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Biomedical subjects

A T Soliman

Publications and source records attributed to A T Soliman.

51 records · Page 3Linked to original sources
PubMed1994

Hyperammonemia in Marasmic children.

The amino acids citrulline, ornithine and arginine, total serum proteins, serum enzymes glutamic oxalacetic and glutamic pyruvic transaminases, blood ammonia and urea were measured in 20 marasmic children with manifest psychomotor changes, before and after nutritional rehabilitation, as well as in 10 healthy age-matched children. Serum protein levels were significantly low and plasma ammonia concentrations were significantly elevated in marasmic children before refeeding (177 +/- 66 micrograms/dl). Plasma ammonia concentrations decreased significantly after 4 weeks of nutritional rehabilitation (38 +/- 18 micrograms/dl). The levels of blood urea, serum enzymes, citrulline arginine, and ornithine did not differ among the study groups. These findings denote that hyperammonemia in marasmic children is neither due to defective hepatic function nor due to enzymatic blockade in the urea cycle.

Alanine Transaminase↗
PubMed1992

Evaluation of captopril versus reserpine and frusemide in treating hypertensive children with acute post-streptococcal glomerulonephritis.

We have evaluated the effect of oral captopril versus a combination of oral reserpine and frusemide in the treatment of 20 children with post-streptococcal glomerulonephritis (APGN) with hypertension. Captopril produced a significantly greater reduction in systolic and diastolic blood pressure in both the standing and supine positions than reserpine + frusemide at 0.75, 1, 1.25, 8, 24, 48 and 72 h after initiating treatment. Neither postural hypotension nor reflex tachycardia accompanied the therapeutic effect of captopril. Blood urea, serum creatinine and creatinine clearance did not change significantly after therapy in either study group. Three days after initiating treatment, the 24 h urinary catecholamine output increased significantly in children who received captopril but did not change in children treated with frusemide and reserpine.

Acute Disease↗
PubMed1991

Circulating growth hormone, insulin-like growth factor I, cortisol and free thyroxine in children with schistosomiasis with and without hepatic fibrosis.

Serum insulin, growth hormone (GH), cortisol, free thyroxine (T4) and plasma insulin-like growth factor I(IGF-I) concentrations were measured in 20 children suffering from schistosomiasis as well as 10 healthy age-matched controls. Circulating GH and insulin levels were determined after an intravenous infusion of arginine HCl (10 per cent solution, 0.5 g/kg). Children with schistosomal hepatic fibrosis (n = 10) had heights more than 2 SD below the mean for their age and sex. Their circulating IGF-I, free T4, and cortisol levels were significantly reduced. They had markedly elevated serum insulin concentrations with normal response to arginine infusion. Their basal GH levels were normal with significantly reduced GH response to arginine provocation. Compared to controls, they had significantly lower serum albumin concentrations, prolonged prothrombin time and elevated alanine transferase (ALT) levels. Free T4 and IGF-I concentrations, and GH increments after provocation correlated significantly with the percentile heights of these patients (r = 0.90, 0.70, and 0.83, P less than or equal to 0.001, less than or equal to 0.05 and less than or equal to 0.01 respectively). Their IGF-I levels correlated closely with the prothrombin time and ALT concentrations (r = 0.87 and 0.77, P less than or equal to 0.002 and less than or equal to 0.01, respectively). It is suggested that the depressed circulating IGF-I and free T4 levels in addition to deficient GH reserve may be responsible for stunted stature in patients with schistosomal hepatic fibrosis.

Anthropometry↗
PubMed1990

Study on some hepatic functions and prevalence of hepatitis B surface antigenaemia in Egyptian children with schistosomal hepatic fibrosis.

Several different hepatic parenchymal lesions, including chronic hepatitis and cirrhosis, have been increasingly reported in children with schistosomal hepatic fibrosis (SHF) despite the known mesenchymal nature of the disease. The prevalence of persistent hepatitis (B) surface (HBs) antigenaemia and some hepatic functions have been determined in 52 children with SHF as well as in 100 age-matched healthy children. High prevalence of chronic HBs antigenaemia (58 per cent) has been demonstrated in children with SHF, but only in 2 per cent of the normal children. This denotes that children with SHF represent a dangerous reservoir for hepatitis B infection to the community. Serum alanine transferase (ALT) was higher than normal in 58 per cent of HBS seropositive patients and in none of the seronegative patients. This points to the risk of continual hepatic parenchymal injury to the HBs seropositive patients with schistosomiasis.

Adolescent↗
PubMed1986

Serum insulin-like growth factors I and II concentrations and growth hormone and insulin responses to arginine infusion in children with protein-energy malnutrition before and after nutritional rehabilitation.

