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With the results of the START study (see ART chapter) purchase 40 mg propranolol mastercard blood vessels more visible, almost all patients will begin ART discount propranolol 40 mg fast delivery cardiovascular stress test. The current EACS guidelines (November 2014) recommend to screen for and, when appropriate, to perform the diagnostic steps for HAND. In case of established diag- nosis, CNS-active drugs should be considered. The US DHHS guidelines (April 2015) recommend to initiate ART at any stage of HIV infection, but does not recommend specific antiretroviral drugs in HAND-affected patients. Some evidence suggests an early initiation of ART for the prevention of HAND (Ellis 2011), but the value of CNS-penetrating compounds is unclear. Depression is frequent in HIV infection (Pence 2012). Depressed people tend to over- report cognitive symptoms (Thames 2011), while on formal testing, a skilled neuropsychologist/neurologist will find normal or near-normal cognition. Patients complaining of cognitive symptoms should therefore be examined for depression as the depression may actually be the cause of the cognitive complaints (so called “pseudodementia”). HIV-1-associated Neurocognitive Disorder (HAND) and Myelopathy 633 Table 5: Differential diagnoses of HIV encephalopathy and diagnostic workup Condition Adequate diagnostic step (commentary) Neurosyphilis Antibody testing and CSF analysis (pleocytosis >15/μl) (serological findings may be atypical for active neurosyphilis) CMV encephalitis CSF (pleocytosis, potentially granulocytic; decreased glucose elevated total protein) PCR for CMV in CSF, CMV antigen (pp65) in blood antibody testing in blood and CSF (IgG and antibody index may be increased) MRI (potentially subependymal hyperintensity and contrast enhancement) Occurs mostly in association with manifestation of other organs (retinitis, colitis, pneumonitis, esophagitis) Toxoplasmosis CT / MRI (single or multiple lesions found most frequently in basal ganglia or thalamus, space occupying effect, edema, frequently with contrast enhancement [patchy or ring-shaped]) Presence of toxoplasma specific IgG in blood and CSF (rarely total seronegativity). PCR for Toxo DNA in CSF has low sensitivity (Disease may rarely run as diffuse microglial nodule encephalitis) Primary CNS CT / MRI (single or multiple lesions most frequently adjacent to ventricles, lymphoma space occupying effect, edema, contrast enhancement) CSF cytology EBV PCR in CSF (HIV-associated CNS lymphomas EBV-induced) PET or SPECT (tracer enhancement in lesion) VZV encephalitis CSF (marked inflammatory signs) VZV specific IgG in blood and CSF (IgM may be absent) VZV PCR in CSF Mostly antecedent or accompanying cutaneous zoster lesions Cryptococcal CSF (opening pressure frequently elevated, cell count and protein may be meningitis normal), India ink stain Cryptococcal antigen in blood and CSF, fungal culture Tuberculous meningitis CSF, culture, PCR for mycobacteria and other bacterial appropriate tests infections Progressive multifocal MRI (single or multiple lesions of white matter, no space occupying effect, leukoencephalopathy no edema, no contrast enhancement) (PML), classical form CSF (no signs of inflammation but PCR for JC virus positive) PML in the context of MRI (white matter lesions with contrast enhancement, space occupying immune reconstitution effect) inflammatory syndrome CSF (variable signs of inflammation, JCV DNA PCR positive) Intoxication Determination of drug levels / screening for illicit drugs Metabolic Determination of electrolytes, renal and hepatic markers, hormones encephalopathy and (thyroid, cortisol), blood count, vitamin B12 deficiency impaired general Hypoxemia? The histopathological hallmarks are prominent vacuoles in the cervical and thoracic parts of the spinal cord and lipid- laden macrophages, hence the term “vacuolar myelopathy” (Petito 1985). These changes are reminiscent of severe combined degeneration (i. As HIV viral products have only inconsistently been shown to be part of the lesions, the role of HIV is uncertain. A disturbance of cobalamin-dependent transmethyla- tion has been discussed. Like HAND, HIVM occurs mainly with advanced immuno- suppression. Not all patients with autopsy findings of vacuolar myelopathy had shown clinically apparent myelopathy during life (dal Pan 1994). A patient may be suspected of having HIVM if he has a spastic-atactic gait, hyper- reflexia with positive Babinski sign, disturbance of sphincter control, erectile dys- function, and slight signs of sensory dysfunction in a glove and stocking distribu- tion. The diagnosis of an independent HIVM should only be made when the concomitant cognitive impairment is significantly less prominent than the myelopa- thy. Increased latencies of somatosensory-evoked potentials (SEP) and motor-evoked potentials on transcranial magnetic stimulation (MEP) are compatible with the diag- nosis. CSF, microbiological and spinal imaging