Endoscopic and histopathological evaluation of preschool children with chronic diarrhoea.

Fifty-seven children with chronic diarrhoea, aged 1-5 years, were studied. Protein-energy malnutrition was present in 49 (85.9 per cent) children. Anaemia (89.5 per cent), presence of mucus and blood in stool (66.6 per cent), abdominal distension (52.6 per cent), and abdominal pain (28.1 per cent) were the common clinical findings at admission. The enteropathogens isolated from the stool of 68.4 per cent of patients were Escherichia coli (19.3 per cent), Candida albicans (12.3 per cent), E. histolytica (8.8 per cent), and Giardia lamblia (7 per cent). Secondary lactose intolerance was present in 21 per cent of children, endoscopic appearance was abnormal in 23.3 per cent of children and the commonest finding was chronic duodenitis (16.7 per cent). Abnormal histopathology was observed in 73.3 per cent of cases and villous atrophy with mononuclear cell infiltration (56.7 per cent) was the most common abnormality detected. The mean duration of diarrhoea had no impact on endoscopic appearance but it significantly affected the histopathological changes. However, no correlation was found in endoscopic and histopathological lesions in relation to malnutrition and aetiological agents.

Acardiac anomaly spectrum.

BACKGROUND: Acardiac anomaly spectrum is a rare congenital malformation found in monozygotic twin pregnancy. Besides the absence of heart, the condition is associated with variable grades of developmental disruption. Thus, no two cases are similar. METHODS: This case report is based on physical examination and autopsy findings. RESULTS: The twin had acardia and partial development of head and face. There was complete absence of upper extremities. CONCLUSIONS: The twin reversed arterial perfusion (TRAP) theory is the most accepted etiology of the disorder. Normally, the cephalic pole is the most severely affected, being most distal to the retrograde perfusion. In acardia, partial development of head, face, and brain is usually associated with the development of the upper extremities. However, in the present case, there was extensive cephalic development in the absence of upper extremity development.

Serum magnesium levels in protein-energy malnutrition.

Serum magnesium levels were measured by atomic absorption spectrophotometry in 46 malnourished and 12 healthy children, aged 3 months to 5 years. The nutritional status of children was classified in relation to weight for age and height for age using the Indian Academy of Pediatrics and the Waterlow classifications, respectively. NCHS data were used for the purposes of comparison. Serum magnesium levels were significantly low in children with moderate (weight for age 61-70 per cent) and severe (weight < or = 60 per cent) malnutrition, and in children with marked linear growth retardation (height for age < 85 per cent). Nearly half of the marasmic children had serum magnesium levels in the hypomagnesemic range (below 1.56 mg/dl). Serum magnesium levels had significant correlations with height for age and serum albumin.

Blood lead levels in children with neurological disorders.

Blood lead levels were measured by atomic absorption spectrometry in 82 children suffering from various neurological disorders (cerebral palsy 42, seizure disorders 35, acute encephalopathy of unknown origin 5) and in 28 healthy children, aged 1 to 12 years. Mean blood lead levels were 11.96 +/- 10.97 micrograms/dl in control children and 19.30 +/- 17.65 micrograms/dl in children with neurological disorders. A significant number of control children as well as those who had neurological disorders were found to have blood lead concentrations of > or = 10 micrograms/dl and > or = 20 micrograms/dl, the cut-off limits for lead poisoning and medical evaluation, respectively. Blood lead levels were, statistically, elevated in children with cerebral palsy compared to controls. Children with pica behaviour exhibited higher blood lead concentrations.

Fetal growth in maternal anaemia.

The effect of maternal iron deficiency anemia on fetal growth was studied in 54 anaemic (haemoglobin < 11.0 g/dl) mothers. Twenty-two mothers served as controls (haemoglobin > or = 11.0 g/dl). All the women had singleton live births at term gestation. The maternal iron status was assessed by serum ferritin estimation. The birth weight, head circumference, chest circumference, mid-arm circumference, and crown heel length were significantly low in infants born to women with moderate (haemoglobin 6.1 +/- 8.5 g/dl) and severe anaemia (haemoglobin < or = 6.0 g/dl), in comparison to infants born to non-anaemic women. Similarly, birth weight, mid-arm circumference, and crown-heel length were significantly low in infants of women with depleted iron stores (serum ferritin < 10 micrograms/l) than in infants of women with serum ferritin levels of 20 micrograms/l or more. All indices of fetal growth showed linear relationships with maternal haemoglobin, as well as with serum ferritin. The growth retarding effect of maternal anaemia was more on fetal birth weight and mid-arm circumference than on other anthropometric indices of the newborn.

