Iron Profile Estimations in Children of Behavioural Disorders.

Background: Iron deficiency causes abnormal dopaminergic neurotransmission and may contribute to behavioral disorders. Objective: Iron Profile Estimation in Children (5-14 yrs) of Behavioral Disorders. Design : Cross-sectional study. Setting: Child Guidance Clinic of University College of Medical Sciences and Guru Tegh Bahadur Hospital. The sample consisted of Forty children in the age group of 5 to 14 years suffering from behavioral disorders. Haemoglobin , Mean Corpuscular Volume, Mean Corpuscular Hemoglobin, Serum Iron ,Total Iron Binding Capacity, Peripheral smear, Percentage transferrin saturation , serum ferritin estimations were done. The behavioral symptoms were scored on Achenback Child Behavior Checklist. Results: Iron deficiency anemia was present in 75% of the children with behavioral symptoms. Serum ferritin was abnormal (<20micrograms/litre) in 67.8% of the children. There was statistically significant association between pica and iron deficiency anemia(p<0.001).Serum ferrittin levels correlated negatively with behavioral symptoms (r=-.067), though not significant.

Red cell indices and discriminant functions in the detection of beta-thalassaemia trait in a population with high prevalence of iron deficiency anaemia.

Red cell indices and discriminant functions were studied in 463 heterozygous beta-thalassaemics (337 without iron deficiency, 126 with iron deficiency) and 195 patients of iron deficiency anaemia (IDA) to ascertain their utility in the detection of betathalassaemia trait (BTT). Majority of traits in both groups had an elevated RBC count (> or = 5.0 x 10(12)/L). The counts were significantly higher than of patients with IDA, only 4.6% of whom had this degree of erythrocytosis. Mean Hb concentration was significantly higher in traits as compared to iron deficient subjects (p < 0.0001). Mean MCV and MCH were significantly (p < 0.0001) lower in traits more so in those with ID as compared to patients of IDA. MCV < 80 fl and MCH < 27 pg were found to be sensitive markers in the detection of traits even in the presence of ID. Of the four discriminant functions studied MCSQ was found to be most sensitive in detection of BTT and it identified 97.9% traits. DF of England and Fraser was most specific for BTT being < 8.4 in only 6.2% patients with IDA. Detection of erythrocytosis especially in the presence of mild anaemia and calculation of discriminant functions derived from red cell indices were found to play an important role in screening for BTT even in the presence of ID and helped identify those patients who required further laboratory evaluation.

Haematological parameters and HbA2 levels in beta-thalassaemia trait with coincident iron deficiency.

Iron status was estimated in 463 heterozygous beta-thalassaemics to delineate the effect of iron deficiency (ID) on the haematological parameters and expression of HbA2 in these patients. One hundred and twenty six (27.2%) traits had coincident ID. These iron deficient traits had a significantly (p < 0.0002), higher prevalence of anaemia (90.5%) as compared to iron replete traits (71.5%). Mean haemoglobin concentration was significantly lower (p < 0.0001) in beta-thalassaemics with ID (10.7 +/- 1.5) g/al as compared to those without ID (11.6 +/- 1.6 g/dl). Mean MCV and MCH were significantly lowered (p < 0.0001) in patients of beta-thalassaemia trait (BTT) with ID than in these without ID. Mean HbA2 was not significantly different in the two groups of traits and was elevated (> or = 3.5%) in all except one patient. However, mean HbA2/cell was significantly (p < 0.05) lower in traits with ID. The effect of ID in BTT was apparent with significant lowering of haemoglobin concentration and increased prevalence of anaemia. Iron therapy is warranted in iron deficient traits and would help in significantly raising their haemoglobin concentration. Elevation in HbA2 values was striking and could be used with reliability for diagnosis of BTT even in the presence of ID.

Prevalence & etiology of nutritional anaemias in early childhood in an urban slum.