studies are inconspicuous or non-spe- cific, and they have their importance in the exclusion of other diagnoses, as listed in Table 7. Spinal imaging should include MRI of the cervical cord and possibly the thoracic cord. Treatment Early observations of significant improvement with AZT monotherapy (Oksen- hendler 1990) were later confirmed with ART. A controlled trial showed L-methionine to bring about improvement on electrophysiological but not clinical parameters. HIV-1-associated Neurocognitive Disorder (HAND) and Myelopathy 635 Table 7: Differential diagnoses of HIV myelopathy and diagnostic workup Condition Adequate diagnostic step (commentary) Mechanic compression Degenerative changes of the cervical spine of the myelon (cervical MRI shows reduced CSF spaces around the spinal cord with hyperintense myelopathy, disk lesions of the myelon herniation) Neurosyphilis Antibody testing and CSF analysis (pleocytosis >45/3) (serological findings may be atypical) CMV myelopathy CSF (signs of inflammation), PCR for CMV in CSF Antibody testing in blood and CSF (IgG and antibody index may be increased) Toxoplasmosis Contrast enhancing cord lesion on MRI VZV myelitis CSF (marked inflammatory signs) VZV specific IgG in blood and CSF (IgM may be absent) VZV PCR in CSF Mostly antecedent or accompanying cutaneous zoster HSV myelitis CSF (inflammatory signs may be absent), HSV PCR in CSF HTLV-1 (tropical spastic Travel to the Caribbean, West Africa or East Asia paraparesis) Slow evolution of symptoms, bladder dysfunction charac-teristic, CSF inflammation, HTLV-1 specific antibodies Severe combined Vitamin B12 levels, increased MCV, homocysteine, holo-transcobalamin degeneration Heredodegenerative Appropriate tests diseases (hereditary spastic paraparesis, adrenoleukodystrophy, Friedreich ataxia, etc. An Observed Performance Test of Medication Management Ability in HIV: Relation to Neuropsychological Status and Medication Adherence Outcomes. Updated research nosology for HIV-associated neurocognitive disorders. Changes in the incidence and predictors of human immunodeficiency virus-associated dementia in the era of highly active antiretroviral therapy. Evidence for a change in AIDS dementia complex in the era of highly active antiretroviral therapy and the possibility of new forms of AIDS dementia complex. A better screening tool for HIV-associated neurocognitive disorders: is it what clinicians need? Discordance between cerebral spinal fluid and plasma HIV replica- tion in patients with neurological symptoms who are receiving suppressive antiretroviral therapy. Absence of neurocognitive effect of hepatitis C infection in HIV-coinfected people. Longitudinally preserved psychomotor performance in long-term asympto- matic HIV-infected individuals. Low prevalence of neurocognitive impairment in early diag- nosed and managed HIV-infected persons. Higher CNS penetration-effectiveness of long-term combination antiretro- viral therapy is associated with better HIV-1 viral suppression in cerebrospinal fluid. Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology 2013;62:28-35. Dynamics of cognitive change in impaired HIV-positive patients initiating antiretroviral therapy. Central nervous system antiretroviral efficacy in HIV infection: a qualitative and quantitative review and implications for future research. Clinicopathologic correlations of HIV-1-associated vacuolar myelopathy: an autopsy-based case-control study. Marked improvement in survival following AIDS dementia complex in the era of HAART. Immune activation of the central nervous system is still present after >4 years of effective highly active antiretroviral therapy. Delayed CNS virus suppression during HAART is associated with HIV encephalopathy, but not with viral drug resistance or poor CNS drug penetration. Genetic shift of env V3 loop viral sequences in patients with HIV-associ- ated neurocognitive disorder during antiretroviral therapy. HIV infection of the central nervous system is characterized by rapid turnover of viral RNA in cerebrospinal fluid. Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology 1999;20:259-264. CD4 nadir is a predictor of HIV neurocognitive impairment in the era of combi- nation antiretroviral therapy. Randomized trial of central nervous system-targeted antiretrovirals for HIV- associated neurocognitive disorder. Cliniconeuropathologic correlates of human immunodeficiency virus in the era of antiretroviral therapy. Increased microglia activation in neurologically asymptomatic HIV-infected patients receiving effective ART; An 11C-PK11195 PET study. Asymptomatic HIV-associated neurocognitive impairment increases risk for symptomatic decline. Improved neurocognitive test performance in both arms of the SMART study: impact of practice effect. Randomized controlled study demonstrating failure of LPV/r monother- apy in HIV: the role of compartment and CD4-nadir. HIV-associated neurocognitive disorders persist in the era of potent antiretroviral therapy: CHARTER Study.