Fetal iron status in maternal anemia.

Hemoglobin, serum iron, transferrin saturation and ferritin were measured on paired maternal and cord blood samples in 54 anemic (hemoglobin < 110 g/L) and 22 non-anemic (hemoglobin > or = 110 g/L) pregnant women at term gestation. The levels of hemoglobin, serum iron, transferrin saturation and ferritin were significantly low in the cord blood of anemic women, suggesting that iron supply to the fetus was reduced in maternal anemia. The linear relationships of these parameters with both maternal hemoglobin and maternal serum ferritin indicated that the fetus extracted iron in amounts proportional to the levels available in the mother. Infants of mothers with moderate and severe anemia had significantly lower cord serum ferritin levels and hence poor iron stores at birth. It is concluded that iron deficiency anemia during pregnancy adversely affects the iron endowment of the infant at birth.

Serum, zinc and copper levels in children with protein energy malnutrition.

Serum zinc and copper were measured by atomic absorption spectrophotometry in 58 children (3 months-5 years); of these, 46 children had protein energy malnutrition (PEM), and 12 children served as controls. The levels of serum zinc and copper were found to be significantly low in children with severe malnutrition (grades III and IV PEM). There was a significant positive correlation between serum zinc and height-for-age (r = 0.8809, p < 0.001). Serum copper was found low only in children exhibiting marked linear growth retardation (height-for-age < 85% of the normal). Hypoalbuminemia (serum albumin < 2.5 g/dl), and anemia (hemoglobin < or = 8.0 g/dl) in malnourished children were associated with significant decline in serum zinc and copper levels, respectively.

Biochemical abnormalities in neonatal seizures.

Early diagnosis and appropriate treatment of biochemical abnormalities accompanying neonatal seizures is important for effective seizure control and to avoid further brain damage. The present study was carried out on 35 neonates to determine the frequency of various biochemical abnormalities in neonatal seizures. Diagnostic evaluation included estimation of levels of serum calcium, phosphorus, magnesium, sodium, potassium, zinc, and blood glucose. Two-thirds of the neonates with seizures had biochemical disturbances in their sera. A variety of abnormalities occurred in asphyxiated infants, including hyponatremia, hypoglycemia, hypocalcemia, and hypomagnesemia. Primary metabolic disorders accounted for one-forth of the cases of neonatal seizures, the most common being hypoglycemia, hypoglycemia/hypocalcemia, and hypocalcemia/hyperphosphatemia. Inappropriate intrauterine growth, inadequate feeding, and feeding with cow's milk were the main risk factors for primary metabolic seizures. Hyponatremia was a frequent finding in seizures resulting from brain damage like birth asphyxia, meningitis, and intracranial hemorrhage. No infant had hypernatremia, hyperkalemia, hypokalemia, or low serum zinc.

Quantitation of T cells in venous blood of healthy neonates.

Quantitation of T Cells in blood is the part of the diagnostic workup for cellular immunity. Specimens of venous blood were collected within 24 hours of birth from 51 healthy, appropriate for gestational age infants. T lymphocytes were identified on the basis of their ability to form rosettes with sheep erythrocytes. The lymphocytes were harvested from peripheral venous blood, which is considered to be more representative of the immune status in the newborn than the cord blood. In the newborn infants the proportion in T cells was found to be considerably diminished in comparison to previously reported values for adults. Preterm infants, especially those with gestational age of 34 wk or less had significantly lower percentage of T cells in their blood as compared with term infants. The proportion of T cells was statistically reduced in infants weighing 2000 g or less in contrast to those weighing 2500 g or more.

Storage iron in human foetal organs.

Maternal plasma iron and storage iron (non-heme) in the foetal liver were estimated in 108 foetuses whose gestational ages ranged from 12-44 weeks. Simultaneous estimations of storage iron were also made on the spleen and kidney in 70 and 69 of these foetuses respectively. Although the concentration of iron per g wet tissue in these organs remained practically the same at all gestations, the total storage iron content increased with the increase in gestation due to growth of these organs. The liver, in particular, showed a steep rise in total iron content in the last 8 weeks of gestation. There was a significant positive correlation between the total storage iron content in the foetal organs and the birth weight and gestational age of the foetus, suggesting that the preterm infants had smaller iron stores at birth as compared to infants born at term. The direct relation of the concentration as well as the total content of storage iron in the foetal liver with the maternal plasma iron levels suggested that babies born to iron deficient mothers had poor iron stores in their livers.