Hemolytic anemia historical perspective: Difference between revisions
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*In '''1962''', Alving's group showed that acute hemolytic anemia could be triggered by primaquine.<ref name="pmid24372186">{{cite journal| author=Luzzatto L, Seneca E| title=G6PD deficiency: a classic example of pharmacogenetics with on-going clinical implications. | journal=Br J Haematol | year= 2014 | volume= 164 | issue= 4 | pages= 469-80 | pmid=24372186 | doi=10.1111/bjh.12665 | pmc=4153881 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24372186 }} </ref> | *In '''1962''', Alving's group showed that acute hemolytic anemia could be triggered by primaquine.<ref name="pmid24372186">{{cite journal| author=Luzzatto L, Seneca E| title=G6PD deficiency: a classic example of pharmacogenetics with on-going clinical implications. | journal=Br J Haematol | year= 2014 | volume= 164 | issue= 4 | pages= 469-80 | pmid=24372186 | doi=10.1111/bjh.12665 | pmc=4153881 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24372186 }} </ref> | ||
In the '''mid-1500s''', seminal experiments were conducted by Richard Lower and Jean-Baptiste Denis on transfusion of blood.<ref name="pmid26696795">{{cite journal| author=Freedman J| title=Autoimmune Hemolysis: A Journey through Time. | journal=Transfus Med Hemother | year= 2015 | volume= 42 | issue= 5 | pages= 278-85 | pmid=26696795 | doi=10.1159/000437195 | pmc=4678316 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26696795 }} </ref> | |||
In the '''1661''', Malpighi observed red blood cells using a microscope and noted that red blood cells were within capillaries.<ref name="pmid26696795">{{cite journal| author=Freedman J| title=Autoimmune Hemolysis: A Journey through Time. | journal=Transfus Med Hemother | year= 2015 | volume= 42 | issue= 5 | pages= 278-85 | pmid=26696795 | doi=10.1159/000437195 | pmc=4678316 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26696795 }} </ref> | |||
In '''1663''', Swammerdam described minute globules in the blood of a frog.<ref name="pmid26696795">{{cite journal| author=Freedman J| title=Autoimmune Hemolysis: A Journey through Time. | journal=Transfus Med Hemother | year= 2015 | volume= 42 | issue= 5 | pages= 278-85 | pmid=26696795 | doi=10.1159/000437195 | pmc=4678316 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26696795 }} </ref> | |||
In '''1673''', van Leeuwenhoek described red blood cells in detail.<ref name="pmid26696795">{{cite journal| author=Freedman J| title=Autoimmune Hemolysis: A Journey through Time. | journal=Transfus Med Hemother | year= 2015 | volume= 42 | issue= 5 | pages= 278-85 | pmid=26696795 | doi=10.1159/000437195 | pmc=4678316 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26696795 }} </ref> | |||
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.<ref name="pmid26696795">{{cite journal| author=Freedman J| title=Autoimmune Hemolysis: A Journey through Time. | journal=Transfus Med Hemother | year= 2015 | volume= 42 | issue= 5 | pages= 278-85 | pmid=26696795 | doi=10.1159/000437195 | pmc=4678316 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26696795 }} </ref> | |||
In '''1843''', Andral proposed the idea that anemia was due to possible destruction of blood, which we now know as hemolysis.<ref name="pmid26696795">{{cite journal| author=Freedman J| title=Autoimmune Hemolysis: A Journey through Time. | journal=Transfus Med Hemother | year= 2015 | volume= 42 | issue= 5 | pages= 278-85 | pmid=26696795 | doi=10.1159/000437195 | pmc=4678316 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26696795 }} </ref> | |||
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.<ref name="pmid26696795">{{cite journal| author=Freedman J| title=Autoimmune Hemolysis: A Journey through Time. | journal=Transfus Med Hemother | year= 2015 | volume= 42 | issue= 5 | pages= 278-85 | pmid=26696795 | doi=10.1159/000437195 | pmc=4678316 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26696795 }} </ref> 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 '''1900''', Minkowski showed that jaundice could be from either hemolytic anemia or liver disease.<ref name="pmid26696795">{{cite journal| author=Freedman J| title=Autoimmune Hemolysis: A Journey through Time. | journal=Transfus Med Hemother | year= 2015 | volume= 42 | issue= 5 | pages= 278-85 | pmid=26696795 | doi=10.1159/000437195 | pmc=4678316 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26696795 }} </ref> | |||
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.<ref name="pmid18886314">{{cite journal| author=WAGLEY PF, SHEN SC| title=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). | journal=J Lab Clin Med | year= 1948 | volume= 33 | issue= 10 | pages= 1197-1203 | pmid=18886314 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18886314 }} </ref> | |||
In ''''1951''', Young and colleagues created the term "autoimmune hemolytic anemia." Glucocorticoids were used to treat warm autoimmune hemolytic anemia. | |||
In '''1962''', Iafusco and Biffa described a case of warm autoimmune hemolytic anemia in a newborn.<ref name="pmid13956038">{{cite journal| author=IAFUSCO F, BUFFA V| title=[Autoimmune hemolytic anemia in a newborn infant]. | journal=Pediatria (Napoli) | year= 1962 | volume= 70 | issue= | pages= 1256-64 | pmid=13956038 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13956038 }} </ref> | |||
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== | ==References== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]
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Overview
Historical Perspective
- In 1891, Paul Ehrlich discovered that methylene blue had activity against malaria.[1]
- In 1920, it was noted that primaquine was an effective anti-malarial medication.
- 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.[1]
- In 1956, Carson's group showed that people who experienced hemolysis from primaquine had decreased level of G6PD.[1]
- In 1962, Alving's group showed that acute hemolytic anemia could be triggered by primaquine.[1]
In the mid-1500s, seminal experiments were conducted by Richard Lower and Jean-Baptiste Denis on transfusion of blood.[2]
In the 1661, Malpighi observed red blood cells using a microscope and noted that red blood cells were within capillaries.[2]
In 1663, Swammerdam described minute globules in the blood of a frog.[2]
In 1673, van Leeuwenhoek described red blood cells in detail.[2]
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.[2]
In 1843, Andral proposed the idea that anemia was due to possible destruction of blood, which we now know as hemolysis.[2]
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.[2] 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 1900, Minkowski showed that jaundice could be from either hemolytic anemia or liver disease.[2]
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 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 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.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Freedman J (2015). "Autoimmune Hemolysis: A Journey through Time". Transfus Med Hemother. 42 (5): 278–85. doi:10.1159/000437195. PMC 4678316. PMID 26696795.
- ↑ 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.