Interleukin -2 ( Il-2 ) and Gamma Interferon ( Ifn ? ) of Lymphocyte Culture Supernatant in Iron Deficiency Anemia Patients with Infection

Iron is an essential nutrient for every living cells because of it role as molecule fortransport of oxygen, as well as DNA synthesis through synthesis of ribonucleotidereductase. Iron deficiency anemia patients, especially pregnant women and children aremore susceptible to infection because of deterioration of their immune response. This wassupported by findings of decreased in phagocytic activities of white blood cells and Tcelllymphocyte proliferation impairment. Iron deficiency anemia (IDA) patients alsoaffect working capacities hence diminishing working outcomes. Although the underlyingmechanism of immune defect in iron deficiency anemia is not clearly understood,multifactor events considered play their contributing roles such as abnormality ofribonucleotide reductase enzym, impairment of T-cell proliferation and activities, alteredcytokine production of IL-2 and IFN?.The study was done to asses the relationship of IL-2 and gamma IFN withinfection in IDA patients on lymphocyte culture supernatant of IDA patients. Study wasconducted on cross-sectional analytic design. Sixty-four iron deficiency anemia patientstreated in Sanglah General Teaching Hospital were recruited, and 31 (48.4%) out of 64IDA patients were man and 33 (51.6%) women, have been selected for the study. Thisstudy found 17 (26.7%) IDA patients with infection, aged 38 ± 14.48 years and 47(73.3%) IDA patients without infection, with age average of 40.5 ± 14.4 years. Allvariables of data characteristics examined did not indicate any statistical significantdifference between group of IDA patients with infection and those without infection. Theaverage level of hemoglobin between the two groups did not differ statistically. Similarresult was obtained if samples were differentiated into severe (Hb< 7g/dl) and mildanemia. The study also revealed that there were no differences of cytokine level observedbetween older and younger age (upper and below 44.5 years) in IDA patients withinfection and without infection. Furthermore, no differences of cytokine level were foundbased on gender between IDA male 10.9 (8.60 – 12,65) (pg/l) patients and IDA femalepatients 10.6 (7.50 – 13.43) (pg/l) with Z -0.490, p =0.624. Nevertheless, significantdifferences were noted between supernatant of IL-2 and IFN? in IDA patients withinfection when compared to IDA patients without infection (Z= - 2.509, p= 0.012 forsupernatant IL-2; and Z= -2.569, p= 0.010 for supernatant IFN?).The study conclusion is that level of IL-2 and IFN? from lymphocyte culturesupernatant of patient suffered from IDA with infection is significantly lower whencompared to IDA patient without infection. It therefore summarized that lower level ofIL-2 and gamma IFN in patients suffered from iron deficiency impaired their immune response to certain infections therefore this findings support the theory that IDA patientsmore susceptible to get infected

Macrocytosis may be associated with mortality in chronic hemodialysis patients: a prospective study

<p>Abstract</p> <p>Background</p> <p>Macrocytosis occurs in chronic hemodialysis (CHD) patients; however, its significance is unknown. The purpose of this study was to establish the prevalence and distribution of macrocytosis, to identify its clinical associations and to determine if macrocytosis is associated with mortality in stable, chronic hemodialysis patients.</p> <p>Methods</p> <p>We conducted a single-centre prospective cohort study of 150 stable, adult CHD patients followed for nine months. Macrocytosis was defined as a mean corpuscular volume (MCV) > 97 fl. We analyzed MCV as a continuous variable, in tertiles and using a cutoff point of 102 fl.</p> <p>Results</p> <p>The mean MCV was 99.1 ± 6.4 fl, (range 66-120 fl). MCV was normally distributed. 92 (61%) of patients had an MCV > 97 fl and 45 (30%) > 102 fl. Patients were not B12 or folate deficient in those with available data and three patients with an MCV > 102 fl had hypothyroidism. In a logistic regression analysis, an MCV > 102 fl was associated with a higher Charlson-Age Comorbidity Index (CACI) and higher ratios of darbepoetin alfa to hemoglobin (Hb), [(weekly darbepoetin alfa dose in micrograms per kg body weight / Hb in g/L)*1000]. There were 23 deaths at nine months in this study. Unadjusted MCV > 102 fl was associated with mortality (HR 3.24, 95% CI 1.42-7.39, P = 0.005). Adjusting for the CACI, an MCV > 102 fl was still associated with mortality (HR 2.47, 95% CI 1.07-5.71, P = 0.035).</p> <p>Conclusions</p> <p>Macrocytosis may be associated with mortality in stable, chronic hemodialysis patients. Future studies will need to be conducted to confirm this finding.</p

Erthropoiesis-stimulating agent hyporesponsiveness

Approximately 5-10% of patients with chronic kidney disease demonstrate hyporesponsiveness to erythropoiesis-stimulating agents (ESA), defined as a continued need for greater than 300 IU/kg per week erythropoietin or 1.5 mug/kg per week darbepoetin administered by the subcutaneous route. Such hyporesponsiveness contributes significantly to morbidity, mortality and health-care economic burden in chronic kidney disease and represents an important diagnostic and management challenge. The commonest causes of ESA resistance are non-compliance, absolute or functional iron deficiency and inflammation. It is widely accepted that maintaining adequate iron stores, ideally by administering iron parenterally, is the most important strategy for reducing the requirements for, and enhancing the efficacy of ESA. There have been recent epidemiologic studies linking parenteral iron therapy to an increased risk of infection and atherosclerosis, although other investigations have refuted this. Inflammatory ESA hyporesponsiveness has been reported to be improved by a number of interventions, including the use of biocompatible membranes, ultrapure dialysate, transplant nephrectomy, ascorbic acid therapy, vitamin E supplementation, statins and oxpentifylline administration. Other variably well-established causes of ESA hyporesponsiveness include inadequate dialysis, hyperparathyroidism, nutrient deficiencies (vitamin B12, folate, vitamin C, carnitine), angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aluminium overload, antibody-mediated pure red cell aplasia, primary bone marrow disorders, myelosuppressive agents, haemoglobinopathies, haemolysis and hypersplenism. This paper reviews the causes of ESA hyporesponsiveness and the clinical evidence for proposed therapeutic interventions. A practical algorithm for approaching the investigation and management of patients with ESA hyporesponsiveness is also provided