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This excess cellular iron deposition ultimately exceeds the capacity of iron-binding proteins generic lamictal 25 mg symptoms when pregnant, thereby leading to cellular damage buy lamictal 100mg on line medication 3 checks, organ dysfunction order 50 mg lamictal visa symptoms yellow fever, and eventually to clinical symptoms cheap lamictal 200 mg online symptoms 5 weeks 3 days. Introduction Iron is an essential metal for many biological processes due to its Ferritin is the primary intracellular iron storage protein, which ability to transfer electrons in reduction/oxidation reactions. This forms multimeric complexes that facilitate iron sequestration and reactivity also provides the potential for great damage to biological mobilization depending on cellular need. In contrast, hemosiderin is systems if iron is not chaperoned through a tightly regulated an amorphous and poorly bioavailable iron-containing conglomer- network of iron-binding proteins and transporters. If the capacity of ate the presence of which is generally a pathologic sign of cellular these iron-binding proteins is exceeded, “free” iron is capable of iron excess. A soluble form of ferritin is also found in the plasma forming reactive oxygen species that may damage macromolecular and is expelled primarily from reticuloendothelial macrophages and cellular components such as nucleic acids, proteins, and lipids and the liver; however, its biological role remains unclear. Iron homeostasis in humans is maintained ferritin correlates with iron stores in many conditions; however, almost exclusively at the level of intestinal absorption because caution must be taken before interpreting in the setting of inflamma- evolution has not provided a physiologically regulated mechanism tion and cellular injury. The large size and electrochemical properties of iron require that it Iron homeostasis be transported across the mammalian cell membranes by specific transmembrane proteins that mediate cellular iron uptake (import) Iron recycling and storage and iron release (export). Although hepatocytes, intestinal mucosal The primary role of iron in mammals is to provide a binding site for cells, and macrophages possess specific carriers for iron import and oxygen in the heme moiety of hemoglobin. The average adult male export, erythroid cells only import iron and do not “release” iron has a total body iron content of 4g, 2/3 of which is contained in until they are lysed or phagocytosed within the reticuloendothelial the erythroid compartment. When iron stores are depleted through decreased dietary intake cyte cytoplasm as ferritin and the remainder is exported through the or intestinal absorption, increased requirements (eg, pregnancy) or enterocyte basolateral membrane into the plasma via the transmem- loss (eg, intestinal blood loss), erythropoiesis becomes iron re- brane iron exporter ferroportin (FPN; described more fully in the stricted and eventually results in the characteristic microcytic, Cellular iron export section). In contrast, erythropoiesis in most iron overload states is relatively unperturbed; however, Nonheme iron is imported into nonintestinal cell types from the HFE hemochromatosis is associated with increases in hemoglobin, plasma by the transferrin (TF) cycle (for review, see Chen and 202 American Society of Hematology Paw6). Almost all plasma iron exists bound to the abundant hepcidin leads to enhanced intestinal absorption and macrophage glycoprotein TF. Each TF molecule binds 2 Fe3 iron atoms with iron release, elevated plasma iron levels, and iron loading. The TF cycle begins with Hepcidin exerts its central role in iron homeostasis through its iron-loaded plasma TF binding with high affinity to TF receptor 1 effect on FPN, the only known receptor for hepcidin and cellular (TFR1) on the cell surface and being endocytosed. Hepcidin binds to FPN at the cell surface, resulting then acidified, prompting the release of iron from TF and the empty in endocytosis and lysosomal degradation,19 blocking of iron TF and TFR1 return to the cell surface and are available to repeat the efflux into the plasma, hypoferremia, and iron-restricted cycle again. The unbound Fe3 iron in the acidified endosome is erythropoiesis. Clinically, plasma hepcidin concentration is modulated by several “regulators. It is unclear whether intestinal heme absorption uses The physiologic regulation of hepcidin expression is controlled at membrane-bound transporters or endocytic uptake. Although a responsive gene-1, (HRG-1), initially identified by homology to great deal remains to be elucidated regarding the molecular control heme transporters found in Caenorhabditis elegans. Most intracellular heme will have its iron liberated Hepcidin regulation by plasma iron and tissue iron stores is by hemoxygenase, allowing