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Biomedical subjects

A T Soliman

Publications and source records attributed to A T Soliman.

At least 37 records · Page 2Linked to original sources
PubMed1996

High prevalence of islet cell antibody and defective insulin release in children with schistosomiasis.

The importance of islet cell antibodies (ICA) as a predictor of insulin dependent diabetes mellitus (IDDM) has been emphasized by several investigators since 1974. The ICA was also detected in patients with various immune-mediated diseases such as auto-immune thyroiditis. Schistosomiasis is a wide-spread helminthic disease which affects more than 200 million patients all over the world. Immunological abnormalities and pancreatic affection are features of the disease. We studied the prevalence of ICA in 40 children with schistosomiasis (20 males and 20 females), 14 children with IDDM, and 30 of the non-diabetic siblings of patients with IDDM, and evaluated the oral glucose tolerance and early release of insulin after an i.v. load of glucose in children with schistosomiasis, diabetics' siblings, and 10 normal age-matched controls. The age of onset of IDDM and duration of the disease were 6.5 +/- 2.3 and 4.1 +/- 1.2, respectively, and the age of onset and duration of schistosomiasis were 8.3 +/- 2.7 and 2.5 +/- 1.5 years, respectively. Sex, consanguinity, history of previous virus diseases (mumps, measles and rubella), and sex maturity rating did not differ among the three study groups; however, children with schistosomiasis were significantly older. The prevalence of ICA was 50 per cent in children with IDDM, 13 per cent in the diabetics' siblings, and 25 per cent of children with schistosomiasis. Glucose tolerance was normal in children with schistosomiasis and diabetics' siblings. Early release of insulin after i.v. glucose load was significantly lower in children with schistosomiasis compared to the other two groups. In conclusion, the high prevalence of ICA and the decreased early release of insulin in response to an i.v. glucose load in children with schistosomiasis suggest that auto-immune aggression against the islet cells contributes in the pathogenesis of pancreatic disease in these patients, and might increase the risk for developing glucose intolerance and diabetes.

Autoantibodies↗
PubMed1996

Maternal and neonatal prevalence of toxoplasma and cytomegalovirus (CMV) antibodies and hepatitis-B antigens in an Egyptian rural area.

To determine the seroprevalence of maternal and neonatal toxoplasmosis and cytomegalovirus (CMV) antibodies and hepatitis-B (HB) antigenaemia in a rural Egyptian area, a prospective serological study was done on a randomly selected sample of pregnant women (n = 150) and their newborn infants (n = 150). Sera were collected from the mothers during the first antenatal visit, and at the time of delivery and cord blood specimens (paired samples) taken from their infants to be tested for toxoplasma-IgG and IgM antibodies, CMV-IgG and IgM antibodies surface antigen (HBsAg) and HBe antigen (HBeAg). Maternal infection was indicated in cases where specific IgM antibody was present or where an initial maternal specimen gave negative result for IgG antibody, but the second blood specimen gave positive result. Specific IgM antibody in a cord blood specimen indicated fetal infection. Out of the 150 pregnant women, 64 (43 percent) were toxoplasma immune at their first antenatal visit and their newborns were toxoplasma IgG positive. Toxoplasma specific IgM antibody was detected in only three mothers at the time of deliver. The rate of maternal infection in susceptible pregnancies was 4 percent and the maternal-fetal transmission rate was estimated to be 33 percent, as only one newborn infant had toxoplasma-IgM antibody at birth. This denoted a prevalence of congenital toxoplasma infection = < 1.0 percent to non-immune mothers. There were no clinical features of congenital infection in the infant with toxoplasma-IgM antibody, but he will require long-term follow-up. All the mothers infected during pregnancy had known risk factors for toxoplasma infection. One-hundred-and-forty-three (96 percent) of the pregnant women were CMV-IgG seropositive at their first antenatal visit. At the time of delivery 143 (96 percent) of the mothers and their newborn infants were CMV-IgG seropositive. None of the mothers or their infants was CMV-IgM seropositive. HBsAg was detected in 8 per cent of pregnant mothers (n = 12) and in two (17 percent) of their newborn infants. None of the mothers was HBeAg positive. In conclusion, the prevalence of toxoplasma infection during pregnancy and its transplacental transmission rate in a rural Egyptian area are high compared to other countries. A toxoplasmosis antenatal screening and public education programmes for pregnant mothers is justifiable in rural Egypt. However, it appears that an antenatal screening programme for CMV is, at present, not warranted.