Serum insulin, growth hormone (GH), insulin-like growth factors (IGFs) I and II, cortisol, and albumin concentrations were measured in 15 children with kwashiorkor, 15 with marasmic-kwashiorkor, and 21 with marasmus, before and in the survivors, after nutritional rehabilitation, as well as in 10 underweight and eight normal Egyptian children. We also evaluated arginine-induced insulin and GH secretion. IGF-I concentrations were reduced in the three severely malnourished groups (0.07 +/- 0.03, 0.05 +/- 0.03, and 0.09 +/- 0.09 U/ml, respectively) but returned to normal after refeeding. IGF-II concentrations were low in the kwashiorkor (175 +/- 79 ng/ml), marasmic-kwashiorkor (111 +/- 57 ng/ml), and marasmic children (128 +/- 70.9 ng/ml) and returned to normal after nutritional rehabilitation. Basal GH levels were high in the three severely malnourished groups (21.9, 28.8, and 16.6 ng/ml, respectively) and returned to normal after refeeding (8.1, 6.5, and 6.0 ng/ml, respectively). GH responses to arginine were depressed in the three malnourished groups and improved significantly in marasmic-kwashiorkor and marasmic children after nutritional rehabilitation. Insulin responses to arginine were impaired in kwashiorkor, and marasmic-kwashiorkor children and improved significantly after refeeding. IGF-I levels correlated significantly with percent of expected weight (r = 0.52, p less than 0.001), percent of expected height (r = 0.42, p less than 0.001), and weight/(height)2 index (r = 0.34, p less than 0.01). IGF-I levels correlated positively with insulin levels (r = 0.421, p less than 0.001) and negatively with cortisol concentrations (r = -0.400, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Anthropometry↗
PubMedDate not supplied

Defective growth hormone secretion and hypogonadism in the new syndrome of congenital hypoparathyroidism, growth failure and dysmorphic features.

A child with extreme growth failure, dysmorphic features, hypoparathyroidism, and abnormal skeletal survey was studied. He was a product of first degree consaguineous marriage who had intrauterine growth retardation and presented at 14 days of age with hypocalcemic tetany with normal cardiovascular system and immune function. Endocrine evaluation after infancy revealed defective growth hormone (GH) secretion in 2 provocation tests and lack of clinical and testosterone response to human chorionic gonadotrophin (HCG) therapy.

Child, Preschool↗
PubMedDate not supplied

Defective growth hormone (GH) secretion and short-term treatment in Noonan syndrome.

Auxological and endocrine data from 12 prepubertal children (3 males, 9 females) with Noonan syndrome (NS) were compared with those of 15 children with constitutional short stature (CSS), 20 children with partial GH deficiency (GHD), and 6 children with Turner syndrome (TS). Four children with NS were treated with human growth hormone (hGH) (n = 4) (25 units/m2 week, divided on daily s.c. doses). In children with NS, the peak serum GH response to clonidine (5.4 +/- 2.7 ug/L) and glucagon (7.4 +/- 3.4 ug/L) were significantly lower than those for children with CSS (14.8 +/- 3.4 and 12.8 +/- 2.8 ug/L respectively). Nine out of the 12 (75%) children with NS did not mount normal GH peak (10 ug/L or more) after provocation. The 12-h integrated GH secretion in the 3 children with NS who had normal GH response to provocation (2.7 +/- 0.7 ug/L) was markedly lower compared to that for children with CSS (6.7 +/- 1.2 ug/L). The serum insulin-like growth factor-1 (IGF-I) concentrations were lower in children with NS (67 +/- 32 ng/ml) vs CSS (165 +/- 35 ng/ml), but not different from those for GHD children (59 +/- 33 ng/ml). In 4 children with NS, hGH therapy for a year increased height growth velocity from 4.1 +/- 0.3 cm/yr to 7.4 +/- 0.6 cm/yr and height standard deviation score (Ht SDS) from -2.2 +/- 0.6 to -1.45 +/- 0.3. This growth acceleration was accompanied by an increase in IGF-I concentration (from 52 +/- 21 ng/ml to 89 +/- 25 ng/ml). In summary, these results prove a defect of the GH secretion in children with NS and suggest that GH therapy has an important role in the management of their short stature.

Child↗
PubMedDate not supplied

Empty sella in short children with and without hypothalamic-pituitary abnormalities.