storage in ferritin or export via FPN. In the of cellular detoxification and transfer of heme between cells. The sensor for iron repletion is not nearly as clear, but (MRP-5)13 have been implicated as heme exporters. The only known mammalian iron exporter is FPN,14,15 which is expressed at all sites involved in cellular Fe2 Hepcidin up-regulation by inflammation appears independent of iron export to the plasma, including the basolateral membranes of 16 BMP6 and HJV and mediated by inflammatory cytokines, espe- duodenal enterocyte, macrophages, hepatocytes, and in the placenta. These enzymes oxidize 24 2 3 fully activate hepcidin. The inflammatory cytokine Activin B also exported Fe iron, returning it to its Fe state and thus promoting induces SMAD signaling and acts synergistically with IL-6 JAK2/ its binding to plasma TF. Deficiencies of these ferroxidases appear 25 STAT-3 signaling to up-regulate hepcidin expression. The most commonly held hypothesis is that the tinal iron absorption, cellular iron import/export, and iron storage. BM produces a hepcidin-suppressing mediator in response to Because humans have no physiological mechanism for iron excre- physiologic erythropoietin or pathophysiologic ineffective erythro- tion, the control of intestinal iron absorption is the primary poiesis. Growth differentiation factor 15 (GDF15) and twisted- mechanism for determining overall iron balance. A small fraction of gastrulation 1 (TWSG1) are BMP family members postulated to be dietary iron is imported into the enterocyte and only a fraction is suppressors of hepcidin in thalassemia26,27; however, their contribu- exported from the enterocyte into the plasma. Inappropriately elevated levels of liver and filtered into the urine. As a negative regulator, decreased iron-refractory iron deficiency anemia). Conversely, inappropriately Hematology 2014 203 Figure 1. Hepcidin is a common effector of 4 known regulators of iron homeostasis. Iron stores, erythropoietic demand, hypoxia, and inflammation all act by modulating hepatocyte production of hepcidin. Increased iron stores and inflammation both appear to increase hepcidin expression, primarily through signal transduction via the SMAD and JAK/STAT pathways, respectively. Increased/ineffective erythropoietic drive and hypoxia appear to decrease hepcidin expression, although the mechanisms of their control of hepcidin expression remain to be fully elucidated. Although HFE hemochromatosis has a worldwide distribution, it is Iron overload states the most common autosomal recessive disorder of northern Euro- Although the earth is an iron-rich environment, acquired iron pean heritage, apparently having descended from a common Celtic ancestor. The estimated iron metabolism result in iron overload rather than iron deficiency. Clinically significant hereditary iron overload is almost exclusively an adult phenomenon, but there are rare pediatric forms. Some clinical laboratories commonly report other HFE mutations. A summary of these disorders and their genetics can be found in The p. His63Asp (H63D) amino acid substitution is occurs in 20% Table 1. Ser65Cys (S65C) amino acid substitution is also reported by some, but the clinical relevance is HFE hemochromatosis not clear. Other very rare (“private”) HFE mutations can be found in Originally recognized in the mid-19th century, this form of heredi- trans to the C282Y and can explain some cases of rapid iron overload out of keeping with the C282Y carrier status. HFE is widely expressed and is known to bind with TFR131 to decrease its affinity for iron-loaded TF. Only a small fraction of matosis, whichi s associated with a predilection for hepatocellular C282Y/H63D heterozygotes appear to develop biochemical evi- iron deposition. FPN1 hemochromatosis FPN1 hemochromatosis appears to be the most common form of HFE hemochromatosis was classically described as the triad of 51 non-HFE hemochromatosis. It is distinguished from other iron cirrhosis, diabetes mellitus, and skin hyperpigmentation developing th th overload disorders by its autosomal-dominant inheritance and 2 in the in the 4 -7 decade of life and thus earning the description phenotypic subtypes depending on the functional consequences of “bronze diabetes. Serum ferritin levels rise early and quency of classically related nonspecific symptoms (eg, fatigue, out of proportion to TF saturation, a pattern in contrast to the early arthralgias, affective disorders) and symptoms of end organ damage elevation in TF saturation seen in HFE hemochromatosis. Although (eg, cardiomyopathy, arrhythmias, diabetes mellitus, sexual dysfunc- 41 FPN1 hemochromatosis is generally milder than HFE hemochroma- tion) are uncommon, and in one study they did not differ 37 tosis, the complete spectrum of iron overload morbidity has been significantly from wild-type controls.