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Cohort study: An observational study in which a defined group of people (the cohort) is followed over time and compared with a group of people who were exposed or not exposed to a particular intervention or other factor of interest 40mg propranolol with mastercard cardiovascular vocabulary. A prospective cohort study assembles participants and follows them into the future purchase propranolol without a prescription cardiovascular fitness benefits. A retrospective cohort study identifies subjects from past records and follows them from the time of those records to the present. Combination Therapy: The use of two or more therapies and especially drugs to treat a disease or condition. Confidence interval: The range of values calculated from the data such that there is a level of confidence, or certainty, that it contains the true value. The 95% confidence interval is generally used in Drug Effectiveness Review Project reports. If the report were hypothetically repeated on a collection of 100 random samples of studies, the resulting 95% confidence intervals would include the true population value 95% of the time. Confounder: A factor that is associated with both an intervention and an outcome of interest. Controlled clinical trial: A clinical trial that includes a control group but no or inadequate methods of randomization. Control group: In a research study, the group of people who do not receive the treatment being tested. The control group might receive a placebo, a different treatment for the disease, or no treatment at all. Convenience sample: A group of individuals being studied because they are conveniently accessible in some way. Convenience samples may or may not be representative of a population that would normally be receiving an intervention. Crossover trial: A type of clinical trial comparing two or more interventions in which the participants, upon completion of the course of one treatment, are switched to another. Direct analysis: The practice of using data from head-to-head trials to draw conclusions about the comparative effectiveness of drugs within a class or group. Results of direct analysis are the preferred source of data in Drug Effectiveness Review Project reports. Dosage form: The physical form of a dose of medication, such as a capsule, injection, or liquid. The route of administration is dependent on the dosage form of a given drug. Various dosage forms may exist for the same compound, since different medical conditions may warrant different routes of administration. Dose-response relationship: The relationship between the quantity of treatment given and its effect on outcome. In meta-analysis, dose-response relationships can be investigated using meta- regression. Double-blind: The process of preventing those involved in a trial from knowing to which comparison group a particular participant belongs. While double-blind is a frequently used term Neuropathic pain 68 of 92 Final Update 1 Report Drug Effectiveness Review Project in trials, its meaning can vary to include blinding of patients, caregivers, investigators, or other study staff. Double-dummy: The use of two placebos in a trial that match the active interventions when they vary in appearance or method of administrations (for example, when an oral agent is compared with an injectable agent). Effectiveness: The extent to which a specific intervention used under ordinary circumstances does what it is intended to do. Effectiveness outcomes: Outcomes that are generally important to patients and caregivers, such as quality of life, responder rates, number and length of hospitalizations, and ability to work. Data on effectiveness outcomes usually comes from longer-term studies of a “real-world” population. Effect size/estimate of effect: The amount of change in a condition or symptom because of a treatment (compared to not receiving the treatment). It is commonly expressed as a risk ratio (relative risk), odds ratio, or difference in risk. Efficacy: The extent to which an intervention produces a beneficial result under ideal conditions in a selected and controlled population. Equivalence level: The amount which an outcome from two treatments can differ but still be considered equivalent, as in an equivalence trial, or the amount which an outcome from treatment A can be worse than that of treatment B but still be considered noninferior, as in a noninferiority trial. Equivalence trial: A trial designed to determine whether the response to two or more treatments differs by an amount that is clinically