A study was conducted on growth hormone (GH) response to oral clonidine (0.15 mg/m2), GH and cortisol responses to i.m. glucagon (0.1 mg/kg), and glucose response to an oral load of glucose (1.75 g/kg). Measurements were made on the circulating concentrations of free thyroxine (FT4), thyroid stimulating hormone (TSH) and different growth parameters and CT sellar images in 25 GH deficient children (Peak GH response to clonidine and glucagon < 7 ug/ml), 15 growth retarded children (Ht < 5th percentile for age and gender) with sickle cell disease (SCD) and GH deficiency, 30 randomly selected children with normal variant short stature (NVSS) (HtSDS 2SD below the mean for age and gender with normal GH response to stimulation (> 10 ug/ml) and 20 age-matched normal children were evaluated. Out of the 25 children with GH deficiency, five had multiple pituitary hormonal deficiency (GH < TSH and/or ACTH. deficiencies), and 20 had isolated GH deficiency. Empty sella, either complete or partial, was detected in 9 out the 20 children with isolated GH deficiency (45%), 4 out of the 5 children with multiple pituitary deficiency (80%), all the children with SCD and GH deficiency (100%), 3 out of the 30 children with NVSS (10%) and in none of the normal children. The insulin-like growth factor-I (IGF-I) concentrations were significantly lower in the two groups of children with GH deficiency compared to those with NVSS. The height standard deviation scores (HTSDS) were significantly lower and the annual growth velocity was slower in children with idiopathic GH deficiency and empty sella compared to those with NVSS and those with empty sella associated with SCD. The bone age delay (yr) did not differ among the 3 groups of children with short stature. All children with isolated GH deficiency associated with empty sella had normal body mass indices (BMI), while all the children with SCD and empty sella had BMI below the 5th percentile for the corresponding age and gender. None of the children had glucose intolerance. In conclusion, children with growth retardation and abnormal hypothalamic pituitary functions have high incidence of empty sella. However, empty sella is detected in considerable number (10%) of short children with normal hypothalamic pituitary function.

Administration, Oral↗
PubMedDate not supplied

Permanent neonatal diabetes mellitus: epidemiology, mode of presentation, pathogenesis and growth.

Permanent neonatal diabetes mellitus (PNIDDM) is a rare form of IDDM with unclear etiology and pathogenesis. We determined the incidence and prevalence rates and studied the clinical and biochemical features of PNIDDM in the Sultanate of Oman. The mean incidence rate during the study period from January 1989 to December 1994 was 1.788 +/- 0.82 per 100,000 live births per year. At the end of December 1994 the prevalence rate was 2.4 per 100,000 children below the age of 5 years. They constituted 41.6% of all cases of IDDM in this age group. Diarrhoea, fever, lethargy, poor feeding and failure to thrive were the most common presenting symptoms. Dehydration and tachypnoea were the most common signs. All patients who developed IDDM during the neonatal period had intrauterine growth retardation and 4.5 presented with diabetic ketoacidosis (plasma glucose 37 +/- 9 mmol/L, pH 7.12 +/- 0.1). Hypertriglyceridemia was a constant feature (19.4 +/- 4.8 mmol/L). They were products of consanguineous marriage with significantly high prevalence of IDDM and NIDDM in their family members. None of the infants had clinical or immunological evidence of congenital viral infection. Three of the five children had HLA-DR2, the diabetes resistance alleles. C-peptide secretion was absent during and after metabolic control of hyperglycemia in all the studied infants and none had circulating islet cell antibody at presentation or during the first year after diagnosis. Despite marked growth retardation at birth, there was a significant improvement of growth after initiating insulin therapy. Four of the 5 patients had normal developmental milestones, one had mild developmental delay following a severe and prolonged attack of hypoglycemia. None of the patients had exocrine pancreatic deficiency. In summary, the very high rate of parental consanguinity, occurrence in both sexes and in two siblings in the same family, absence of islet cell antibodies and the presence of HLA-DR2 loci in 3/5 of patients suggest that PNIDDM is a different disease process to standard IDDM in childhood and an autosomal recessive mode of transmission.

Autoantibodies↗
PubMedDate not supplied

Arginine-induced insulin and growth hormone secretion in children with nutritional rickets.

We evaluated arginine-induced insulin and growth hormone (GH) secretion in ten children with vitamin D deficiency rickets and compared these values with those of eight age-matched control children. All rachitic children had biochemical (increased serum alkaline phosphatase activity and decreased calcium x phosphate product) and clinical evidence for rickets. After an intravenous infusion of arginine-HCl (10% solution, 0.5 g/kg), blood samples were obtained for the measurement of serum insulin and GH concentrations. The mean insulin level 30 min after the start of the infusion was 22.2 +/- 17.1 microU/ml for the rachitic children. This value is significantly below that for the normal children, 63.4 +/- 38.7 microU/ml (p = 0.004). Neither the fasting insulin level nor any others after the arginine infusion differed significantly from those for the control children. There were no significant differences in the fasting or the arginine-stimulated GH levels between the rachitic and control children. The concentrations of insulin-like growth factors did not differ between the two groups.

Alkaline Phosphatase↗