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Zolpidem dependence in a patient with former polysubstance abuse buy cheap lamictal 50 mg symptoms stomach flu. Zolpidem dependence case series: Possible neurobiological mechanisms and clinical management purchase lamictal 100 mg visa medicine dictionary prescription drugs. Three cases of zolpidem dependence treated with fluoxetine: the serotonin hypothesis 100 mg lamictal mastercard medicine gif. Zolpidem tolerance and dependence - Two case reports lamictal 25mg with visa treatment yellow tongue. Sakkas P, Psarros C, Masdrakis V, Liappas J, Christodoulou GN. Vartzopoulos D, Bozikas V, Phocas C, Karavatos A, Kaprinis G. Insomnia Page 55 of 86 Final Report Update 2 Drug Effectiveness Review Project 160. Haasen C, Mueller-Thomsen T, Fink T, Bussopulos A, Reimer J. Zopiclone dependence after insomnia related to torticollis. A case of parenteral zolpidem dependence with opioid-like withdrawal symptoms. International Journal of Psychiatry in Clinical Practice. Quaglio G, Lugoboni F, Fornasiero A, Lechi A, Gerra G, Mezzelani P. Dependence on zolpidem: Two case reports of detoxification with flumazenil infusion. Physical dependence following zopiclone usage: A case report. Hajak G, Muller WE, Wittchen HU, Pittrow D, Kirch W. Abuse and dependence potential for the non-benzodiazepine hypnotics zolpidem and zopiclone: A review of case reports and epidemiological data. New-onset transient hallucinations possibly due to eszopiclone: a case study. Primary Care Companion to the Journal of Clinical Psychiatry. Zaleplon overdose associated with sleepwalking and complex behavior. Journal of the American Academy of Child & Adolescent Psychiatry. Incidence of cancer in individuals receiving chronic zopiclone or eszopiclone requires prospective study. Fatal overdose of zopiclone in an elderly woman with bronchogenic carcinoma. Zopiclone withdrawal: an unusual cause of delirium in the elderly. Zolpidem, vascular headache, and hallucinations in an adolescent. Insomnia Page 56 of 86 Final Report Update 2 Drug Effectiveness Review Project 180. Amnesia possibly associated with zolpidem administration. Worsening hepatic encephalopathy secondary to zolpidem. Zolpidem-associated hallucinations and serotonin reuptake inhibition: a possible interaction. Zolpidem-related delirium: A case report Journal of Clinical Psychiatry. Zolpidem-induced delirium with mania in an elderly woman. Journal of the American Academy of Child & Adolescent Psychiatry. Zolpidem and hallucinations Annals of Emergency Medicine. Amnestic sleep-related eating disorder associated with zolpidem. Zolpidem after long-acting benzodiazepines: Possible interaction. Zolpidem-induced psychosis in an older woman Journal of the American Geriatrics Society. Somnambulism due to probable interaction of valproic acid and zolpidem. Insomnia Page 57 of 86 Final Report Update 2 Drug Effectiveness Review Project 201. Toner LC, Tsambiras BM, Catalano G, Catalano MC, Cooper DS. Central nervous system side effects associated with zolpidem treatment. Tripodianakis J, Potagas C, Papageorgiou P, Lazaridou M, Matikas N. A Novel Clinical Pattern of Visual Hallucination after Zolpidem Use. Visual hallucinations and amnesia associated with the use of zolpidem International Journal of Clinical Pharmacology and Therapeutics. One rare side effect of zolpidem--sleepwalking: a case report. Zolpidem addiction in a pregnant woman with a history of second-trimester bleeding. Progress in Neuro-Psychopharmacology & Biological Psychiatry. Pseudohallucinations after zolpidem intake: a case report. Visual hallucinations and amnesia associated with zolpidem triggered by fluvoxamine: a possible interaction. Letsas KP, Filippatos GS, Kounas SP, Efremidis M, Sideris A, Kardaras F.

