Page 680 - Williams Hematology ( PDFDrive )
P. 680

654  Part VI:  The Erythrocyte           Chapter 44:  Anemia Resulting From Other Nutritional Deficiencies            655




                     In addition to folate deficiency, chronic alcoholics frequently     20.  Lane M, Alfrey CP Jr: The anemia of human riboflavin deficiency. Blood 25:432–442,
                  demonstrate multiple other micronutrient deficiencies, including thia-  1965.
                                                                   101
                  mine, pyridoxine, and vitamin A, which aggravate the risk of anemia.      21.  Foy H, Kondi A: A case of true red cell aplastic anaemia successfully treated with ribo-
                                                                           flavin. J Pathol Bacteriol 65(2):559–564, 1953.
                  Although decreased dietary folate intake appears to be a necessary fac-    22.  Powers HJ: Riboflavin (vitamin B-2) and health. Am J Clin Nutr 77(6):1352–1360, 2003.
                  tor in the etiology of the megaloblastic anemia, ethanol itself interferes     23.  Hodges RE, Bean WB, Ohlson MA, et al: Human pantothenic acid deficiency produced
                                                                           by omega-methyl pantothenic acid. J Clin Invest 38(8):1421–1425, 1959.
                  with folate metabolism (Chap. 41). 102,103              24.  Spivak JL, Jackson DL: Pellagra: An analysis of 18 patients and a review of the literature.
                     Macrocytosis, however, does not always indicate the presence   Johns Hopkins Med J 140(6):295–309, 1977.
                                    97
                  of  megaloblastic  anemia,   reticulocytosis  secondary  to  hemolysis  or     25.  Bay A, Keskin M, Hizli S, et al: Thiamine-responsive megaloblastic anemia syndrome.
                  bleeding, or liver disease. So-called macrocytosis of alcoholism is found   Int J Hematol 92(3):524–526, 2010.
                  in as many as 96 percent of alcoholics.  In these patients, the macrocy-    26.  Boros LG, Steinkamp MP, Fleming JC, et al: Defective RNA ribose synthesis in fibrob-
                                             104
                                                                           lasts from patients with thiamine-responsive megaloblastic anemia (TRMA).  Blood
                  tosis usually is mild, with MCV in the range of 100 to 110 fL, and ane-  102(10):3556–3561, 2003.
                  mia is usually absent. In the blood film, macrocytes are typically round     27.  Beshlawi I, Al Zadjali S, Bashir W, et al: Thiamine responsive megaloblastic anemia: The
                                                                           puzzling phenotype. Pediatr Blood Cancer 61(3):528–531, 2014.
                  rather than oval and neutrophil hypersegmentation is not present. The     28.  Zhao R, Goldman ID: Folate and thiamine transporters mediated by facilitative carriers
                  macrocytosis persists until the patient abstains from alcohol. Even then,   (SLC19A1–3 and SLC46A1) and folate receptors. Mol Aspects Med 34(2–3):373–385,
                  MCV does not become completely normal for a period of 2 to 4 months   2013.
                  in view of the life span of erythrocytes. 103           29.  Reuler JB, Broudy VC, Cooney TG: Adult scurvy. JAMA 253(6):805–807, 1985.
                                                                          30.  Hodges RE, Baker EM, Hood J, et al: Experimental scurvy in man. Am J Clin Nutr
                     Alcohol ingestion for 5 to 7 days produces vacuolization of early   22(5):535–548, 1969.
                  red cell precursors, and formation of vacuoles can be observed in in     31.  Zalusky R, Herbert V: Megaloblastic anemia in scurvy with response to 50 microgm. of
                  vitro marrow cell cultures. 99,105  These changes disappear promptly when   folic acid daily. N Engl J Med 265:1033–1038, 1961.
                  alcohol ingestion is discontinued. Vacuolization with a similar appear-    32.  Stokes PL, Melikian V, Leeming RL, et al: Folate metabolism in scurvy. Am J Clin Nutr
                                                                           28(2):126–129, 1975.
                  ance occurs in subjects who are fed a phenylalanine-deficient diet,     33.  Cox EV, Meynell MJ, Northam BE, et al: The anaemia of scurvy.  Am J Med 42(2):
                  patients treated with chloramphenicol or pyrazinamide, patients in   220–227, 1967.
                  hyperosmolar coma, and individuals deficient in copper or riboflavin. 104    34.  Clark NG, Sheard NF, Kelleher JF: Treatment of iron-deficiency anemia complicated by
                                                                           scurvy and folic acid deficiency. Nutr Rev 50(5):134–137, 1992.