Animals↗
PubMed1996

Effect of passive smoking on frequency of respiratory illnesses and serum immunoglobulin-E (IgE) and interleukin-4 (IL-4) concentrations in exposed children.

We studied the relationship of serum immunoglobulin-E (Ig-E) and interleukin-4 (IL-4) concentrations, eosinophil counts, and frequency of respiratory illness with passive smoking in 70 randomly selected children of smoking parents. Fifty randomly selected age-matched children of non-smoking parents served as controls. Children of smoking parents had higher frequency of respiratory illnesses per year (P < 0.01), significantly higher total leucocytic and eosinophil counts, higher percentage of eosinophils (P < 0.01), and higher serum IgE and IL-4 concentrations (P < 0.05) compared to the control group. Serum IgE level was correlated positively with the average number of smoked cigarettes/day, number of siblings, and total leucocytic count. Interleukin-4 concentrations were significantly correlated with the number of smoked cigarettes and IgE levels. Although IgE levels were higher in children of smoking parents (587 +/- 359 IU/ml) compared to controls (189 +/- 21 IU/ml), they did not differ significantly between children with and those without frequent respiratory illness (605 +/- 365 and 557 +/- 354 IU/ml, respectively). Interleukin-4 concentrations were significantly higher in children of smoking parents with frequent respiratory illness (1.8 +/- 0.5 pg/ml) v. those without frequent respiratory illness (1.3 +/- 0.45 pg/ml). Multiple logistic regression analysis revealed that the overall positivity of the risk factors predisposing to respiratory diseases in the study children was 79 percent, and the highest odds ratio was that for IL-4 (OR = 5.15). In conclusion, there is a significant increase in IL-4 and Ig-E concentrations, high eosinophil count and frequent respiratory symptoms in children of smoking parents. It remains that the current state of knowledge on health risks associated with passive smoking warrants that strong preventive action be promoted.

Analysis of Variance↗
PubMed1996

Growth parameters, growth hormone (GH) response to clonidine and circulating insulin-like growth factor-I (IGF-I), free thyroxine (FT4) and cortisol concentrations in relation to glycaemic control in children with insulin-dependent diabetes mellitus.

The objective of this paper was to determine the effect of glycaemic control and endocrine functions on linear growth in children with IDDM. We studied 45 prepubertal children with IDDM (30 males, 15 females) over 1 year period. The mean +/- SD for age of onset and duration of IDDM were 6.2 +/- 2.3 years and 3.5 +/- 1.3 years, respectively. At each clinic visit (every 3 months), glycaemic control was assessed by measuring glycosylated haemoglobin (HbA1C). Growth hormone and cortisol responses to high dose clonidine (0.15 mg/m2) and ACTH, respectively, were evaluated and circulating concentrations of free thyroxine (FT4) and TSH estimated. The average insulin dose (unit/kg/day) during this period was calculated for each patient. Growth was assessed by determining both height standard deviation score (HtSDS) and growth velocity standard deviation scores (GVSDS) and bone age determined according to the atlas of Greulich and Pyle. Two-hundred-and-fifty age- and sex-matched normal children served as controls for growth data, and 20 normal age-matched children and 20 normal children with short stature (NVSS) served as controls for the hormonal studies. Growth velocity (GV) (cm/year) and GVSDS were significantly lower in children with IDDM compared to normal children, and significantly lower in children with poorly controlled diabetes compared to those with good glycaemic control. GV and GVSDS were inversely correlated to HbA1C (r = -0.356, P < 0.01 and r = 0.335, P < 0.01 respectively). GVSDS was correlated with serum IGF-I (r = 0.22, P < 0.01), FT4 (r = 0.321, P < 0.01) and inversely with basal GH (r = -0.362, P < 0.01) concentrations, but was not correlated with cortisol levels or peak GH concentrations in response to clonidine. GVSDS was correlated with HtSDS (r = 0.222, P < 0.01) and inversely with age (r = -0.43, P < 0.05). There was no significant correlation between GVSDS on the one hand and weight gain or body mass index (BMI) on the other hand. Peak GH response to clonidine was correlated with BMI (r = 0.68, P < 0.001) and insulin dose/kg/day (r = 0.602, P < 0.01). This study confirms that in children with IDDM linear growth velocity is dependent on the age of the child and the degree of glycaemic control, as well as on growth promoting hormones such as IGF-I and FT4. High BMI is associated with more GH secretion in response to clonidine, this might explain the higher requirements of insulin/kg in children with IDDM and high BMI.