unimportant. This lack of clinical importance is usually demonstrated by showing that the true treatment difference is likely to lie between a lower and an upper equivalence level of clinically acceptable differences. Exclusion criteria: The criteria, or standards, set out before a study or review. Exclusion criteria are used to determine whether a person should participate in a research study or whether an individual study should be excluded in a systematic review. Exclusion criteria may include age, previous treatments, and other medical conditions. External validity: The extent to which results provide a correct basis for generalizations to other circumstances. For instance, a meta-analysis of trials of elderly patients may not be generalizable to children. Studies are assumed to be measuring the same overall effect. Fixed-dose combination product: A formulation of two or more active ingredients combined in a single dosage form available in certain fixed doses. Forest plot: A graphical representation of the individual results of each study included in a meta- analysis and the combined result of the meta-analysis. The plot allows viewers to see the heterogeneity among the results of the studies. The results of individual studies are shown as squares centered on each study’s point estimate. A horizontal line runs through each square to show each study’s confidence interval—usually, but not always, a 95% confidence interval. The overall estimate from the meta-analysis and its confidence interval are represented as a diamond. The center of the diamond is at the pooled point estimate, and its horizontal tips show the confidence interval. Neuropathic pain 69 of 92 Final Update 1 Report Drug Effectiveness Review Project Funnel plot: A graphical display of some measure of study precision plotted against effect size that can be used to investigate whether there is a link between study size and treatment effect. Half- life: The time it takes for the plasma concentration or the amount of drug in the body to be reduced by 50%. Harms: See Adverse Event Hazard ratio: The increased risk with which one group is likely to experience an outcome of interest. For example, if the hazard ratio for death for a treatment is 0.

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Beclomethasone compared with flunisolide We did not identify any good or fair quality systematic reviews or head-to-head trials that compared beclomethasone to flunisolide discount propranolol 40mg online cardiovascular disease 2013 statistics. Controller medications for asthma 30 of 369 Final Update 1 Report Drug Effectiveness Review Project 4 generic propranolol 40 mg xylazine cardiovascular effects. Beclomethasone compared with fluticasone Two systematic reviews and 11 head-to-head RCTs comparing fluticasone (FP) to BDP met our 23 inclusion criteria. One systematic review included studies comparing FP compared with BDP or BUD. Of the 71 studies included in this review, 33 compared FP to BDP (nine of those 33 were included in our review). Comparisons were stratified by FP:BDP/BUD dose ratios of 1:2 or 1:1. The pooled treatment effect of FP was compared to the pooled treatment effect for BDP and BUD. For the studies conducted at dose ratios of 1:2, pooled estimates indicate that FP-treated patients had fewer symptoms, required less rescue medication, and had a higher likelihood of pharyngitis (see Key Question 2) than those treated with BDP or BUD. For the studies conducted at dose ratios of 1:1, individual studies and pooled estimates suggest no difference in symptoms, rescue medicine use, or the number of asthma exacerbations. Although we rated the quality of this review as good, the comparison of fluticasone to the combined effect of beclomethasone and budesonide limits possible conclusions regarding the specific comparison of beclomethasone to fluticasone. The review included nine studies (1265 participants) and found no statistically significant difference between treatments for symptom scores and quality of life. The single good-rated trial compared BDP 400 mcg/day (MDI-HFA) to FP 400 mcg/day (MDI) in 172 adults with mild 33 to severe persistent asthma for 6 weeks; both were medium potency doses. The trial was conducted in 30 general practice sites in the United Kingdom and Ireland. There were no significant differences in the improvement of asthma symptoms, sleep disturbance, rescue medicine use, or quality of life (AQLQ mean change from baseline) between the two groups. One was conducted exclusively in a population of 31 children and adolescents aged 4-11 and