The present study was carried out to find out the prevalence and etiology of nutritional anaemia among preschool children from an urban slum. Randomly selected 300 children aged 3 months-3 yr were analysed over a period of one year for estimating prevalence of nutritional anaemia. Prevalence was also assessed by the rise in haemoglobin after 8 wk of haematinic supplementation in 159 of the 300 subjects. Ninety anaemic children were evaluated for the etiology of anaemia. Prevalence of anaemia, as judged by WHO recommended 'cut-off' value of haemoglobin < 11 g/dl, was 76 per cent while comparable value of 74.8 per cent was derived by response to haematinic supplementation. Pure iron deficiency anaemia (IDA) was detected in 41.4 per cent (37/90) of anaemic children. Vitamin B12 deficiency alone or in combination with iron was diagnosed in 14.4 and 22.2 per cent anaemic children respectively. Similarly folate deficiency, IDA with infection and anaemia of chronic diseases (ACD) was diagnosed in 2.2, 3.3 and 12.2 per cent cases respectively. Childhood anaemia continues to be a significant public health problem in preschoolers and iron deficiency is by far the commonest nutritional cause of anaemia. Vitamin B12 deficiency per se or in combination with iron is an important yet not commonly recognised cause of anaemias in preschool children in the community.

Beta-thalassaemia mutations in northern India (Delhi).

The present study was undertaken to define beta-thalassaemia mutations prevalent in northern India (Delhi). Forty six children of beta-thalassaemia major and their families were investigated. DNA was extracted from leucocytes and screened for mutations prevalent in the Indian population. These mutations included 619bp deletion, IVS 1-1 (G-T), IVS 1-5 (G-C), frameshift mutations FS 8/9 (+G), FS 41/42 (-CTTT), Codon 16(-C), Codon 15 (G-A), codon 30 (G-C), IVS 1-110 (G-A) and -88 (C-T). 619 bp deletion mutation was detected directly by amplification of DNA by PCR followed by agarose gel electrophoresis. Other mutations were studied by DNA amplification and dot blot hybridization using synthetic normal and mutant oligonucleotide probes labelled at 5' end with gamma-32 P-ATP. Five mutations accounted for all the chromosomes in 46 patients. 619 bp deletion mutation was found to be the commonest mutation (34.8%) followed by IVS 1-5 (G-C) in 22.8 per cent, IVS 1-1 (G-T) in 19.6 per cent, FS 8/9 (+G) in 13 per cent and FS 41/42 (-CTTT) in 9.8 per cent. Nineteen (41.3%) patients were homozygous and 27 (58.7%) double heterozygous for different beta-thalassaemia mutations. This observation of limited number of mutations is significant and will be useful in planning strategies for prenatal diagnosis of beta-thalassaemia in northern India.

ESR and iron status in pregnancy.

ESR (Westergen) correlated significantly with the iron status (as measured by Hb concentration, haematocrit, red cell count, MCH, P/H ratio, serum iron, TIBC and percent saturation of transferrin) in a group of pregnant women (PW) at term. Serum ferritin correlated negatively with the ESR but the correlation was not statistically significant. Serum ferritin levels of < 50 micrograms/L were present in 9 (34.6%) PW with ESR > or = 50 mm 1st hour and 5 (19.2%) PW with ESR < 50 mm 1st hour. The mean ESR in PW was 55.7 (+/- 22.9) and was > or = 50 mm 1st hour in 50% and < 75 mm 1st hour in 82.7%. The difference in the mean ESR in anaemic and nonanaemic PW was highly significant (p < 0.001), 87.5% anaemic PW with serum ferritin > 50 micrograms/L had ESR > or = 50 mm 1st hour, suggesting the possible effect of chronic infection in raising ferritin levels in these PW.

Haemostatic function in coronary artery disease (CAD).

Tests to evaluate haemostatic function bleeding time (BT), prothrombin time (PT) partial thromboplastin time with kaolin (PTTK), thrombin time (TT), platelet count, platelet function tests (platelet adhesiveness and microthrombus index) and plasma fibrinogen levels were performed in 30 patients of coronary artery disease (14 myocardial infarction, 16 angina pectoris) and 20 age and sex matched controls. There was no statistically significant difference in platelet adhesiveness and mean microthrombus index in patients and controls. The BT, PT, PTTK and TT were normal in all patients and controls. Stepwise logistic regression analysis showed that plasma fibrinogen was an independent risk factor in the production of CAD.

Proliferating cell nuclear antigen immunostaining in breast carcinoma and its relationship to clinical and pathological variables.

Tumour proliferative activity of 74 breast lesions was assessed by determining mitotic index and immunostaining for proliferative cell nuclear antigen using Peroxidase antiperoxidase method. The indices were correlated with histomorphology and clinical stage of the disease. Positively stained nuclei and mitotic figures were counted per 1000 cells to calculate Proliferating Cell Nuclear Antigen (PCNA) and mitotic index respectively. Sixty four cases stained positive for PCNA. The index ranged between 0 to 98. PCNA index was significantly low in benign lesions as compared to malignant lesions (p < 0.0002). There was a linear correlation between the mitotic index and PCNA index. PCNA index also showed significant correlation with tumour size and histologic grade; however, it had no correlation with axillary lymph node status.

