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Journal articles on the topic 'Anemia perniciosa'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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1

Kurdi, Barnabás, Zoltán András Mezei, Ádám Kellner, and Miklós Egyed. "Thalassaemiás betegen észlelt anaemia perniciosa – a diagnózis nehézségei." Orvosi Hetilap 159, no. 33 (August 2018): 1368–71. http://dx.doi.org/10.1556/650.2018.31097.

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Abstract: The bone marrow aspiration, which was done in a leukopenic, hypochromic, microcytic, progressive anemic, thalassemic patient, revealed megaloblastic morphology. The low level of vitamin B12 and the reticulocytosis following the B12 supportation strenghtened the diagnosis of pernicious anemia. The set of the right diagnosis has been delayed by the fact that even in severe anemia one could not obtain the typical signs of B12 deficiency, having a hypochromic, microcytic erythrocyte morphology, due to the thalassemia minor disorder. Orv Hetil. 2018; 159(33): 1368–1371.

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2

Junior, Rudival Faial de Moraes, Andrea Negrão Costa, Rodrigo Bona Maneschy, Maria Silvia de Brito Barbosa, Carla Daniele Nascimento Pontes, Lucianna Serfaty de Holanda, Vanessa Kelly Guimaraes Cavalcante, et al. "Anemia perniciosa: um relato de caso." Revista Eletrônica Acervo Saúde Esp., no. 12 (2018): S1412—S1417. http://dx.doi.org/10.25248/reas280_2018.

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3

Cabeza, S., P. Martínez, C. Moreno, and F. De Miguel. "Anemia perniciosa y enfermedad de graves." Gaceta Médica de Bilbao 98, no. 4 (January 2001): 116. http://dx.doi.org/10.1016/s0304-4858(01)74380-6.

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4

Rodríguez de Santiago, E., C. Ferre Aracil, A. García García de Paredes, and V. F. Moreira Vicente. "Anemia perniciosa. Del pasado al presente." Revista Clínica Española 215, no. 5 (June 2015): 276–84. http://dx.doi.org/10.1016/j.rce.2014.12.013.

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5

Gómez del Río, María Zulema, María José Sánchez Soberón, María Teresa Saiz Careaga, María Luisa Gutiérrez López, María Carmen de la Hoz Regules, and Ana Bringas Roldán. "Trastorno de la memoria secundario a anemia perniciosa." Medicina General y de Familia 8, no. 4 (2019): 178–80. http://dx.doi.org/10.24038/mgyf.2019.043.

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6

Mòdol Deltell, Josep, Jordi Juncà Piera, Pere Tudela Hita, and Alonso Flores López. "Anemia perniciosa: enmascaramiento por la toma de folatos." Medicina Clínica 128, no. 9 (March 2007): 359. http://dx.doi.org/10.1016/s0025-7753(07)72591-5.

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7

Castillo-Torres, Sergio A., Alexandro Atilano-Díaz, and David Gómez-Almaguer. "Hematopoyesis extramedular pleural secundaria a anemia perniciosa grave." Medicina Clínica 153, no. 2 (July 2019): e7-e8. http://dx.doi.org/10.1016/j.medcli.2018.09.020.

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8

Calvo Romero, J. M. "Hipotiroidismo primario autoinmune en pacientes con anemia perniciosa." Revista Clínica Española 210, no. 6 (June 2010): 311–12. http://dx.doi.org/10.1016/j.rce.2009.11.017.

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9

Grau, Javier, Josep Maria Ribera, Jordi Juncà, and Fuensanta Millá. "Anemia perniciosa en el curso de una aplasia medular." Medicina Clínica 116, no. 2 (January 2001): 78. http://dx.doi.org/10.1016/s0025-7753(01)71728-9.

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10

Baretta, Giorgio Alfredo Pedroso, João Batista Marchesini, João Caetano Dallegrave Marchesini, Sérgio Brenner, and Maria Elize Rocha Sanches. "Anemia pós-cirurgia bariátrica: as causas nem sempre são relacionadas à cirurgia." ABCD. Arquivos Brasileiros de Cirurgia Digestiva (São Paulo) 21, no. 2 (June 2008): 95–97. http://dx.doi.org/10.1590/s0102-67202008000200012.

