China
Africa
Explore chapters and articles related to this topic
Unexplained Fever In Hematologic Disorders Section 1. Benign Hematologic Disorders
Published in Benedict Isaac, Serge Kernbaum, Michael Burke, Unexplained Fever, 2019
An infrequent cause of iron deficiency is massive hemosiderinuria. Loss of iron in the urine is the result of repeated intravascular hemolysis. Such rare disorders as black water fever due to malaria falciparum or paroxysmal nocturnal hemoglobinuria or valvular aortic disease may cause iron deficiency. In such cases, there may be no reticulocytosis as the hemolysis may be masked by an inadequate response of the iron deficient bone marrow. It is to emphasize that bacterial virulence correlates with ability to acquire iron.53,54
Section 9
Published in Padmanabhan Ramnarayan, MCQs in Paediatrics for the MRCPCH, Part 1, 2017
Unconjugated bilirubin is elevated in haemolysis and reduces levels of haptoglobulin (a bilirubin binding protein in the serum). Intravascular haemolysis causes leakage of haemoglobin into the urine and causes haemosiderinuria in the renal tubular cells. Polychromasia is a reflection of high reticulocyte count. Relative deficiency of folate occurs due to high demand and causes a megaloblastic marrow picture.
Haematology
Published in Fazal-I-Akbar Danish, Essential Lists of Differential Diagnoses for MRCP with diagnostic hints, 2017
Findings in haemolysis:1 ↑ reticulocyte index.2 ↑ unconjugated bilirubin.3 ↑ LDH.4 ↓ or absent serum haptoglobin.5 Haemosiderinuria (in cases of moderate haemolysis).96 Haemoglobinuria (in cases of severe haemolysis).
Strategies to overcome the diagnostic challenges of autoimmune hemolytic anemias
Published in Expert Review of Hematology, 2023
Wilma Barcellini, Bruno Fattizzo
Hemolytic markers are quite known by most hematologist, and include unconjugated bilirubin, LDH haptoglobin and reticulocytes [40]. They may be variably altered in the different forms of AIHAs, mostly reflecting the acuteness of the hemolytic process and degree of intravascular versus extravascular hemolysis. Symptomatic anemia usually reflects a brisk decrease in hemoglobin, typical of wAIHA plus complement activation, mixed forms, or the fulminant warm IgM AIHAs. LDH is highly elevated, as a marker of intravascular hemolysis, related to massive complement activation until the membrane attack complex (MAC); unconjugated bilirubin, is increased as well, although to a lesser extent, and reflects extravascular hemolysis in lymphoid organs, mainly in the spleen for wAIHA and in the liver for CAD. The mechanism is the so-called antibody-dependent or complement-dependent cellular cytotoxicity by macrophages or activated lymphocytes expressing Fc or complement receptors [3,16,40,41]. CAD is more frequently a chronic disease with possible flares associated with exposure to cold or infections due to concomitant massive complement activation. Regarding cold exposure, it is important to remember that agglutination and hemolysis occur only when the optimal temperature of action of the cold IgM is compatible with body temperature particularly in acral sites [2,41]. Haptoglobin, the scavenger of free hemoglobin is invariably consumed, and is the most sensitive hemolytic marker, often remaining measurable for months; its increase and normalization is a definitely sign of full recovery of the hemolytic process. It is worth reminding the presence of free hemoglobin (when haptoglobin scavenger activity is saturated), and hemoglobinuria/hemosiderinuria (when intravascular hemolysis is intense and prolonged). Finally, as in many chronic hemolytic conditions, ferritin may be increased, particularly for transfused patients or concomitant hemochromatosis genetic mutations, even in heterozygosity [40].
Systemic loxoscelism induced warm autoimmune hemolytic anemia: clinical series and review
Published in Hematology, 2022
Brandon Calhoun, Andrew Moore, Andrew Dickey, D. Matthew Shoemaker
Urinalysis demonstrates proteinuria, hemosiderinuria, increased urobilinogen, and hemoglobinuria [4,33] (Table 4). With severe hemolysis, high concentrations of free urine hemoglobin can predispose to nephrotoxic acute tubular necrosis [21].