                     Two relatively uncommon hematologic complications of alcohol-    35.  Wapnick AA, Lynch SR, Krawitz P, et al: Effects of iron overload on ascorbic acid
                  ism are Zieve syndrome, 106,107  consisting of alcohol-induced liver disease,   metabolism. Br Med J 3(5620):704–707, 1968.
                  often hyperlipidemia, jaundice, and transient spherocytic hemolytic     36.  Wapnick AA, Lynch SR, Charlton RW, et al: The effect of ascorbic acid deficiency on
                                                                           desferrioxamine-induced urinary iron excretion. Br J Haematol 17(6):563–568, 1969.
                  anemia; and spur cell hemolytic anemia, associated with severe      37.  Chapman RW, Hussain MA, Gorman A, et al: Effect of ascorbic acid deficiency on
                  alcohol-induced liver disease often requiring hepatic transplantation for   serum ferritin concentration in patients with beta-thalassaemia major and iron over-
                  resolution. 108,109  Chapter 45 discusses these syndromes.  load. J Clin Pathol 35(5):487–491, 1982.
                                                                          38.  Cohen A, Cohen IJ, Schwartz E: Scurvy and altered iron stores in thalassemia major.
                                                                           N Engl J Med 304(3):158–160, 1981.
                  REFERENCES                                              39.  Lipschitz DA, Bothwell TH, Seftel HC, et al: The role of ascorbic acid in the metabolism
                                                                           of storage iron. Br J Haematol 20(2):155–163, 1971.
                    1.  Blackfan KD, Wolbach SB: Vitamin A deficiency in infants, a clinical and pathological     40.  Bothwell TH, Abrahams C, Bradlow BA, et al: Idiopathic and Bantu Hemochromatosis.
                     study. J Pediatr 3:679–706, 1933.                     Comparative Histological Study. Arch Pathol 79:163–168, 1965.
                    2.  Vitamin A and iron deficiency. Nutr Rev 47(4):119–121, 1989.    41.  Williams ML, Shoot RJ, O’Neal PL, et al: Role of dietary iron and fat on vitamin E defi-
                    3.  Majia LA, Hodges RE, Arroyave G, et al: Vitamin A deficiency and anemia in Central   ciency anemia of infancy. N Engl J Med 292(17):887–890, 1975.
                     American children. Am J Clin Nutr 30(7):1175–1184, 1977.    42.  Oski FA, Barness LA: Hemolytic anemia in vitamin E deficiency.  Am J Clin Nutr
                    4.  Hodges RE, Sauberlich HE, Canham JE, et al: Hematopoietic studies in vitamin A defi-  21(1):45–50, 1968.
                     ciency. Am J Clin Nutr 31(5):876–885, 1978.          43.  Ritchie JH, Fish MB, McMasters V, et al: Edema and hemolytic anemia in premature
                    5.  Lynch S: Influence of infection/inflammation, thalassemia and nutritional status on   infants. A vitamin E deficiency syndrome. N Engl J Med 279(22):1185–1190, 1968.
                     iron absorption. Int J Vitam Nutr Res 77(3):217–223, 2007.    44.  Zipursky A: Vitamin E deficiency anemia in newborn infants. Clin Perinatol 11(2):
                    6.  Citelli M, Bittencourt LL, da Silva SV, et al: Vitamin A modulates the expression of   393–402, 1984.
                     genes involved in iron bioavailability. Biol Trace Elem Res 149(1):64–70, 2012.    45.  Wilfond BS, Farrell PM, Laxova A, et al: Severe hemolytic anemia associated with vita-
                    7.  Kolsteren P, Rahman SR, Hilderbrand K, et al: Treatment for iron deficiency anaemia   min E deficiency in infants with cystic fibrosis. Implications for neonatal screening.
                     with a combined supplementation of iron, vitamin A and zinc in women of Dinajpur,   Clin Pediatr (Phila) 33(1):2–7, 1994.
                     Bangladesh. Eur J Clin Nutr 53(2):102–106, 1999.     46.  Farrell PM, Bieri JG, Fratantoni JF, et al: The occurrence and effects of human vitamin
                    8.  Walczyk T, Davidsson L, Rossander-Hulthen L, et al: No enhancing effect of vitamin A   E deficiency. A study in patients with cystic fibrosis. J Clin Invest 60(1):233–241, 1977.
                     on iron absorption in humans. Am J Clin Nutr 77(1):144–149, 2003.    47.  Corash L, Spielberg S, Bartsocas C, et al: Reduced chronic hemolysis during high-dose
                    9.  Mejia LA, Chew F: Hematological effect of supplementing anemic children with     vitamin E administration in Mediterranean-type glucose-6-phosphate dehydrogenase
                     vitamin A alone and in combination with iron. Am J Clin Nutr 48(3):595–600, 1988.  deficiency. N Engl J Med 303(8):416–420, 1980.