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RACIONAL: As anemias ferropriva, perniciosa e megaloblástica são comuns após procedimentos bariátricos como o bypass e as derivações biliopancreáticas. As principais causas devem-se ao desvio duodenal e do jejuno proximal do trânsito alimentar e, em menor grau, às úlceras anastomóticas. Entretanto a dieta pobre em nutrientes, a suplementação vitamínica inadequada, medicamentos, uso de álcool e neoplasias devem ser lembrados. RELATO DOS CASOS: Os autores relatam dois casos de pacientes pós-procedimentos bariátricos com anemia severa sem controle clínico e cuja investigação identificou melanoma metastático em um caso e neoplasia colônica no segundo, ambos tratados cirurgicamente com bons resultados. CONCLUSÃO: Anemias são comuns após procedimentos bariátricos, porém causas atípicas como neoplasias devem ser suspeitadas nos pacientes mais idosos e principalmente naqueles refratários ao controle clínico.

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11

Gil-Ruiz Gil-Esparza, M. A., J. Huerta Aragonés, C. Garrido Colino, and F. González Martínez. "Anemia hemolítica y pancitopenia en un lactante hijo de madre con anemia perniciosa mal controlada." Anales de Pediatría 75, no. 4 (October 2011): 288–90. http://dx.doi.org/10.1016/j.anpedi.2011.05.019.

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12

Pons Muzzo, Julio. "Los ácidos grasos totales y el colesterol total del plasma en la enfermedad de Carrión y en la bartonellosis del perro." Anales de la Facultad de Medicina 24, no. 1 (October 18, 2014): 89. http://dx.doi.org/10.15381/anales.v24i1.9729.

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Hace algún tiempo, nos propusimos estudiar los lípidos sanguíneos en la Enfermedad de Carrión y en la Bartonellosis del perro, inducidos por los importantes hallazgos de Williams y asociados en el plasma y eritrocitos de sujetos con anemia perniciosa, y el trabajo de Wintger en perros con lesión hepática por el tetracloruro de carbono.

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13

Fernández-Sabé, Nuria, and Roger Llatjós. "Varón de 38 años con anemia perniciosa y formaciones polipoides gástricas." Medicina Clínica 114, no. 18 (January 2000): 712–16. http://dx.doi.org/10.1016/s0025-7753(00)71409-6.

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14

Fernández-Miranda, C., M. Yebra Yebra, C. Ribera Casado, T. Toledo Urgarte, M. Martín Mola, and P. Gómez González. "Tromboembolia venosa e hiperhomocisteinemia como primera manifestación de una anemia perniciosa." Revista Clínica Española 205, no. 10 (October 2005): 489–92. http://dx.doi.org/10.1157/13079763.

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15

Fernández-Fernández, F. J., E. Ameneiros-Lago, and P. Sesma. "Anemia perniciosa: ferritina normal y un posible déficit de hierro oculto." Revista Clínica Española 215, no. 8 (November 2015): 478. http://dx.doi.org/10.1016/j.rce.2015.07.005.

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16

Jeney, András. "History of the therapy of pernicious anemia." Orvosi Hetilap 154, no. 44 (November 2013): 1754–58. http://dx.doi.org/10.1556/oh.2013.29743.

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Increased blood cell regeneration in exsanguinated experimental animals treated either with liver or with aqueous liver extracts was reported by Whipple and by Jeney and Jobling, respectively. These findings stimulated Minot and Murphy to provide evidence for the efficacy of liver against anaemia in clinical studies. After oral administration of liver (45–50 g per day) for 45 patients with anaemia perniciosa improvement of the hematological status was demonstrated. Consequently, for proving the therapeutic value of liver therapy Whipple, Minot and Murphy received Nobel price in 1934. The isolation of the antianemic factor from the liver has been succeded in 1948 and designated as vitamin B12. At the same time Lucy Wills applied yeast for the treatment of pregnant women with anemia related to undernourisment. The conclusions of this study inspired the discovery of folate. The detailed investigation of the mode of action of vitamin B12and folate enriched our knowledge in the area of pathophysiology and extended the clinical application of these two drugs. Orv. Hetil., 154 (44), 1754–1758.

