 1197–1203. PMID 18886314.
- ↑ IAFUSCO F, BUFFA V (1962). "[Autoimmune hemolytic anemia in a newborn infant]". Pediatria (Napoli). 70: 1256–64. PMID 13956038.