Body Mass Index↗
PubMed1996

Growth parameters and predictors of growth in short children with and without growth hormone (GH) deficiency treated with human GH: a randomized controlled study.

Seventy-seven prepubertal short children with heights below the third centile for age and gender were divided into three groups according to their peak GH response to clonidine and insulin provocation. Group (I) included 30 children with peak GH response < 7 micrograms/l, group (II) included 19 children, with GH peak response between 7 and 10 micrograms/l, and group (III) included 24 children with GH peak > 10 micrograms/l. Each group was divided into two subgroups, a and b. Subgroups (I)b, (II)a and (III)b were treated daily for 1 year with subcutaneous recombinant human growth hormone (GH) 15 U/m2/week, and group (I)a was treated with GH (30 U/m2/week). Before initiation of treatment, the chronological age, the height standard deviation score (HtSDS), and the bone age delay did not differ among the study subgroups. The height growth velocity (GV) and insulin-like growth factor-I concentrations were significantly higher in group (III), with normal GH response to provocation, compared to those for group (I) with GH deficiency. All the children had normal thyroid function and normal glucose tolerance. CT examination of the hypothalamic-pituitary area revealed a picture of empty sella (either partial or complete) in 35 per cent of the children in group (I) and 21 per cent of children in group (II). After 1 year of GH therapy, the HtSDS, GV, and IGF-I concentrations increased significantly in the four subgroups treated with GH compared to their pretreatment values and to their controls. All the children in group (I) were responders (increment in GV of 2 cm2/year above the pretreatment GV), of the nine subjects treated in group (II)a, one child was a non-responder and of the 12 children in group (III)a three children were non-responders. GV was non-significantly higher in group (I)a (30 U/m2/week) v. group (I)b (15 U/m2/week). GV of children in groups (I)b, with abnormal GH response to provocation, was significantly higher than GV of children in group (III)a. Bone age advanced by less than 1 year in the treated groups (0.84 +/- 0.14 years) v. the untreated groups (0.73 +/- 0.3 years). None of the children had impaired glucose tolerance or abnormal thyroid function after 1 year of GH therapy. In all the treated children, GV after 1 year of GH treatment was correlated significantly with the pretreatment GV (r = -0.63, P < 0.01), peak GH response to provocation (r = -0.59, P < 0.01), IGF-I concentration (r = -0.54, P < 0.01), and positively with the GH dose (r = 0.589, P < 0.01). In group (III) children, with normal GH reserve, GV correlated significantly with the pretreatment GV (r = -0.48, P < 0.01) and negatively with the GH peak response to provocation (r = -0.25, P < 0.05). In conclusion, GH therapy improved GV of children growing along or parallel to the 3rd centile, irrespective of their GH response to provocation, without untoward effect on skeletal maturation, thyroid function or glucose tolerance.

Analysis of Variance↗
PubMed1996

Insulin and glucagon responses to provocation with glucose and arginine in prepubertal children with thalassemia major before and after long-term blood transfusion.