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17

Velarde-Mayol, Cristina, Benito de la Hoz-García, Carlos del Cañizo-Fernández-Roldán, Alba Marina Hernández-López, Isabel Loza-Candia, and Andrea Cardona-Hernández. "Anemia perniciosa y enfermedades tiroideas autoinmunes en una población mayor de 65 años." Revista Española de Geriatría y Gerontología 50, no. 3 (May 2015): 126–28. http://dx.doi.org/10.1016/j.regg.2014.10.004.

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18

Arce, Julián. "Lecciones sobre la verruga peruana o "Enfermedad de Carrión"." Anales de la Facultad de Medicina 1 (November 23, 2014): 130. http://dx.doi.org/10.15381/anales.v1i0.10691.

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La verruga peruana, es una enfermedad infecciosa, inoculable al hombre y a los animales, de distribución geográfica limitada a determinadas zonas del Perú y que está caracterizada por los dos sindromas anatomo-clínicos siguientes: 1° anemia, que puede ser simple, en unos casos (verruga benigna), o aguda y perniciosa, en otros (verruga maligna); y 2° brote, más o menos abundante, de tumores granulomatosos, muy vasculares, conocidos con el nombre impropio de verrugas. La trasmisión de esta enfermedad, se realiza, probablemente, por intermedio de algún insecto chupador de sangre.

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19

Guzmán Barrón, Alberto, and Leonidas Delgado Butrón. "Estudio de la uropepsina en condiciones normales y patológicas." Anales de la Facultad de Medicina 37, no. 2 (October 18, 2014): 167. http://dx.doi.org/10.15381/anales.v37i2.9437.

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Se ha estudiado la concentración horaria de uropepsina en hombres y habiéndose obtenido un promedio de 32 unidades y en mujeres de 19, todos ellos normales. El estudio de la enzima en úlceras gástricas y duodenales dán resultados más altos que la media normal, en las neoplasias gástricas las cifras son bajas, pero como las variaciones individuales son amplias, es muy dudoso que esta determinación pueda prestar utilidad clínica, reemplazando al tubaje gástrico. El estudio de la uropepsina en los gastrectomizados revela que en la parcial por úlcera o cáncer la concentración disminuye. En las gastrectomías totales desaparece la uropepsina. En las anemias con aclorhidria del jugo gástrico, la investigación de la enzima presta gran utilidad diagnóstica; en las anemias perniciosas hay ausencia de uropepsina, en las de otro tipo, incluyendo la aplástica hasy disminución. La utilización de la hormona adrenocorticotrópica (A.C.T.H.) y Cortisona en el estudio de la excreción de uropepsina presta valiosos servicios. En sujetos normales, con la administración de 25 mgrs. de A.C.T.H. hemos obtenido un incremento de un 100% en la excreción de uropepsina. En los casos de anemia perniciosa el A.C.T.H. ni la cortisona son capaces de hacer aparecer a la enzima en la orina, pero en anemias de otro tipo el incremento es similar al de los sujetos normales. En la enfermedad de Addison la administración de A.C.T.H. no logra aumentar la uropepsina, pero en éstos casos la administración de cortisona incrementa la excreción de la enzima, por lo que consideramos que representa una prueba fácil de efectuarse, con fines de diagnóstico. Dada la sencillez del método y los útiles servicios que puede prestar, creemos que la determinación de uropepsina debe añadirse a los métodos de rutina en nuestros laboratorios clínicos.

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20

Orsini, Marco, Mariana Pimentel de Mello, Jhon Peter Botelho Reis, Carlos Henrique Melo Reis, Marcos RG de Freitas, and Osvaldo JM Nascimento. "Reabilitação física na Paraparesia Espástica por deficiência de vitamina B12:." Revista Neurociências 16, no. 3 (April 30, 1999): 242–47. http://dx.doi.org/10.34024/rnc.2008.v16.8639.