one included children, adolescents, and young adults 34 aged 4-19. Asthma severity ranged from mild- to severe-persistent. Doses ranged from low to high; all studies included comparisons of equipotent doses of BDP and FP. All but two trials assessed asthma symptoms and rescue medicine use. The majority of trials reported no difference between BPD- and FP-treated patients for the outcomes of interest reported. Four studies found FP to be better than BDP for at least one 37 36 outcome: symptoms, nighttime symptoms, rescue medicine use—increase in percent of 34 37 32 rescue free days or mean change in rescue puffs per day, or exacerbations. One study found 36 BDP-treated patients to have lower daytime symptom scores. Beclomethasone compared with mometasone 38, 39 Two fair-quality RCTs compared treatment with BDP and mometasone for 12 weeks. Both compared medium-dose BDP MDI (336 mcg/d), multiple doses of mometasone DPI (low-dose 38 200 mcg/d and medium-dose 400 mcg/d in both studies, and high-dose 800 mcg/d in only one), and placebo in patients at least 12 years old with persistent asthma. Both studies found no statistically significant differences between BDP and mometasone for symptoms, nocturnal awakenings, and rescue medicine use. Controller medications for asthma 31 of 369 Final Update 1 Report Drug Effectiveness Review Project 6. Beclomethasone compared with triamcinolone 40, 41 We found two fair-quality multicenter RCTs comparing BDP to triamcinolone (TAA). Both compared medium-dose BDP (336 mcg/d), medium-dose TAA (800 mcg/d), and placebo for eight weeks in adult subjects. Both found no difference between the active treatment groups for 41 rescue medicine use and one found no difference in nighttime awakenings. They reported conflicting results for improvement of symptoms: one reported greater improvement with BDP 41 40 than TAA and one reported no difference. Budesonide compared with ciclesonide Five fair-quality multicenter RCTs meeting our inclusion criteria compared BUD with 58-62 62 ciclesonide. One was conducted in children age 6-11 61 and one in adolescents 12-17 years old. One was conducted using subjects with mild to moderate persistent asthma, two with mild to severe, one with moderate to severe, and one with severe persistent asthma. Two trials only compared nonequivalent doses with ciclesonide given 58, 60 at a higher relative dose than BUD. The three studies comparing equivalent doses were non- inferiority trials. All studies used dry powder formulations of BUD and HFA-MDI for ciclesonide. All five trials evaluated outcomes for asthma symptoms and rescue medicine use 59 and all but one reported exacerbations. All five trials were funded by pharmaceutical companies. Overall, the evidence from the three studies comparing equivalent doses (low versus low or medium versus medium doses of ICSs) was consistent, finding ciclesonide to be non-inferior to 59, 61, 62 BUD. All three studies reported similar improvement in symptoms, rescue medication 59, 61, 62 61, 62 use, and quality of life for subjects treated with ciclesonide and those treated with BUD. Budesonide compared with flunisolide We found one fair-quality multicenter RCT comparing BUD (1200 mcg/d) to flunisolide (1500 42 mcg/d) in adults (N = 154) with moderate persistent asthma for 6 weeks. They reported no statistically significant differences between BUD and flunisolide in change from baseline in asthma symptoms, nocturnal awakenings, or rescue medicine use. Budesonide compared with fluticasone One previously described systematic review and eight head-to-head RCTs comparing FP to BUD 23 met our inclusion criteria. The systematic review included studies comparing FP with BDP or BUD. Of the 71 studies included in this review, 37 compared FP to BUD. Comparisons were stratified by FP: BDP/BUD dose ratios of 1:2 or 1:1. The pooled treatment effect of FP was compared to the pooled treatment effect for BDP and BUD. For the studies conducted at dose ratios of 1:2, pooled estimates indicate that FP-treated patients had fewer symptoms, required less rescue medication, and had a higher likelihood of pharyngitis (see Key Question 2) than those treated with BDP or BUD. For the studies conducted at dose ratios of 1:1, individual studies and pooled estimates suggest no difference in symptoms, rescue medicine use, or the number of asthma exacerbations. Although we rated the quality of this review as good, the comparison of the effectiveness of BUD and FP cannot be 23 clearly ascertained from this systematic review because the comparator group contains both BUD and BDP.