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CGI scores did not show significant differences generic 25mg lamictal visa symptoms 9f diabetes, but MADRS score were significantly greater at week 1 in the mirtazapine group generic lamictal 100 mg otc hb treatment. The Changes in Sexual Functioning Questionnaire did not show significant differences although for mirtazapine the trend was positive cheap 25 mg lamictal fast delivery treatment non hodgkins lymphoma. A significantly higher number of patients withdrew because of adverse events in the mirtazapine group (12 buy cheap lamictal 25 mg line treatment interventions. Venlafaxine compared with citalopram A fair European 6-month study compared venlafaxine ER (37. No statistical differences in any outcome measures (MADRS, CGI-S, CGI-I) could be detected at study endpoint. The remission rates were 19 percent for venlafaxine and 23 percent for citalopram. Both treatment groups reached a 93 percent response rate. Venlafaxine compared with escitalopram Two fair 8-week studies assessed the comparative effectiveness of venlafaxine XR and 93, 94 escitalopram. A fair European, multinational study assigned 293 patients to escitalopram 93 (10-20 mg/d) or venlafaxine XR (75-150 mg/d). Results presented no statistically significant differences in response (venlafaxine XR: 79. Survival analysis of the intention-to-treat population indicated that escitalopram-treated patients achieved sustained remission 6. Significantly more patients on venlafaxine XR than on escitalopram reported nausea (26% compared with 17%; P<0. No statistically significant differences were apparent between venlafaxine XR and escitalopram in response (48% compared with 58. Significantly more patients in the venlafaxine group withdrew because of Second-generation antidepressants 28 of 190 Final Update 5 Report Drug Effectiveness Review Project adverse events (16% compared with 4%; P<0. Venlafaxine compared with fluoxetine A South American multicenter study with a good quality rating randomized 382 patients to 95 venlafaxine (75-150 mg/d) or fluoxetine (20-40 mg/d) for 8 weeks. Patients were predominantly female and moderately to severely ill. The majority had a previous history of depression (venlafaxine, 79. LOCF analysis yielded no significant differences between study groups in any primary efficacy measures (HAM-D, MADRS, CGI, Hopkins Symptom Checklist). Both treatment groups showed significant decreases of HAM-D and MADRS scores from baseline (P<0. Response rates were similar in both treatment groups (venlafaxine, 80. No significant differences in adverse events were observed. Three fair-rated studies reported mixed results about the efficacy of venlafaxine and 96, 97 98, 99 fluoxetine in comorbid patients with high anxiety or GAD. Only one study reported significantly greater response rates on HAM-D (71. All three studies presented greater improvements on anxiety scales (HAM-A, Covi Anxiety Scale) in patients treated with venlafaxine than with fluoxetine. However, differences were only statistically significant in one trial (Covi Anxiety 96 scale: P=0. Two studies reported significantly more dizziness (P<0. Seven additional trials also provided predominantly consistent evidence on a similar 45-48, 100-102 efficacy of venlafaxine and fluoxetine. Only one study reported a significantly higher 101 response rate of venlafaxine than fluoxetine (72% compared with 60%; P=0. Three 46, 48, 95 studies were excluded because of missing data. The main outcome measure was the response to treatment on HAM-D at study endpoint. Results (Exhibit 5), based on 2,593 patients, show no statistical difference between venlafaxine and fluoxetine (RR 0. Funnel plot, Kendell’s test, and L’Abbe plot did not indicate major biases. However, given the small number of component studies results of these tests must be viewed cautiously. These findings are similar to results of a meta-analysis recently reported by Smith et al. Venlafaxine showed a modest but statistically significantly greater standardized effect size (-0. The OR for response was numerically greater for venlafaxine but did not reach statistical significance (OR: 1. This study included inpatients and therefore did not meet the eligibility criteria for this report. Venlafaxine compared with paroxetine 104, 105 Two fair studies compared venlafaxine to paroxetine. A Spanish study compared venlafaxine (75-150 mg/d) to paroxetine (20-40 mg/d) in outpatients (N=84) with either MDD or 104 dysthymia over 24 weeks. The percentage of dysthymic patients was not reported, and the authors did not differentiate between dysthymia and Second-generation antidepressants 29 of 190 Final Update 5 Report Drug Effectiveness Review Project mild or moderate depression. Loss to follow-up was 32 percent, with a substantially higher loss to follow-up in the venlafaxine group (39% compared with 26%). Intention-to-treat analysis yielded no significant differences between treatment groups on any primary outcome measures (HAM-D, MADRS, CGI) at 24 weeks. However, sample size for this study was small, and it was underpowered because it had been designed as a pilot study. A 12-week, British fixed-dose trial randomized 361 mainly moderately ill patients (based on CGI severity score) treated in 43 general practices to either venlafaxine XR (75 mg/d) or 105 paroxetine (20 mg/d). Results revealed no significant differences in efficacy measures, quality of life scores, or adverse events between study groups. Venlafaxine compared with sertraline 106, 107 37 Two good trials and one fair trial compared the efficacy of sertraline to venlafaxine. A good quality Scandinavian trial compared venlafaxine (75-150 mg/d) to sertraline (50-100 mg/d) 107 in 147 patients who were mainly moderately to markedly ill. Study duration was 8 weeks; loss to follow-up was 19 percent. Both treatment groups showed statistically significant reductions in MADRS, HAM-D, and CGI scores. Response rates on the HAM-D scale were higher for venlafaxine at the endpoint (83% compared with 68%; P=0.