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A deficiência de vitamina B12 manifesta-se através de distúrbios neurológicos, psiquiátricos, gastrointestinais e hematológicos. É mais freqüente entre idosos, vegetarianos e indivíduos que adotam baixa dieta protéica ou apresentam distúrbios da absorção gastrintestinal. Sua prevalência é próxima a 20% na população geral, tendo como causa mais freqüente a anemia perniciosa. A degeneração combinada subaguda (DCS), é uma das manifestações neurológicas mais freqüentes na deficiência de vitamina B12, sendo marcada por lesões nas colunas posteriores e laterais, que acarretam déficits sensoriais e motores. Relatamos o caso de um paciente com degeneração subaguda combinada e revisamos a literatura acerca das principais estratégias fisioterapêuticas empregadas na reabilitação de pacientes acometidos por essa condição patológica.

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21

SILVA, MARCUS TULIUS TEIXEIRA DA, JOSÉ LUIS DE SÁ CAVALCANTI, and DENISE MADEIRA MOREIRA. "Alterações neurorradiológicas cerebrais na degeneração combinada de medula: relato de caso." Arquivos de Neuro-Psiquiatria 58, no. 3A (September 2000): 752–55. http://dx.doi.org/10.1590/s0004-282x2000000400026.

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A carência da vitamina B12 em muitas situações manifesta-se também por alterações neuropsiquiátricas, sendo a mais comum a degeneração combinada subaguda da medula espinhal. No sistema nervoso central a repercussão maior é na mielina, sendo a degeneração esponjosa e a desmielinização difusa das colunas lateral e posterior da medula as mais típicas alterações patológicas. O mesmo ocorre nos hemisférios cerebrais, sendo que anormalidades nas imagens por ressonância magnética são esperadas. No entanto muito pouco tem sido relatado e a carência da cobalamina não figura habitualmente na lista de diagnósticos diferenciais de lesões desmielinizantes. Relatamos caso de anemia perniciosa com manifestações neurológicas em que a ressonância magnética mostrou alterações compatíveis com desmielinização do feixe piramidal, consequentes, possivelmente, à carência da vitamina B12. Discutimos os achados neuropatológicos da hipovitaminose. Sugerimos que a degeneração combinada subaguda da medula deve fazer parte do diagnóstico diferencial radiológico das lesões desmielinizantes no sistema nervoso central.

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22

Barrera Valencia, Mariana. "Endocrinopatía múltiple autoinmune." Revista Repertorio de Medicina y Cirugía 29, no. 2 (March 11, 2020): 131–34. http://dx.doi.org/10.31260/repertmedcir.01217273.1025.

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Los autoanticuerpos son proteínas producidas en el organismo por la inducción de un antígeno propio del individuo el cual no reconocen y rechazan. Su aparición en sangre puede iniciarse tiempo antes de la presentación de síntomas o signos. El deterioro funcional de dos o más glándulas es una afectación endocrinológica múltiple que puede asociarse con otras patologías autoinmunes no endocrinas, tales como vitiligo, alopecia areata, gastritis autoinmune y anemia perniciosa. Se clasifica en tres síndromes poliendocrinos autoinmunes (SPA). En Europa la incidencia del tipo I es menor a 1:100000 por año y los 2 y 3 varían entre 1–2:100000 por año. Colombia no cuenta con registros que permitan calcularla. Se reporta el caso de un hombre de 18 años diagnosticado con hipotiroidismo autoinmune, a los 15 años de edad debutó con cetoacidosis diabética y a los 17 con posterior aparición de vitiligo. El manejo inicial se realizó con levotiroxina sódica y análogos de insulina. Este caso corresponde a un SPA tipo IIIA, ya que cursa con hipotiroidismo autoinmune, diabetes mellitus y como último hallazgo cronológico la asociación con vitiligo. La detección de una endocrinopatía autoinmune en pacientes jóvenes debe alertar sobre la posible existencia de un SPA.

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23

Fernández-Ruiz, Mario, Félix Alonso-Navas, Eva Muro, and Mercedes Pérez-Carreras. "Trombosis venosa portal y mesentérica asociadas a hiperhomocisteinemia y anemia perniciosa en un paciente heterocigoto para la mutación C677T del gen de la MTHFR." Medicina Clínica 136, no. 5 (February 2011): 225–26. http://dx.doi.org/10.1016/j.medcli.2010.01.011.