Congenital deficiency of factor VII.

A case of congenital factor VII deficiency in a five-year-old child is reported. The patient, born of a non-consanguineous marriage, presented with repeated bouts of epistaxis since childhood. The prothrombin time (PT) was markedly prolonged with a normal bleeding time (BT), partial thromboplastin time with Kaolin (PTTK) and platelet count. The patient has been on follow up for the last four years and is doing apparently well.

Effect of maternal iron deficiency anaemia on foetal outcome.

One hundred and two pregnant women and their neonates were examined to evaluate the effect of maternal haemoglobin concentration (Hb. conc) and iron deficiency anaemia on the placental weight and the foetal outcome. Haematological and serum ferritin values were determined. It was observed that 34.3% of the pregnant women were anaemic. Maternal Hb conc. and serum ferritin showed a highly significant correlation (r = 0.40, p < 0.001) indicating that iron deficiency was the most important cause of anaemia amongst them. The maternal Hb conc. showed a significant correlation with placental weight (p < 0.05), birth weight (p < 0.01), Apgar score (p < 0.001) and birth asphyxia. Maternal serum ferritin also correlated positively with cord ferritin (p < 0.001). The study did not reveal any association between high Hb and adverse foetal outcome.

Effect of leukaemic sera & cell-extracts on splenic colony counts (CFU-S).

Sera and leukaemic cell extracts from patients of acute leukaemia were evaluated for their effect on the repopulating ability of the pluripotent stem cells and erythroid differentiation by an in vivo splenic colony count (CFU-S) technique. Normal donor marrow cells of mice were treated with sera and cell extracts from patients of acute leukaemic and healthy controls and injected in the recipient mice. The CFU-S performed on the seventh day to assess repopulating ability of the stem cell showed consistently lower CFU-S counts in the test groups, with leukaemic sera (P less than 0.01) as well as leukaemic cell-extracts (P less than 0.001). The erythroid differentiation assessed by 59Fe uptake by the spleens also showed significantly reduced counts in the two test groups (P less than 0.01 and less than 0.001 respectively). The results indicate that both leukaemic sera and cell-extracts exert a significant suppressive effect on the repopulating ability of the stem cells and on their erythroid differentiation.

Serum & cerebrospinal fluid ferritin levels in children with acute leukaemia.

Serum and CSF ferritin were estimated in 35 consecutive patients of acute leukaemia at the time of admission and on induction of remission. Serum ferritin levels were significantly raised in 94 per cent patients of acute leukaemia. The mean (+/- SD) serum ferritin (314.36 +/- 158.4 micrograms/1) was significantly higher when compared with control values (P less than 0.001). Remission induction resulted in significant fall in serum ferritin values to a mean of 149 (+/- 98.7) micrograms/l (P less than 0.05). Serum ferritin is thus of value in assessing the state of remission and is a sensitive indicator of the leukaemic cell mass and the state of activity of the disease. CSF ferritin levels in acute leukaemia were comparable to normal control values. CSF ferritin did not reflect CNS involvement in acute leukaemia and therefore its value as a tumour marker of CNS infiltration is doubtful.

Supplementary iron dose in pregnancy anemia prophylaxis.

This study was conducted to determine the optimum dose of supplemental iron for prophylaxis against pregnancy anemia. One hundred and ten pregnant women were randomly allocated to three groups: Group A receiving equivalent of 60 mg, group B 120 mg and Group C 240 mg, elemental iron as ferrous sulphate daily; the content of folic acid was constant in all the three groups (0.5 mg). These women had at least consumed 90 tablets in 100 +/- 10 days. Blood was drawn at the beginning and at the end of the treatment. Fifty percent were anemic (less than 11 g/100 ml). The hemoglobin levels rose similarly in all groups and the differences were statistically not significant. Fifty-six percent had depleted iron stores (serum ferritin value less than 12 micrograms/l) at the beginning of the study. Following therapy a statistically significant increase in iron stores was observed in group B and C as compared to group A. The difference between group B and C was not significant. The side effects increased with increasing doses of iron; 32.4%, 40.3% and 72% in group A, B and C respectively. Based on these findings, the authors advocate that optimum dose of iron should be 120 mg instead of 60 mg as is currently being used in the National Nutritional Anemia Prophylaxis Programme.