The importance of iron deficiency as a public health problem is based ultimately on the seriousness of its consequences on health. The most extensively investigated consequences of iron deficiency involve work performance and immune function. The significance of the effects on work performance is generally accepted. In contrast, data on the influence of iron deficiency on immune function are often perceived as being confusing and contradictory.We aimed to evaluate the effect of iron deficiency anemia on humoral, cellular, nonspecific immunity, and also the effect on the cytokines that are the key factors of many immunologic steps.Forty children with iron deficiency anemia and 20 age and sex-matched healthy children were included. All children were subjected to full medical history, thorough clinical examination, complete blood count, iron indices (serum iron, serum total iron-binding capacity, serum ferritin, and transferrin saturation), immunoglobulin assay (IgA, IgG, and IgM), interleukin (IL)-6 serum level, study of T-lymphocyte subsets, and evaluation of phagocytic function of macrophages and oxidative burst activity of neutrophils.Patients had significantly lower IgG levels, IL-6, phagocytic activity, and oxidative burst of neutrophils than controls, although there was no significant difference between patients and controls with regard to other immunoglobulins and CD4/CD8 ratio. There was significantly positive correlation between serum iron and IL-6 serum level.We concluded that humoral, nonspecific immunity (phagocytic activity and oxidative burst), and the IL-6 are influenced in patients with iron deficiency anemia. Study of these abnormalities after correction of iron deficiency is strongly needed.

Luteinizing-hormone-releasing hormone (LHRH) is distributed in several extrahypothalamic areas, suggesting that it might act as a neurotransmitter or neuromodulator in the central nervous system. This study was undertaken to characterize and localize LHRH receptors in the rat brain by using slide-mounted frozen sections. The radioligand used was an iodinated stable LHRH agonist, [D-Ser(TBU)6, des-Gly-NH2(10)]LHRH ethylamide. It was clearly established that LHRH receptors with characteristics similar to those of pituitary LHRH receptors were present in the brain. They were found in high concentrations in the dorsal hippocampus, amygdala, septum, and subiculum and in very low amounts in the hypothalamus. Generally, a good correlation could be observed between receptor distribution and immunohistologically localized LHRH. These results strongly suggest that LHRH has multiple sites of action in the rat brain and reinforce the hypothesis that the peptide could act as a neurotransmitter/neuromodulator in the central nervous system.

Abstract. Chemotherapy-induced neutropenia (CIN) is the major dose-limiting toxicity of systemic chemotherapy and it is associated with significant morbidity, mortality and treatment cost. The aim of the present study was to identify the risk factors that may predispose pediatric cancer patients who receive myelosuppressive chemotherapy to CIN and associated sequelae. A total of 113 neutropenia episodes were analyzed and the risk factors for CIN were classified as patient-specific, disease-specific and regimen-specific, while the consequences of CIN were divided into infectious and dose-modifying sequelae. The risks and consequences were analyzed to target high-risk patients with appropriate preventive strategies. Among our patients, 28% presented with a single neutropenia attack, while 72% experienced recurrent attacks during their treatment cycles. The mean absolute neutrophil count was 225.5±128.5 x10 9 ̸l (range, 10-497 x10 9 ̸l), starting 14.2±16.3 days (range, 2-100 days) after the onset of chemotherapy and resolving within 11.2±7.3 days, either with (45.1%) or without (54.9%) granulocyte colony-stimulating factor (G-CSF). No significant association was observed between any patient characteristics or disease stage and the risk for CIN. However, certain malignancies, such as acute lymphocytic leukemia (ALL), neuroblastoma and Burkitt's lymphoma, and certain regimens, such as induction block for ALL and acute myelocytic leukemia, exerted the most potent myelotoxic effect, with severe and prolonged episodes of neutropenia. G-CSF significantly shortened the duration of the episodes and enhanced bone marrow recovery. Febrile neutropenia was the leading complication among our cases (73.5%) and was associated with several documented infections, particularly mucositis (54.9%), respiratory (45.1%), gastrointestinal tract (38.9%) and skin (23.9%) infections. A total of 6% of our patients succumbed to infection-related complications. Neutropenia was responsible for treatment discontinuation (13.3%), dose delay (13.3%) and dose reduction (5.3%) in our patients.