Hypertransfusion therapy has dramatically increased the duration and quality of life in patients with B-thalassemia major; however, it leads to chronic iron overload, and is frequently complicated by the development of diabetes mellitus or impaired glucose tolerance. To determine the early effect of iron overload on the endocrine pancreatic function, we studied glucose, insulin, and glucagon responses to oral load of glucose and to arginine provocation in 15 children with B-thalassemia major, before and after (3.1 +/- 0.6 years) high-transfusion and iron chelation and compared them with 15 age matched normal controls. In addition, we evaluated growth hormone (GH) responses to oral clonidine and measured the circulating insulin-like growth factor-I concentration in thalassemic children on long-term transfusion and controls. After long-term high-transfusion, thalassemic children had significantly decreased serum insulin concentrations and low insulin/glucose ratios at 60 and 120 min after an oral glucose load (1.75 g/kg) in comparison with values before therapy and those for controls. None of the thalassemic children had glucose intolerance after this period of frequent blood transfusion; however, their serum glucose levels at 60 and 120 min after the oral glucose load were significantly higher compared to control children. Thirty minutes after starting arginine infusion, serum insulin concentration was significantly lower in thalassemic children compared to before therapy. Basal and arginine-stimulated glucagon secretions were significantly elevated in thalassemic children on long-term blood transfusion with significantly low serum insulin/glucagon ratios. In addition, the high basal serum glucagon concentrations were not suppressed after the oral glucose load. Despite hyperglucagonaemia in all thalassemic children, their blood glucose dropped appropriately below 50 per cent of the fasting glucose level after an intravenous insulin dose (0.1 U/kg) ruling out any significant insulin-resistance. GH responses to clonidine provocation were subnormal in thalassemic children after long-term blood transfusion compared to controls. In summary, thalassemic children on long-term blood transfusion and iron chelation have progressive and early loss of B-cell mass, manifested by decreased insulin release in response to secretagogues, before the development of significant insulin resistance or impairment of glucose tolerance.

Arginine↗
PubMed1996

Hypoinsulinaemia has an important role in the development of oedema and hepatomegaly during malnutrition.

Various alterations in hormonal levels have been suggested to contribute to the development of nutritional oedema and fatty liver in children with kwashiorkor. We present an infant who underwent near-total pancreatectomy at the age of 4 weeks and developed kwashiorkor after 11 weeks. The sequence of events following surgery can be divided into two phases. The first phase was characterized by hyperinsulinaemia and hypoglycaemia before feeds. During this phase, although the weight gain was slow (10 g/day) serum albumin (32 g/I) and prealbumin (0.23 g/I) concentrations were maintained with no oedema or hepatomegaly. In the second phase, insulin deficiency prevailed and he was receiving the same amount of milk (protein)/day (enriched with starch). During that phase he rapidly developed hypoalbuminaemia (18 g/l), hypoprealbuminaemia (0.1 g/l), oedema, hepatomegaly, and dermatosis. This case demonstrates clearly the important role of defective insulin secretion in the development of nutritional oedema and hepatomegaly.

Edema↗
PubMed1996

Interleukin-1-beta, tumour necrosis factor-alpha, islet-cell antibody, and insulin secretion in children with thalassemia major on long-term blood transfusion.

In vitro, cytokines like interleukin-1-beta (IL-1-B) and tumour necrosis factor-alpha (TNF-A) inhibit insulin release and can destroy islet B-cells. We measured blood levels of IL-1-B, TNF-A, and islet cell antibody (ICA) in 20 children with IDDM, 20 of their non-diabetic siblings, 20 children with thalassemia major on long-term hypertransfusion therapy and iron chelation, and 10 normal age-matched children. In the non-diabetic and thalassemic children we investigated the early phase of insulin release after i.v. glucose (0.5 g/kg, 30 per cent solution) and evaluated tolerance to oral glucose (1.75 g/ kg). Circulating IL-1-B and TNF-A concentrations were significantly higher in IDDM-siblings (33.7 +/- 12.7 pg/ml and 655 +/- 165 pg/ml, respectively) v. normal children (21.1 +/- 6.4 pg/ml and 383 +/- 122 pg/ml, respectively). Thalassemic children had no detectable circulating ICA. The prevalence of ICA was 30 per cent in children with IDDM and 60 per cent of their siblings. Impaired oral glucose tolerance was detected in five children with thalassemia (25 per cent), but in none of the IDDM-siblings. The early phase of insulin release was significantly depressed in thalassemic children (peak insulin = 29.2 +/- 5.1 mIU/ml) v. normal children (52.3 +/- 9.5 mIU/ml) and IDDM-siblings (45.3 +/- 12.4 mIU/ml). It appears that thalassemic children had significantly decreased insulin secretion and impaired glucose tolerance, however, the mechanism of B-cell dysfunction is not mediated by ICA nor by cytokines.