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It is very encouraging to witness recent developments in our Semin Thromb Hemost purchase 100mg lamictal with amex medicine 513. Efficacy and safety of low-dose that these new options can provide to patients purchase lamictal with paypal medicine xalatan. Correlation of blood counts combined with data from clinical trials underpin these improve- with vascular complications in essential thrombocythemia: analysis of the prospective PT1 cohort best purchase for lamictal medicine you can take while breastfeeding. There is an urgent need to complete studies to assess the 15 generic 200mg lamictal free shipping symptoms 9 days before period. Hydroxyurea compared with relative benefits of HU and IFN as first-line therapies for both ET anagrelide in high-risk essential thrombocythemia. A greater understanding of the biological aspects of these 2005;353(1):33-45. Anagrelide compared patients in need of novel therapies and to the development of more with hydroxyurea in WHO-classified essential thrombocythemia: the meaningful and practical trial end points. Bone marrow pathology in Disclosures essential thrombocythemia: interobserver reliability and utility for Conflict-of-interest disclosures: C. Distinct clustering of symptom- Gilead, and SBio; has received honoraria from Novartis and Sanofi; atic burden amongst myeloproliferative neoplasm patients: retrospective and has been affiliated with the speakers’ bureau for Novartis, assessment in 1470 patients. Development and validation of Off-label drug use: JAK inhibition and other novel therapies such as an International Prognostic Score of thrombosis in World Health Smo inhibitors for management of thrombocytosis. A prospective study of 338 Correspondence patients with polycythemia vera: the impact of JAK2 (V617F) allele Claire Harrison, Department of Haematology, Guy’s and St Thomas’ burden and leukocytosis on fibrotic or leukemic disease transformation Foundation Trust, London SE1 9RT, UK; Phone: 442071882742; and vascular complications. Observation versus antiplatelet therapy as primary prophylaxis for thrombosis in low-risk essential thrombocythemia. Somatic CALR mutations in venous haematocrit in primary proliferative polycythaemia. Revised response criteria for regarding WHO-defined diagnosis of early/prefibrotic primary myelofi- polycythemia vera and essential thrombocythemia: an ELN and IWG- brosis versus essential thrombocythemia. Diagnosis and management of congenital and idiopathic patterns for essential thrombocythemia in Europe. Experience with pegylated in a family with hereditary thrombocytosis. CALR and ASXL1 progenitors suggests that pegylated interferon alpha-2a treatment targets mutations-based molecular prognostication in primary myelofibrosis: an JAK2V617F clones without affecting TET2 mutant cells. Quintas-Cardama A, Kantarjian H, Manshouri T, et al. Pegylated mutations on clinical and hematological phenotype and outcome in interferon alfa-2a yields high rates of hematologic and molecular essential thrombocythemia. Efficacy and safety of tracking of minimal residual disease in JAK2-V617F-associated my- AOP2014/P1101, a novel, investigational mono-pegylated proline- eloproliferative neoplasms: a joint European LeukemiaNet/MPN&MPNr- interferon alpha-2b, in patients with polycythemia vera (PV): update on EuroNet (COST action BM0902) study. Hernandez-Boluda JC, Alvarez-Larran A, Gomez M, et al. Clinical droxyurea (HU): the RESPONSE trial [abstract]. Serious adverse events during ruxolitinib essential thrombocythaemia. CEP-701 in patients with JAK2 V617F-positive PV and ET: update of 38. A phase II study of 39 enrolled patients [abstract]. A phase II study of the JAK1/ JAK2 inhibitor, INCB018424, in patients with polycythemia Givinostat in combination with hydroxycarbamide in patients with vera (PV) and essential thrombocythemia (ET) refractory or intolerant polycythaemia vera unresponsive to hydroxycarbamide monotherapy. A phase 2 study of induces and maintains substantial hematologic and molecular responses ruxolitinib, an oral JAK1 