                    10.  Calis JC, Phiri KS, Faragher EB, et al: Severe anemia in Malawian children. N Engl J Med     48.  Eldamhougy S, Elhelw Z, Yamamah G, et al: The vitamin E status among glucose-6
                     358(9):888–899, 2008.                                 phosphate dehydrogenase deficient patients and effectiveness of oral vitamin E. Int J
                    11.  Tatala SR, Kihamia CM, Kyungu LH, et al: Risk factors for anaemia in schoolchildren in   Vitam Nutr Res 58(2):184–188, 1988.
                     Tanga Region, Tanzania. Tanzan J Health Res 10(4):189–202, 2008.    49.  Johnson GJ, Vatassery GT, Finkel B, et al: High-dose vitamin E does not decrease the
                    12.  Snyderman SE, Holt LE Jr, Carretero R, et al: Pyridoxine deficiency in the human   rate of chronic hemolysis in glucose-6-phosphate dehydrogenase deficiency. N Engl J
                     infant. J Clin Nutr 1(3):200–207, 1953.               Med 308(17):1014–1017, 1983.
                    13.  Foy H, Kondi A: Hypochromic anemias of the tropics associated with pyridoxine and     50.  Natta CL, Machlin LJ, Brin M: A decrease in irreversibly sickled erythrocytes in sickle
                     nicotinic acid deficiency. Blood 13(11):1054–1062, 1958.  cell anemia patients given vitamin E. Am J Clin Nutr 33(5):968–971, 1980.
                    14.  Hisano M, Suzuki R, Sago H, et al: Vitamin B6 deficiency and anemia in pregnancy. Eur     51.  Tangney CC, Phillips G, Bell RA, et al: Selected indices of micronutrient status in adult
                     J Clin Nutr 64(2):221–223, 2010.                      patients with sickle cell anemia (SCA). Am J Hematol 32(3):161–166, 1989.
                    15.  McCurdy PR, Donohoe RF, Magovern M: Reversible sideroblastic anemia caused by     52.  Ren H, Ghebremeskel K, Okpala I, et al: Patients with sickle cell disease have reduced
                     pyrazinoic acid (Pyrazinamide). Ann Intern Med 64(6):1280–1284, 1966.  blood antioxidant protection. Int J Vitam Nutr Res 78(3):139–147, 2008.
                    16.  Baumann Kreuziger LM, Wolanskyj AP, Hanson CA, et al: Lack of efficacy of pyri-    53.  Ndombi IO, Kinoti SN: Serum vitamin E and the sickling status in children with sickle
                     doxine (vitamin B6) treatment in acquired idiopathic sideroblastic anaemia, including   cell anaemia. East Afr Med J 67(10):720–725, 1990.
                     refractory anaemia with ring sideroblasts. Eur J Haematol 86(6):512–516, 2011.    54.  Anderson GJ, Frazer DM, McKie AT, et al: The ceruloplasmin homolog hephaestin and
                    17.  Clayton PT: B6-responsive disorders: A model of vitamin dependency. J Inherit Metab   the control of intestinal iron absorption. Blood Cells Mol Dis 29(3):367–375, 2002.
                     Dis 29(2–3):317–326, 2006.                           55.  Graham GG, Cordano A: Copper depletion and deficiency in the malnourished infant.
                    18.  Anderson BB, Newmark PA, Rawlins M, et al: Plasma binding of vitamin B6 com-  Johns Hopkins Med J 124(3):139–150, 1969.
                     pounds. Nature 250(5466):502–504, 1974.              56.  Spiegel JE, Willenbucher RF: Rapid development of severe copper deficiency in a
                    19.  Beutler E, Srivastava SK: Relationship between glutathione reductase activity and   patient with Crohn’s disease receiving parenteral nutrition. JPEN J Parenter Enteral Nutr
                     drug-induced haemolytic anaemia. Nature 226(5247):759–760, 1970.  23(3):169–172, 1999.






          Kaushansky_chapter 44_p0651-0656.indd   655                                                                   9/17/15   6:30 PM
   675   676   677   678   679   680   681   682   683   684   685