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24

Skvortsov, Vsevolod Vladimirovich, and Anastasia Romanovna Ponomareva. "B₁₂-deficiency anemia in the work of the nurse." Medsestra (Nurse), no. 9 (July 21, 2021): 76–80. http://dx.doi.org/10.33920/med-05-2109-10.

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B₁₂-deficiency anemia (megaloblastic anemia, pernicious anemia, Addison-Birmer disease), characterized by progressive hyperchromic, macrocytic anemia, hypersegmentation of neutrophil nuclei, megaloblastic erythropoiesis and morphological abnormalities of other hematopoietic growths in the bone marrow; Unlike other anemias, B₁₂-deficiency anemia is often associated with the development of pathological psycho-neurological symptoms (funicular myelosis).This article deals with problems of etiology, pathogeny, clinical symptomatology, approaches to detection and treatment of B₁₂-deficiency anemia.

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25

Thomes, Reggie M., and Lori J. Rosenstein. "Pernicious anemia." Blood 135, no. 19 (May 7, 2020): 1719. http://dx.doi.org/10.1182/blood.2020005344.

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26

Toh, Ban-Hock, Ian R. van Driel, and Paul A. Gleeson. "Pernicious Anemia." New England Journal of Medicine 337, no. 20 (November 13, 1997): 1441–48. http://dx.doi.org/10.1056/nejm199711133372007.

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27

Hawley, Kelly. "Pernicious Anemia." American Journal of Nursing 96, no. 11 (November 1996): 52–53. http://dx.doi.org/10.1097/00000446-199611000-00040.

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28

Carmel, Ralph. "Pernicious Anemia." Archives of Internal Medicine 148, no. 8 (August 1, 1988): 1712. http://dx.doi.org/10.1001/archinte.1988.00380080016007.

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29

Schrier, S. "Pernicious Anemia." ASH Image Bank 2001, no. 1205 (December 5, 2001): 100231. http://dx.doi.org/10.1182/ashimagebank-2001-100231.

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30

Karnad, Anand B., and Agnes Krozser-Hamati. "Pernicious anemia." Postgraduate Medicine 91, no. 2 (February 1992): 231–37. http://dx.doi.org/10.1080/00325481.1992.11701209.

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31

Hirokawa, Makoto. "3. Pernicious Anemia." Nihon Naika Gakkai Zasshi 103, no. 7 (2014): 1609–12. http://dx.doi.org/10.2169/naika.103.1609.

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32

PRUTHI, RAJIV K., and AYALEW TEFFERI. "Pernicious Anemia Revisited." Mayo Clinic Proceedings 69, no. 2 (February 1994): 144–50. http://dx.doi.org/10.1016/s0025-6196(12)61041-6.

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33

TÖTTERMAN, G., and P. AHRENBERG. "The Age Distribution in Pernicious Tapeworm Anemia and Addisonian Pernicious Anemia." Acta Medica Scandinavica 153, no. 6 (April 24, 2009): 421–26. http://dx.doi.org/10.1111/j.0954-6820.1955.tb18246.x.

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34

Hawley, Kelly. "Clinical Snapshot: Pernicious Anemia." American Journal of Nursing 96, no. 11 (November 1996): 52. http://dx.doi.org/10.2307/3464985.

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35

Bunch, L. C. "144 JUVENILE PERNICIOUS ANEMIA." Journal of Investigative Medicine 53, no. 1 (January 1, 2005): S278.3—S278. http://dx.doi.org/10.2310/6650.2005.00006.143.

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36

Weisse, Allen B. "An Anemia Called Pernicious." Hospital Practice 26, no. 11 (November 15, 1991): 25–40. http://dx.doi.org/10.1080/21548331.1991.11704217.

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37

Egli, Fritz, and Roland Walter. "Vitiligo and Pernicious Anemia." New England Journal of Medicine 350, no. 26 (June 24, 2004): 2698. http://dx.doi.org/10.1056/nejmicm990602.

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38

WRIGHT, PATRICK E., and DAVID A. SEARS. "Hypogammaglobulinemia and Pernicious Anemia." Southern Medical Journal 80, no. 2 (February 1987): 243–46. http://dx.doi.org/10.1097/00007611-198702000-00026.