Analysis of Variance↗
PubMed1996

Growth and endocrine function after near total pancreatectomy for hyperinsulinaemic hypoglycaemia.

Seven children, with a mean (SD) age of 4.6 (2.1) years, who as infants (21 (7.5) days) underwent near total (95-98%) pancreatectomy for persistent hyperinsulinaemic hypoglycaemia of infancy (PHHI) were studied. At birth all the infants were macrosomic. Four infants had been born after a difficult labour, of whom three had moderate birth asphyxia and respiratory distress. All had normal thyroid function. After surgery transient hyperglycaemia was manifest in six of the children and required insulin treatment for 5.8 (3.8) weeks, and transient hypoglycaemia was encountered in one child and responded well to increased carbohydrate intake and diazoxide for three weeks. Six of the children rapidly crossed down their length and weight centiles during the first year after surgery. At the end of the first year these children were at or below the 5th centile of height and weight for their age and gender. After a period of 4.6 (2.1) years, their mean (SD) height score was -2.57 (0.5), growth velocity 3.9 (0.75) cm/year, and growth velocity SD score -2.1 (0.55)l these were significantly low and denoted significant growth retardation. The growth hormone peak responses to provocation with clonidine were normal (13.5 (2.8) micrograms/l). However, the circulating insulin-like growth factor-I (IGF-I) concentrations were significantly decreased (79 (34) ng/ml). Three of the children developed diabetes at two and a half, five, and seven years after surgery, two others had impaired oral glucose tolerance and six out of the seven children had an impaired C peptide response to glucagon. Defective insulin secretion in these children might directly inhibit IGF-I synthesis in the liver. The body mass index of the pancreatectomised children was 14.9 (0.5) and was normal for age and gender; they had a normal 72 hour faecal fat content and normal serum albumin concentration. These data indicated grossly adequate exocrine pancreatic function. It appears that children requiring near total pancreatectomy for PHHI have normal developmental milestones but defective linear growth with impaired insulin secretion and low IGF-I production despite normal growth hormone response to provocation.

Anthropometry↗
PubMed1996

Defective growth hormone secretion in children with pycnodysostosis and improved linear growth after growth hormone treatment.

Short stature is a characteristic feature of pycnodysostosis. We report defective growth hormone secretion in response to provocation and low insulin-like growth factor-I (IGF-I) concentration in five out of six patients with pycnodysostosis. Physiological replacement with growth hormone increased IGF-I concentration and improved linear growth in these children.

Adult↗
PubMed1995

Testosterone treatment in adolescent boys with constitutional delay of growth and development.

Administration of androgens to adolescent boys with constitutional delay in growth has been highly controversial. One hundred forty-eight adolescent boys with constitutional delay of growth and puberty with a mean age of 14.3 +/- 0.7 years were treated with testosterone enanthate 100 mg intramuscularly each month for 6 months. Growth parameters, sexual maturation, and circulating concentrations of testosterone and insulin-like growth factor-I (IGF-I) were compared with those for 50 age-matched adolescent boys with constitutional delay of growth and puberty with a mean age of 14.1 +/- 0.9 years who did not receive any treatment. The mean height growth velocity, height standard deviation score, weight gain, and IGF-I concentration were significantly greater in the treatment group after 1 year of follow-up evaluation. The advancement in bone age equaled that in chronologic age in the treatment group, with no significant change in the bone age to chronologic age ratio (BA/CA) before versus after therapy. All subjects in the treatment group had clearly entered puberty by the end of 1 year. Testicular size increased significantly in the treatment group and they had significantly higher serum testosterone concentrations 6 months after the end of testosterone therapy as compared with the control group, denoting activation of the hypothalamic-pituitary testicular axis. All subjects in the treatment group were psychologically satisfied with the enhanced growth and increased muscle mass, versus only 40% of those in the control group. In conclusion, our regimen appears to be efficacious and safe for treatment of boys with constitutional delay of growth and puberty and has no deleterious effect on skeletal age.