Using this simplified dosage schedule, bactericidal efficacy was maintained and most subjects had serum vancomycin concentrations within the therapeutic range.

In β-thalassemia, certain mutations cause a complete absence of β-globin chain synthesis, termed β-thalassemia, while others may allow certain β-globin production and are termed β- or β-thalassemia. The homozygous state results in severe anemia, which requires regular blood transfusion. By contrast, frequent blood transfusion can in turn lead to iron overload, which may result in several endocrinal complications. The present study aimed to investigate the impact of genotype on the development of endocrine complications in β-thalassemia patients. A cross-sectional study was conducted on 100 thalassemia patients >10 years. A data abstraction form was designed to capture the appropriate information from the individual medical records, including full clinical, laboratory, transfusion and chelation data. The genotype of the patients was identified by the DNA sequencing technique. Growth retardation and hypogonadism were the most prominent endocrinal complications (70 and 67%, respectively) followed by hypothyroidism, diabetes mellitus and hypoparathyrodism (8, 8 and 7%, respectively). The most common mutations identified were IVS-1-110, IVS-1-1 and IVS-1-6 (63, 47 and 41%, respectively). Patients with the ββ genotype had a significantly higher prevalence of growth retardation, hypogonadism, hypothyroidism and hypoparathyrodism compared to those with the ββ and ββ genotypes (P<0.001, P<0.001, P<0.001 and P=0.037, respectively). Patients with the homozygous IVS-11-745 mutation had a significantly higher prevalence of diabetes (P=0.001). The underlying genetic defect in thalassemia patients is a contributing factor for the development of endocrinal complications, as patients with the more severe defects have a greater rate of iron loading through higher red cell consumption.

The functional independence score in haemophilia (FISH) is a performance-based instrument used to assess musculoskeletal function in patients with haemophilia. We aimed to evaluate the functional independence of haemophilia A adolescents and its correlation to radiological joint scores. A cross-sectional study was carried out on 50 adolescent haemophilia A patients. Musculoskeletal function was assessed using the FISH and individual joints were assessed radiologically using the Pettersson score and MRI scale. The mean age of our patients was 16 ± 1.1 with a mean FISH of 23.32 ± 4.69 (range 13-28) and a mean Pettersson score of 2.32 ± 3.09 (range 0-13) for the knees, 1.86 ± 2.67 (range 0-11) for ankles and 1.42 ± 2.17 (range 0-10) for elbows. The mean MRI score for the knees was 3.92 ± 2.74 (range 0-10) while that for ankles was 3.16 ± 2.64 (range 0-10) and for elbows was 2.34 ± 2.63 (range 0-10). There was highly significant correlation between both radiological joint scores and FISH and between degree of factor VIII deficiency and each of FISH, Pettersson score and MRI score. MRI was superior to conventional radiography in detection of subchondral cyst formation and erosions at joint margins. Given the highly significant correlation with both radiological joint scores, FISH appears to be a reliable tool for assessment of functional independence in adolescents with haemophilia A. MRI is more sensitive than conventional radiography in detection of early joint abnormalities.

Haemophilia A is characterized by the occurrence of frequent spontaneous intra-articular and intramuscular bleeding. If inadequately treated, it results in progressive damage to joints and muscles leading to crippling deformities and musculoskeletal dysfunction. These complications result in lifelong chronic pain and disability that may greatly affect the patients' mood. We aimed to evaluate the musculoskeletal function in our haemophilia A patients and its correlation to depressed mood in these patients and determine the impact of degree of factor VIII deficiency, different replacement therapy regimens and frequency of hemarthrosis, on both musculoskeletal function and mood. A cross-sectional study was carried out on 50 adolescent haemophilia A patients. Musculoskeletal function was assessed using Functional Independence Score for Hemophilia (FISH) and mood status was assessed using Beck Depression Inventory-Short Form (BDI-SF). The mean FISH score was 23.32 ± 4.69 (range 13-28) and the tasks that obtained lower scores were step climbing, squatting and walking. Of our 50 patients included, 16(32%) were not depressed, 18(36%) were with mild depression, 11(22%) were with moderate depression and 5(10%) were with severe depression. There was a highly significant negative correlation between mean FISH score and mean BDI-SF score (P < 0.001). The better the replacement therapy regimen, the better the musculoskeletal function that could be obtained in haemophilia A patients and the better the mood.

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