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This process is associated with septicemia propranolol 80mg overnight delivery cardiovascular system lab tests, bowel or suggested that these might be a “reaction to parasitism rather than an respiratory tract infections cheap propranolol 80 mg without prescription cardiovascular system review, wound infections, or processes that independent process. In many situations, the infecting microbe does not attack the RBC directly and cause intravascular hemolysis, but instead may cause T-activation. Anti-T develops after about 3 months of age and is hemolysis indirectly or accelerated RBC destruction usually via the present in all adults, probably as a result of exposure to various liver and spleen. Several mechanism have been proposed including: bacteria and environmental stimuli. The T antigen is present on the absorption of immune complexes and complement onto the RBC surface of RBCs, but normally is masked by N-acetyl neuraminic surface, development of cross-reacting antibodies, and true autoim- (sialic) acid. This acid can be removed from the RBC surface by munity with loss of tolerance secondary to the infectious agent. The anti-T/T antigen reaction causes polyagglutination; Alterations of the RBC causing immunologic clearance that is, sera from all donors cause RBC agglutination in vitro. Rarely, the anti-T may cause intravascular patients infected with M. Because the cholecystitis, hepatic abscess, or amniocentesis. The alpha toxin of Cromer antigen is the receptor for E. GPs are Such a mechanism is clearer with the P blood group system. Some receptors for some bacterial toxins, especially E. Inhibition of RBC production coli is GPA containing the M antigen. The P antigen is a receptor for parvovirus B-19,18 although it alone is not sufficient for attachment of the virus There are associations between the Lewis (b) determinant and to the RBC. Erythroid precursors, but not mature RBCs, are invaded binding to Helicobacter pylori. Therefore, Therefore, parvovirus B-19 infection causes direct inhibition of whereas many people harbor H. This is especially likely to become infected and develop pyloric ulcers. Individuals negative for the P antigen (pp) are for Mycobacterium tuberculosis and M. Some alternate resistant to infection with parvovirus B-19. In patients with infectious mononucleosis, autoimmune hemolytic anemia is said to occur 0. Hemolysis occurs during the first 2–3 weeks of 1 that are probably involved in adhesion to mucosal cells, but that also infection and spontaneously clears in 2-3 months. The underly- agglutinate most RBCs except those of the AnWj-negative ing mechanism is not clear. The parvovirus B19 adheres to globoside of the P blood RBC aplasia by T-cell suppression of erythroid colony forming 18 group system. Enteroviruses such as coxsackievirus or echovirus units. Poliovirus may use the CD44 molecule containing the Indian blood group Acquired RBC antigens due to infectious agents antigens in its adhesive process. Bacterial enzymes, possibly deacetylases, may convert the blood group A determinant sugar into a form similar to the blood group B determinant sugar. This then gives the Receptors and adhesion molecules appearance that a type A individual has become type B. These Some RBC surface proteins resemble receptor or adhesion mol- individuals continue to produce anti-B, but this does not react with ecules (Table 2). The role of the RBC chemokine receptors is to their own apparent type B RBCs. Bacteria shown to cause this bind and thus inactivate chemokines in the blood, and several RBC phenomenon in vitro are C. It is not known whether any of these RBC receptors and adhesion molecules are targets of or play a role in infection. However, because they are part of such a crucial RBC blood group antigens in infection and complex system, such a role could exist. The RBC may be involved in infection of other tissues indirectly. Many RBC antigens are located on molecules with important physiologic functions, some of which involve infectious agents. On Complement regulatory molecules other tissues, these may involve adhesion molecules, complement Three blood group systems are part of molecules involved in the receptors, or microbial receptors. The Chido/Rogers antigens are part of the C4 molecule,21 which is absorbed onto RBCs from the circula- Blood group antigens as microbial receptors tion. The Cromer antigens are located on the DAF RBC membrane molecule,22 the role of which is to protect RBCs from Blood group antigens play a central role in host pathogen relations. As a first step in infection, an invading organism must bind they are involved with complement in infectious processes. RBC blood group antigens in infection* Blood group antigens as microbial receptors Microorganism Receptor Clinical effect E. Blood groups on red cells, platelets and neutrophils. In: causing accelerated clearance Porwit A, McCullough J, Erber WN, eds. Philadelphia: Churchill Livingstone Elsevier; As part of most infections, there is generation of cytokines and 2011:599-617. A receptor for the malarial membrane damage, altering the structure, leading to immunologic parasite Plasmodium vivax: the erythrocyte cytokine receptor. Because these are general patho- 1993;261(5125):1182-1184. Identification of an erythrocyte component carrying the Duffy blood group Fya antigen. The RBC may be a target of infections in several different ways, 5. Erythrocyte receptors for ranging from direct attack by the microbe to damage, accelerated Plasmodium knowlesi malaria, Duffy blood group determinants. Sci- clearance, or lysis due to toxins produced by the infecting agent or ence.