Adolescent↗
PubMed1995

Study of hepatic functions and prevalence of hepatitis-B surface antigenaemia in Omani children with sickle cell disease.

The prevalence of persistent hepatitis-B surface (HBS) antigenaemia and hepatic functions have been determined in 125 children with sickle cell disease (SCD) as well as in 100 age-matched healthy children. Hepatic functions and the presence of HBS antigenaemia have been followed for 1 year in six children with SCD and 10 normal children following acute hepatitis-B infection. The prevalence of chronic HBS antigenaemia (3 per cent) in children with SCD is not higher than in normal children (11 per cent). The significant elevation of serum alanine transferase (ALT) and bilirubin concentrations in sickle cell children denotes a process of mild hepatocellular dysfunction which is unrelated to hepatitis-B viral antigenaemia. The high incidence of chronic HBS antigenaemia accompanied by elevated serum ALT and bilirubin concentrations in sickle cell children following acute hepatitis-B infection, in addition to the significant impairment of hepatic functions in sicklers with chronic HBS antigenaemia compared to those without the antigenaemia, point out to the high risk of continual parenchymal hepatic damage in these children following acute hepatitis-B infection. Vaccination against hepatitis-B virus should eliminate this risk.

Anemia, Sickle Cell↗
PubMed1995

Defective clonidine-induced growth hormone secretion and normal thyroid and adrenal functions in prepubertal children with chronic renal insufficiency (CRF).

We evaluated clonidine-induced growth hormone (GH) secretion, insulin-like factor-I (IGF-I), free thyroxine (FT4), and thyroid stimulating hormone (TSH) concentrations, basal (8-h) as well as adrenocorticotrophic hormone (ACTH) provoked cortisol secretion in 14 prepubertal children suffering from chronic renal failure (CRF) with impaired statural growth [growth velocity (GV) = 3.7 +/- 0.3 cm/year] and compared these values with those of 10 normal age matched children with normal variant short stature (NVSS) (GV = 4.6 +/- 0.4 cm/year). The body mass indices and the bone age delay did not differ between the two groups (14.8 +/- 0.7 kg/m2 and 1.5 +/- 0.35 years v. 13.8 +/- 0.48 kg/m2 and 2 +/- 0.25 years, respectively). The basal GH concentrations in CRF patients (4.1 +/- 0.8 micrograms/l) were significantly higher than those for the NVSS group (1.56 +/- 0.2 micrograms/l). The peak GH response to clonidine was significantly lower in children with CRF (8.4 +/- 1.7 micrograms/l) v. (19.6 +/- 2.3 micrograms/l) for the control group (P < 0.01). Eight out of the 14 children with CRF did not mount a proper GH response (> 10 micrograms/l) to clonidine stimulation whereas the GH response of all the children with NVSS was above 10 micrograms/l. IGF-I concentrations were higher in patients with CRF (35.6 +/- 10.9 IU/l) compared to those for the NVSS group (22.1 +/- 4.9 IU/l). However, the difference was not statistically significant. There was no significant difference in the FT4, TSH as well as basal (8-h) and ACTH-stimulated cortisol concentrations between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Circulating growth hormone (GH), insulin-like growth factor-I (IGF-I) and free thyroxine, GH response to clonidine provocation and CT scanning of the hypothalamic-pituitary area in children with sickle cell disease.

Serum growth hormone (GH), cortisol, free thyroxine (FT4), thyroid-stimulating hormone (TSH), and insulin like growth factor I (IGF-I) concentrations were measured in 15 children with sickle cell disease (SCD) together with their heights < 5th percentile for age and gender, and in 15 healthy age-matched children who had normal variant short stature (NVSS). GH response to an oral dose of clonidine (0.15 mg/m2) and cortisol response to ACTH stimulation were determined in the two groups. Children with SCD had significantly lower serum concentrations of IGF-I and decreased GH response to stimulation. Eight out of the 15 children with SCD did not mount an appropriate GH response to clonidine provocation (> 10 micrograms/l). CT scanning of the hypothalamic-pituitary area in those eight children with SCD revealed a partial or complete empty sella in all of them. It appears that defective GH release, and consequently low IGF-I production and slow growth velocity in children with SCD might be secondary to hypoxic-vascular insults to their hypothalamic-pituitary axis during one or more of the sickling episodes.

