Anemia pathogenesis

Bia MJ, Cooper K, Schnall S, Duffy T, Hendler E, Malluche H, Solomon L. Aluminum induced anemia pathogenesis and treatment in patients on chronic hemodialysis. Kidney Int I989 36(5) 852-8. 

Malkin, D., Koren, G., 8c Saunders, E. F. (1990 Winter). Drug-induced aplastic anemia Pathogenesis and clinical aspects. The American Journal of Pediatric Hematology/Oncology, 12(4), 402—410. 

Paglia DE, Valentine WN, Dahigren JG. 1975. Effects of low-level lead exposure on pyrimidine 5 -nucleotidase and other erythrocyte enzymes Possible role of pyrimidine 5 -nucleotidase in the pathogenesis of lead-induced anemia. J Clin Invest 56 1164-1169. 

Anemia of chronic disease is a hypoproliferative anemia associated with chronic infectious or inflammatory processes, tissue injury, or conditions that release proinflammatory cytokines. The pathogenesis is based on shortened RBC survival, impaired marrow response, and disturbance of iron metabolism. For information on anemia of chronic kidney disease, see Chap. 76. 

The demonstration that iron deficiency was an important risk factor in RLS pathogenesis has led, since the 1950s, to several therapeutic attempts with iron supplements. Initially, these attempts were aimed at subjects with RLS and hyposideremia, with or without anemia later partial supplementation was also tested in patients with the idiopathic form. 

Fia. 11. Scheme of the pathogenesis of congenital Heinz body hemolytic anemia. From (J4), H. S. Jacob, Seminars in Hematology 341 (1970), with permission of the author and publisher. 

Chronic treatment with phenobarbital, phenytoin, and carbamazepine is associated with reduced serum folate concentrations. Although megaloblastic anemia is rare, macrocytic changes in red cells are common in these patients. The fact that serum folate is not reduced by valproate and zonisamide, which do not induce liver enzymes, is consistent with the hypothesis that enzyme induction plays a role in the pathogenesis of folate deficiency (99). 

Semba RD, Bloem MW. The anemia of vitamin A deficiency epidemiology and pathogenesis. Eur J Clin Nutr 2002 56 271-81. 

Patients with CKD are at increased risk of cardiovascular disease, independent of the etiology of their kidney disease. While a clearly unique pathogenesis of cardiovascular disease specific to CKD has not been identified, it is known that manifestations of kidney disease are contributory. Risk factors for cardiovascular disease in this population include hemodynamic and metabolic abnormalities, as well as hypertension, dyslipidemia, elevated homocysteine levels, anemia, hyperparathyroidism, malnutrition, and oxidative stress. Hypertension induced by volume expansion and increased systemic vascular resistance increases myocardial work and contributes to development of left ventricular hypertrophy (LVH). Hyperlipidemia may enhance atherogenesis, while some uremic toxins can decrease myocardial contractflity. In addition, uremic toxins can induce pericarditis, a potentially fatal complication. Currently, measures to screen this high-risk population for cardiovascular risk factors are not routine. ... 

Suboptimal erythropoiesis can be classified by changes in the size of RBCs noted on examination of the peripheral blood. Because the excretory and endocrine functions of the kidney usually mirror each other, renal dysfunction can lead to anemia by reduction in EPO production, resulting in a normochromic, normocytic pattern. Other causes of insufficient erythropoiesis include replacement of bone marrow by fibrosis, solid tumors, or leukemia, as well as defects in erythroid maturation. Relative deficiencies in the cofactors required for heme-RBC synthesis such as iron, folate, and vitamin B may also be important contributors. Structurally, RBC macrocytosis denotes defects in the maturation of the nucleus, whereas microcytosis is indicative of cytoplasmic defects (reduced hemoglobin synthesis). (A detailed description regarding the pathogenesis and treatment of anemic disorders is found in Chap. 99.)... 

ACD is a hypoprolrferative anemia that has traditionally been associated with infectious or inflammatory processes, tissue injury, or conditions associated with the release of proinflammatory cytokines. Alternative names include anemia of inflammation and cytokine-mediated anemia. The pathogenesis of the anemia of chronic disorders is based on three abnormalities shortened erythrocyte survival, impaired marrow response, and disturbance of iron metabolism. Pathologically, the RBCs have a shortened life span, and the bone marrow s capacity to respond to EPO is inadequate to maintain normal Hgb concentration. The cause of this defect is still uncertain, but appears to involve a block in the release of iron from the reticuloendothelial cells of the marrow. Various cytokines, such as interleukin-1, interferon-y, and tumor necrosis factor released during these illnesses may inhibit the production or action of EPO or the production of RBCs. ... 

Moore RD. Anemia and human immunodeficiency virus disease in the era of highly active antiretroviral therapy. Semin Hematol 2000 37 18-23. Means RT, Krantz SB. Progress in understanding the pathogenesis of the anemia of chronic disease. Blood 1992 80 1639-1647. 

So far, laboratory studies have failed to detect any disorder as a specific marker for early detection of the disease or a reliable indicator for differential diagnosis. Laboratory studies have confirmed that Balkan nephropathy is a tubulointerstitial disease so that tubular disorders precede impairment of glomerular filtration. Although anemia is one of the criteria for the diagnosis of the disease, it has not been evidenced that pathogenesis and features of this anemia differ from that observed in other chronic renal diseases. It is only more severe in end-stage Balkan nephropathy patients than in patients with other kidney diseases. 

E. Ivanov, M. Pisanets (1982). Studies on the biosynthesis of porphyrins in erythrocytes after incubation with -aminolevulinic acid An attempt to investigate the pathogenesis of nephrogenic anemia. Acta Biol. Med. Germ., 41, 307-313. 

Singer K. 1951. The pathogenesis of sickle cell anemia A review. Am. J. Clin. Pathol. 21, 858. 

Table 3-2. Pathogenesis of sickle cell anemia Dominant autosomal gene...

Knowledge of the molecular alteration in sickle cell anemia has contributed to an understanding of the pathogenesis of the disease and has also generated some hope for therapy. Two compounds have been used in the treatment of sickle cell anemia urea and cyanate. 

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