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39

Harakati, M. S. E. "Pernicious Anemia in Arabs." Blood Cells, Molecules, and Diseases 22, no. 2 (August 1996): 98–103. http://dx.doi.org/10.1006/bcmd.1996.0015.

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40

Chan, Joyce Chee Wun, Herman Sung Yu Liu, Bonnie Chi Sang Kho, Joycelyn Pui Yin Sim, Thomas Kwan Hang Lau, Yiu Wing Luk, Raymond Wan Chu, Florence Man Fung Cheung, Frankie Pak Tat Choi, and Edmond Shiu Kwan Ma. "Pernicious Anemia in Chinese." Medicine 85, no. 3 (May 2006): 129–38. http://dx.doi.org/10.1097/01.md.0000224710.47263.70.

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41

Banka, Siddharth, Kate Ryan, Wendy Thomson, and William G. Newman. "Pernicious anemia – Genetic insights." Autoimmunity Reviews 10, no. 8 (June 2011): 455–59. http://dx.doi.org/10.1016/j.autrev.2011.01.009.

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42

Fujii, Toshihito, Shigeru Fujinami, Yoshihiro Tagawa, Yoichi Kadota, Sei Nakatani, Yukitoshi Takeuchi, Tadahide Yasuda, et al. "Pernicious anemia associated with autoimmune hemolytic anemia." Journal of the Japan Society of Blood Transfusion 38, no. 4 (1992): 573–76. http://dx.doi.org/10.3925/jjtc1958.38.573.

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43

Yeruva, Sri Lakshmi Hyndavi, Raj Pal Manchandani, and Patricia Oneal. "Pernicious Anemia with Autoimmune Hemolytic Anemia: A Case Report and Literature Review." Case Reports in Hematology 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/7231503.

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Pernicious anemia is a common cause of vitamin B12 deficiency. Here, we discuss a case of a young woman who presented with severe anemia along with a history of iron deficiency anemia. After a review of her clinical presentation and laboratory data, we identified an autoimmune hemolytic anemia and a concomitant pernicious anemia. The concurrence of both these hematological diagnoses in a patient is rare.

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44

Green, Ralph. "Anemias beyond B12 and iron deficiency: the buzz about other B's, elementary, and nonelementary problems." Hematology 2012, no. 1 (December 8, 2012): 492–98. http://dx.doi.org/10.1182/asheducation.v2012.1.492.3800162.

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Abstract The term “unexplained anemia” appears frequently in a request for a hematology consultation. Although most anemia consultations are fairly routine, they occasionally represent challenging problems that require an amalgam of experience, insight, and a modicum of “out-of-the-box” thinking. Problem anemia cases and pitfalls in their recognition can arise for one of several reasons that are discussed in the cases presented herein. “Anemias beyond B12 and iron deficiency” covers a vast domain of everything that lies beyond the commonly encountered anemias caused by simple deficiencies of 2 currently major hematologically relevant micronutrients. However, even these deficiencies may be obscured when they coexist or are not considered because of misleading distractions. They may also be mistakenly identified when other less common nutrient deficiencies occur. I present herein case examples of such situations: a young patient with pancytopenia and schistocytes who was responsive to plasmapheresis, but in whom pernicious anemia was not suspected because of ethnicity and age; a bicytopenic patient with anemia and myelodysplastic features caused by copper deficiency after gastric reduction surgery; and a patient with BM hypoplasia and a dimorphic blood smear who was found to have paroxysmal nocturnal hemoglobinuria. These “pearls” represent but 3 examples of the many varieties of problems in anemia diagnosis and are used to illustrate potential pitfalls and how to avoid them.

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Hagarty, Sarah, Istvan Hüttner, Henry Shibata, and Saul Katz. "Gastric Carcinoid Tumours and Pernicious Anemia: Case Report and Review of the Literature." Canadian Journal of Gastroenterology 14, no. 3 (2000): 241–45. http://dx.doi.org/10.1155/2000/645639.