Case-Control Studies↗
PubMed1995

Prevalence of hepatitis-C antibody seropositivity in healthy Egyptian children and four high risk groups.

We studied the prevalence of HCV antibody seropositivity and serum alanine concentrations in a random sample of healthy Egyptian children (n = 110) as well as in four high risk groups of children. Group 1 included 18 children with thalassemia major, group 2 included 17 children with insulin-dependent diabetes mellitus (IDDM), group 3 included 21 children with schistosomal hepatic fibrosis (SHF), and group 4 included 20 children with chronic rheumatic heart disease (RHD). The prevalence rate of HCV seropositivity was 12 per cent in normal children, 44 per cent in thalassemic children, 29 per cent in children with IDDM, 38 per cent in children with SHF and 0 per cent in patients with RHD. The liver size was significantly larger in HCV seropositive normal children as well as in HCV seropositive children with thalassemia and SHF compared to the seronegative children in each group respectively (P < 0.05). In all groups serum alanine transferase concentrations were significantly higher in HCV seropositive v. seronegative children. This pointed out to the high risk of continuous parenchymal hepatic damage in these children following acute HCV infection. In summary, our data revealed a relatively high prevalence of HCV antibody seropositivity in healthy Egyptian children compared to reports from other countries, and a significantly high prevalence of HCV seropositivity in children with thalassemia, IDDM, and SHF which carries a considerably high risk for development of chronic liver disease in these patients.

Adolescent↗
PubMed1995

Nocturnal growth hormone (GH) secretion and GH response to clonidine provocation in children before and after long-term prednisone therapy.

Glucocorticoids reduce growth hormone (GH) response to the majority of exogenously administered stimuli and can variably inhibit growth in man and animals. Recently, however, glucocorticoids have been shown to have varying effects on GH secretion depending on the time of administration and, furthermore, to be potent secretagogues. We evaluated growth parameters, GH response to high-dose clonidine and integrated (12-h) nocturnal and mean (12-h) nocturnal GH secretion in 10 prepubertal children before and after long-term alternate-day prednisone therapy (LTPT). Height standard deviation scores (HtSDS) and growth velocity standard deviation scores (GVSDS) decreased significantly after LTPT. GH response to clonidine as well as integrated and mean nocturnal GH secretion were significantly after LTPT. GH response to clonidine as well as integrated and mean nocturnal GH secretion were significantly depressed after LTPT v. before treatment. We compared growth parameters and GH data of two groups of children before and after LTPT. Group 1 had low GH peak response to clonidine after LTPT, and group 2 had normal GH response to clonidine. Group 1 children had significantly more impairment of their statural growth and nocturnal GH secretion. Growth parameters (HtSDS and GVSDS) during LTPT correlated significantly with the peak GH response to clonidine (r=0.69 and 0.78, respectively) as well as to the growth parameters before therapy (r > 0.9). It appears that LTPT impairs both physiologic and pharmacologically provoked GH secretion and consequently retards growth in children. However, this effect is variable and is affected by the attained statural growth before therapy.

Adrenergic alpha-Agonists↗
PubMed1995

Growth hormone deficiency and empty sella in DIDMOAD syndrome: an endocrine study.

Two girls with DIDMOAD syndrome are presented. One also had severe megaloblastic-sideroblastic anaemia and the other several neurological manifestations. Both were short with defective growth hormone secretion. Computed tomography revealed empty sella in both girls; one had widespread atrophic cortical and cerebellar changes. High doses of thiamine improved the anaemia in the first case, increased C peptide secretion in both, but had no effect on the neurological abnormalities.

Anemia, Sideroblastic↗