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Overview of hypersensitivity
Published in Gabriel Virella, Medical Immunology, 2019
Intravascular hemolysis is associated with release of free hemoglobin into the circulation (hemoglobinemia), which may be excreted in the urine (hemoglobinuria). Massive hemoglobinuria can induce acute tubular damage and kidney failure, usually reversible. In contrast, extravascular hemolysis is usually associated with increased levels of bilirubin, derived from cellular catabolism of hemoglobin. All hemolytic reactions usually lead to the mobilization of erythrocyte precursors from the bone marrow to compensate for the acute loss. This is reflected by reticulocytosis and, in severe cases, by erythroblastosis.
Concepts of Replacement Therapy: Blood Components, Blood Derivatives, and Medications
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Acute hemolytic reactions can be the result of either immune or nonimmune mechanisms. Immune-mediated hemolytic reactions usually occur when incompatible red blood cells are transfused into a patient with a preexisting antibody. These antibodies, usually a naturally occurring IgM antibody to the group A or B antigens, fix and activate the complement cascade, resulting in intravascular lysis of the red blood cell membrane. Free hemoglobin is released, leading to hemoglobinemia and hemoglobinuria. The potent antigen–antibody interaction also leads to other metabolic pathways that can result in serious clinical effects. These include activation of the coagulation cascade, a neuroendocrine response, and release of complement-derived anaphylatoxins and cytokines. The manifestations of these reactions can result in fever, hypotension and shock, bronchospasm, DIC, and renal failure. Table 3 illustrates the management of a patient when an acute hemolytic reaction is suspected (30).
Primaquine
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Michael D. Edstein, G. Dennis Shanks
The degree of hemolysis induced by primaquine in G6PD-deficient individuals varies with the type of G6PD deficiency and the quantity of primaquine administered. In individuals with the African variant A− form of G6PD deficiency, 15 mg daily for 14 days generally produces a mild, self-limiting, and asymptomatic anemia owing to hemolysis of older red blood cells. In these subjects, hemolysis usually starts 3–4 days after the first dose of primaquine and lasts about 7 days. The African variant A− may be found in up to 10–15% of Africans or African Americans. A 45 mg weekly dose of primaquine over 8 weeks does not cause clinically significant hemolysis in variant A– individuals (Brewer and Zarafonetis, 1967). However, serious hemolysis may occur in individuals with the Mediterranean and Asian variant B− forms and can result in progressive, potentially fatal hemoglobinemia and hemoglobinuria (Clyde, 1981). High levels of hemolysis have been reported in variant B−individuals after a primaquine course of 15 mg daily (Aung Than et al., 1970) or 45 mg single dose (Pannacciulli et al., 1969; Reeve et al., 1992).
The rare Ogilvie’s Syndrome in pregnancy. How to manage? A case report and literature review
Published in Journal of Obstetrics and Gynaecology, 2022
Vittorio Bresadola, Pier Paolo Brollo, Michele Graziano, Carlo Biddau, Tommaso Occhiali, Lorenza Driul
A 37-year-old pregnant patient (30 weeks, P2G4), without a relevant clinical history, presented to the Emergency Department for feelings of abdominal distension with sporadic episodes of cramp-like pain in the lower quadrants, associated with closed alvus and inability to pass stool or gas for four days. The patient reported only one episode of vomiting and no fever in the previous days. The vital parameters of the pregnant woman and the foetus were substantially normal. Clinical examination revealed swelling in the upper quadrants of the abdomen, non-painful superficial and deep palpation on all quadrants, increased entero-colic tympanism, and absence of peristalsis with occasional metallic bowel sounds. Upon digital rectal exploration, the ampoule was empty and without traces of blood. Cardiopulmonary assessment was unremarkable. Laboratory tests at the time of admission showed an increase in inflammation indices (WBC 12630/µL, CRP 25.25 mg/L), hemoglobinemia of 11.0 g/dL, mild hypokalaemia (3.43 mEq/L), and arterial lactate 1.6 mEq/L. An urgent ultrasound of the abdomen revealed diffuse dilation of the small bowel loops. HCV, HBV, CMV and rubella serology results were all negative. Urine culture and urinary Legionella and Pneumococcal antigens were also negative. Plain abdominal radiography, ordered by the consultant general surgeon, revealed a dilation of the ascending colon up to about 10 cm, and dilation in the proximal tract of the descending colon of about 7−8 cm, with associated gas distension of the small bowel loops (Figure 1).
A Case of Hb Aalborg (HBB: c.223G>C) with Chronic Obstructive Pulmonary Disease: A First Familial Presentation in Japan
Published in Hemoglobin, 2021
Kei Takamura, Taku Komori, Yuiko Hashino, Takatoshi Suzuki, Ai Shiwaku, Hajime Kikuchi, Makoto Yamamoto, Hidetoshi Yamauchi, Yasuhiro Yamashiro
We subjected the Hb extracted from the hemolysate to reverse-phase HPLC. The optical density of the eluting solution showed an abnormal peak between the heme and normal β-globin peaks. The estimated Hb ratio was Hb A 61.0%, Hb F 1.0%, Hb A2 2.8%, and unknown Hb 27.0% (Figure 2). We therefore concluded that the patient carried an unknown β chain variant. The sample was sent to Yamaguchi University, Yamaguchi, Japan for further analysis to determine the membrane properties of the erythrocytes. The median glycerol lysis time (GLT50) was within the normal range. Heinz bodies were not detected, however, the isopropanol test was weakly positive, suggestive of a hemoglobinopathy. The cellulose acetate membrane electrophoresis of Hb and isoelecric focusing yielded an abnormal band between Hb F and Hb S (HBB: c.20A>T), the same as our data. These findings strongly suggested an unstable hemoglobinemia.