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Patients with pernicious anemia are at risk of developing carcinoid tumours of the stomach. A patient with pernicious anemia and multifocal carcinoid tumours of the gastric fundus that regressed after antrectomy is presented. The frequent occurrence of gastric carcinoid tumours in patients with long-standing pernicious anemia suggests that surveillance gastroscopy and biopsies of the fundus might be indicated. Compete functional antrectomy may effectively cause these tumours to regress by removing their excessive gastrin hormonal stimulation. However, incomplete antrectomy can result in persistently elevated serum gastrin and failure of total disappearance of the carcinoid tumours.

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Lane, Lenee A., and Carlos Rojas-Fernandez. "Treatment of Vitamin B12–Deficiency Anemia: Oral versus Parenteral Therapy." Annals of Pharmacotherapy 36, no. 7-8 (July 2002): 1268–72. http://dx.doi.org/10.1345/aph.1a122.

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OBJECTIVE: To evaluate the use of oral cyanocobalamin therapy in the treatment of cobalamin (vitamin B12)–deficient anemia. DATA SOURCES: Primary and review articles were identified by MEDLINE search (1966–May 2000) and through secondary sources. DATA SYNTHESIS: Cobalamin-deficient anemia is among the most common diagnoses in older populations. Cobalamin-deficient anemia may be diagnosed as pernicious anemia, resulting from the lack of intrinsic factor required for cobalamin absorption or as protein malabsorption from the inability to displace cobalamin from protein food sources. Several studies provide evidence that daily oral cyanocobalamin as opposed to monthly parenteral formulations may adequately treat both types of cobalamin-deficient anemias. CONCLUSIONS: Daily oral cyanocobalamin at doses of 1000–2000 μg can be used for treatment in most cobalamin-deficient patients who can tolerate oral supplementation. There are inadequate data at the present time to support the use of oral cyanocobalamin replacement in patients with severe neurologic involvement.

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Andreichev, Nail A. "The differential diagnostic of anemia unrelated to iron metabolism." Medical Journal of the Russian Federation 22, no. 5 (October 15, 2016): 259–66. http://dx.doi.org/10.18821/0869-2106-2016-22-5-259-266.

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The anemia continue to be actual problem of health care all over the world, occurring in almost half of population of terrestrial globe. The anemias are very various by their etiology, pathogenesis and clinical hematological manifestations. They are differentiated by leading pathogenic mechanism of development with purpose of choosing schemes of diagnostic and treatment. However, morphological classification and classification by color index are considered for facilitating diagnostic and differentiated diagnosis. The modern diagnosis and differentiated diagnostic of anemia bounded and unbounded with iron metabolism. The differentiated diagnosis of anemia is based on analysis of clinical, laboratory and instrumental data. In case of anemia, the blood analysis is to account indices of Hb, size of erythrocytes, their Hb saturation, average volume of erythrocytes and average content of hemoglobin in erythrocytes, color index, number of reticulocytes, etc., permitting judging about character and activity of erythropoiesis. The article presents algorithm of examination in case of occurrence of normocytic anemia, anemia in case of deficiency of diet, anemia in case of chronic renal insufficiency, hemolytic anemia; diagnostic criteria of autoimmune hemolytic anemia, inherent hemolytic microspherocytic anemia, deficiency of pyruvate kinase, paroxysmal night hemoglobinuria, deficiency of glucose-6-phosphatedehydrogenase, anemia due to primary disorders of bone marrow, aplastic anemia, hyperchrome and macrocytic anemia, deficiency of vitamin B12 (pernicious anemia) and also folic acid.

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Badiga, Murthy S. "Pernicious Anemia and Colorectal Cancer." Annals of Internal Medicine 112, no. 8 (April 15, 1990): 630. http://dx.doi.org/10.7326/0003-4819-112-8-630_2.

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Harakati, Mohammed S., Abdul-Kareem Al-Momen, Fahad I. Al-Mohareb, Dahish S. Ajarim, Shihab A. Al-Mashhadani, Khalid S. Al-Khairy, and Kamal Higgy. "Pernicious Anemia in Saudi Arabs." Annals of Saudi Medicine 12, no. 3 (May 1992): 274–78. http://dx.doi.org/10.5144/0256-4947.1992.274.

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HASHIZUME, Toshihiko. "Good's Syndrome and Pernicious Anemia." Internal Medicine 41, no. 11 (2002): 1062–64. http://dx.doi.org/10.2169/internalmedicine.41.1062.

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