Could the MMR vaccine replace the measles vaccine at one year of age in Egypt?

This cross-sectional study evaluated the immune status of non-vaccinated healthy infants to determine if it is possible to replace both measles vaccine (at 9 months) and measles, mumps and rubella (MMR) vaccine (at 18 months) with a single dose of MMR at 12 months. Serum samples from 566 children in Alexandria, Egypt showed a significant decrease in the seropositive rate to the 3 viral diseases with increasing age, but a significant increase in the seropositive rate among infants who were ranked 1st or 2nd in their family, full-term or born to mothers with no history of hypertension during pregnancy. We recommend administration of the first dose of MMR vaccine between 9 and 12 months of age, and a booster dose of MMR vaccine at 4 years of age.

Could the MMR vaccine replace the measles vaccine at one year of age in Egypt?

This cross-sectional study evaluated the immune status of non-vaccinated healthy infants to determine if it is possible to replace both measles vaccine [at 9 months] and measles, mumps and rubella [MMR] vaccine [at 18 months] with a single dose of MMR at 12 months. Serum samples from 566 children in Alexandria, Egypt showed a significant decrease in the seropositive rate to the 3 viral diseases with increasing age, but a significant increase in the seropositive rate among infants who were ranked 1st or 2nd in their family, full-term or born to mothers with no history of hypertension during pregnancy. We recommend administration of the first dose of MMR vaccine between 9 and 12 months of age, and a booster dose of MMR vaccine at 4 years of age

Interleukin-1-beta, tumor necrosis factor-alpha, insulin secretion and oral glucose tolerance in non-diabetic siblings of children with IDDM.

Recent reports suggest that the pancreas participates in tumor necrosis factor alpha (TNF-A) production during stress, and that the islets are predominantly responsible for such synthesis. In vitro TNF-A and interleukin 1-beta (IL-1-beta) inhibit insulin release from islet beta-cells. We measured the circulating levels of IL-1-beta, TNF-A and islet cell antibody (ICA) in 30 children with IDDM (10 of them at their first presentation), 30 of their non-diabetic siblings, and 30 normal age-matched children. In the non-diabetic children we investigated the early phase of insulin release after intravenous bolus of glucose and evaluated tolerance to oral glucose (OGTT). IL-1-beta and TNF-A concentrations were significantly higher in IDDM-siblings (31.8 +/- 7.7 pg/ml and 650 +/- 155 pg/ml respectively) versus normal children (21.2 +/- 6.4 pg/ml and 383 +/- 122 pg/ml respectively). IL-1-beta and TNF-A concentrations did not differ significantly between the diabetic children and healthy age-matched controls. ICA were detected in 60% of the recently diagnosed diabetic children vs. 30% of those with longer duration of diabetes (3.1 +/- 1.2 years). Despite the significantly high prevalence of ICA in the recently diagnosed children with IDDM, their IL-1-beta and TNF-A concentrations were lower than those for the normal children. In experimental animals these cytokines can induce round cell infiltration (insulinitis) and inhibit insulin secretion by beta-cell. The presence of significantly higher concentrations of these cytokines in IDDM siblings, with high prevalence of ICA (16%), was associated with normal oral glucose tolerance and normal peak insulin response (60 +/- 10.4 mlU/ml) after i.v. glucose bolus compared to normal children (52.3 +/- 9.5 mlU/ml). However, after 2 years of follow up, one of them developed IDDM and another developed IGT but none of the normal controls developed abnormal glucose tolerance. It appears that the process of autoimmune aggression against beta-cells, and its effect on insulin release and glucose homeostasis, is a slow and chronic process. However, the production of these cytokines and consequently the degree of beta-cell destruction, in a genetically susceptible subject, might be enhanced by several factors including viral infections. In summary, IL-1-beta and TNF-A levels can be used as indicators of continuing autoimmune aggression against beta-cells before the development of extensive beta-cell destruction.

Ultrasonographic and Doppler study of the thyroid gland in Graves' disease before and after treatment with antithyroid drugs.

OBJECTIVE: To determine the effects of medical treatment on the thyroid gland, peripheral circulation, and laboratory findings in patients with Graves' disease. METHODS: Twenty patients with Graves' disease were treated with either carbimazole and propranolol (group I) or carbimazole only (group II). Serum free thyroxine (FT(4)), thyroid-stimulating hormone (TSH), and thyrotropin-binding inhibitory immunoglobulins (TBII) were estimated before and after 6 weeks of treatment. Duplex Doppler ultrasonographic examination of the thyroid, inferior thyroid artery (ITA), and common carotid artery (CCA) was performed before and after 2, 4, and 6 weeks of therapy. RESULTS: Serum FT(4) and TBII decreased after treatment in both groups, whereas serum TSH increased in group I only. The volume of the thyroid gland and parenchymal blood velocity were increased in these patients and diminished only with addition of propranolol to carbimazole. A diffuse hypoechogenic pattern in the thyroid gland and increased ITA blood flow and peak velocity were observed in all patients and persisted throughout treatment. The mean CCA peak blood velocity was accelerated in Graves' disease and diminished after 6 weeks of therapy in both groups, whereas increased CCA blood flow diminished only in group I. CONCLUSION: A 6-week period of therapy with carbimazole and propranolol has no effect on the diffuse low echogenic pattern in the thyroid gland and the accelerated ITA blood flow in Graves' disease. The addition of propranolol is associated with early decrements in thyroid volume, parenchymal vascularity, and CCA blood flow as well as early recovery of TSH suppression, but it has no additional effect on thyroid hormone secretion or TBII levels.

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.

A study on beta-adrenergic receptors in children with asthmatic bronchitis.

The function of beta-adrenergic receptors was assessed in 50 children with asthmatic bronchitis and 45 healthy controls by the hyperglycemic, eosinopenic and platelet aggregation responses to epinephrine. The results showed evidence of beta-adrenergic blockade in children with asthmatic bronchitis. It is suggested that this blockade may reflect a functional and/or a structural immaturity of the beta receptors in these children.