and JAK2 Inhibitor, in patients with advanced in patients with essential thrombocythemia (ET) who are refractory or polycythemia vera who are refractory or intolerant to hydroxyurea. Guideline for investigation and prospective, randomized, open-label phase 3 study of ruxolitinib (RUX) management of adults and children presenting with a thrombocytosis. When the microorganism enters the RBC directly, RBC damage becomes a fundamental aspect of the disease process. Malaria is the best example of an organism that directly targets the RBC, but others are Babesia and Bartonella. RBCs can also be indirect targets of infectious agents. This can occur when molecules are bound to the surface of the RBC, leading to immunologic clearance; when microorganism- produced toxins damage the RBC membrane, leading to hemolysis; when previous crypt-antigens are exposed, leading to accelerated removal; when microorganism-produced toxins alter RBC antigens to a different phenotype, or when microorganism suppression of erythropoiesis occurs due to specific binding to RBC precursors. Learning Objective There is rossetting of parasitized cells, with nonparasitized cells ● To understand the variety of infectious agents that affect leading to complement activation on the uninfected RBCs and RBCs directly or indirectly. Several uninfected RBCs are removed from the circulation for each parasite infected RBC, thus magnifying the extent of hemolysis. The osmotic fragility of Introduction nonparasitized cells is increased. Infected RBCs also develop some This chapter reviews the obvious infections in which microorgan- modified receptors binding to endothelial proteins, platelet glycopro- isms specifically enter the RBC and also addresses infectious teins, thrombospondin, intracellular adhesion molecule 1, and some situations in which the RBC may be altered or damaged secondarily vascular adhesion molecules. Litchman1 lists 39 infectious agents that cause hemolytic Infected cells also have a highly irregular surface and there is anemia. Some organisms invade the RBC and others damage the activation of hepatosplenic macrophages that increases RBC clear- RBC, causing premature clearance; cause hemolytic anemia from ance. There are changes on the surface of both parasitized and the hemolysins that they produce or by stimulating an immune nonparasitized RBCs that increase RBC recognition and thus response due to alterations of the RBC surface; stimulate antibodies phagocytosis. The loss of RBC deformity in the parasitized cells to RBC antigens; or deposit immune complexes, causing increased leads to shortened RBC survival. Because this discussion focuses on the RBC, the other IgG and complement on the RBC surface, which also increases diseases are not discussed in detail. RBCs as primary targets of infection (Table 1) Role of the Fy (Duffy) blood group antigens in malaria. Duffy Malaria antibodies are commonly encountered in routine blood banking Upon infection, malaria parasites multiply in hepatocytes and the and transfusion medicine. The Duffy system is composed of 6 engorged cells rupture, releasing merozoites into the circulation. This is a multistep process involving several different and disruption of chemokine gradients. Plasmodium falciparum, the most serious form of for P. In the absence of the malaria, uses multiple ligands, one of which involves the glyco- Duffy molecule, the parasites are not able to establish a junction phorins (GPs) A, B, and C. Therefore, individuals with the Duffy null phenotype receptor containing the Duffy antigen receptor for chemokines Fy(a,b) in which DARC is absent from RBCs, are resistant to (DARC). Low rates of parasitemia may have little frequency varies in different populations and, not surprisingly effect on causing anemia, whereas high rates in which 10% of the Fy(a,b) phenotype is very common, approaching 100% in RBCs are parasitized may cause significant hemolysis. Within the RBC, the parasites multiply, ultimately bursting the RBC Role of ABO blood group antigens in malaria. One of the and releasing more merozoites to invade other RBCs.