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Biomedical subjects

M Asfour

Publications and source records attributed to M Asfour.

At least 37 records · Page 2Linked to original sources

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↗

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↗

[Therapeutical effects of bromocriptine (CB 154) in 10 acromegalic subjects. Study of somatotrophic function and clinical survey (author's transl)].

Plasma GH levels were studied following acute administration of 2.5 mg of bromocriptine (CB 154) in 12 acromegalic patients. In 9 responders, reduction of GH levels was obvious 2 to 4 hours after bromocriptine administration and the lowest values were achieved between 5 and 8 hours following drug absorption. This pattern suggested the use of bromocriptine at a dose of 2.5 mg six-hourly in chronic treatment of acromegaly. Chronic administration of CB-154 in 10 acromegalic patients was followed by a stable reduction of plasma GH levels in seven subjects. No appreciable variation in GH levels were observed in one patient who was unresponsive to acute administration of CB-154 and in two other subjects treated with 2.5 mg 12-hourly. In three patients who had high plasma GH levels inspite of an anterior treatment by hypophyseal surgery and/or physiotherapy, plasma GH values were normalised under bromocriptine therapy. (9 to 24 months). In the four other subjects, high basal plasma GH levels were reduced with at least 50% reduction rate from baseline. Nevertheless, in two subjects from the latter group bromocriptine daily dose was increased to 20 mg divided in four fractions, because of an escape phenomenon to initial dose regimen. Normalisation or reduction of plasma GH levels was associated with considerable clinical improvement. Tolerance of the drug was excellent in all patients but four who experienced nausea and vomiting; these side effects disappeared when treatment was reduced and then increased gradually.

Acromegaly↗