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Background:Mobile phone text messaging has rapidly become a socially popular form of communication. Several studies showed that mobile phone might offer a useful means of providing information between clinic visits and might increase adherence to diabetes therapy regimens.Objectives:We conducted a study to evaluate the effect of mobile phone short message service (SMS) on glycemic control in Saudi patients with type 2 diabetes.Patients and Methods:One hundred patients (mean age, 41 ± 9.5 years) were selected at the Security Forces Hospital, Riyadh, Saudi Arabia, and provided with daily educational, reminding SMS messages for four months. Glycosylated hemoglobin (HbA1c) level, frequency of hypoglycemic and hyperglycemic attacks, and compliance with blood glucose monitoring were recorded before and after the trial.Results:In addition to significant improvement in patients’ knowledge, mean fasting blood glucose level improved from 8.60 ± 3.16 to 7.77 ± 3.11 mmol/L and mean HbA1c decreased from 9.9% ± 1.8% to 9.5% ± 1.7%.Conclusions:Mobile phone text messaging increased adherence to diabetes therapy and improved the clinical outcome in Saudi patients with type 2 diabetes.

Context This study describes the molecular genetics of pseudohypoaldosteronism type 1b (PHA 1b) in the highly consanguineous population of two Arabian Gulf countries, Saudi Arabia and Oman. Patients and Methods This study enrolled 22 patients from 13 unrelated families (two families with five patients from Oman and 11 families with 17 patients from Saudi Arabia). All of these patients had presented within the first 10 days of life with nausea and vomiting, hyponatremia, hyperkalemia and hypotension. We isolated DNA from peripheral blood and PCR-sequenced all exons and exon-intron boundaries of SCNN1A and, if negative, SCNN1B and SCNN1G using the Dideoxy Chain termination method. Results We found a total of eight mutations in 13 families as follows: six mutations in SCNN1A, one in SCNN1B, and one in SCNN1G. All of these mutations were novel except one. SCNN1A mutations were: c.1496A>G, p.Q499R (novel) in one patient; c.1453C>T, p.Q485X (novel) in one patient; c.1322_1322delA, p.N441Tfs*41 (novel) in two patients of one family; c.876 + 2 delGAGT (novel) in three patients of one family; c.203_204 delTC, p.I68Tfs*76 (known mutation) in eight patients of five families; and whole SCNN1A gene deletion (novel) in two patients of two families. In addition, a nonsense SCNN1B mutation c.1694C>A, p.S565X (novel) was found in three siblings from one Omani family, and an SCNN1G deletion mutation c.527_528 delCA, p.T176Rfs*9 (novel) in two siblings form another Omani family. Conclusion We characterized a unique genotype of PHA 1b with several novel gene-structure disrupting mutations in SCNN1A, SCNN1B and SCNN1G in a consanguineous population.

Diagnosis and management of growth disorders comprises an important area of pediatric practice. Current procedures in the different stages of the identification, referral, investigation, and treatment of growth disorders in the Gulf Cooperation Council (GCC) countries have been summarized. Evidence-based procedures, relating specifically to height screening for identification of short stature, auxological criteria for patient referral from primary to secondary pediatric care, and general and endocrine investigations and diagnosis have been discussed and outlined. The management issues related to key disorders that are licensed for growth hormone (hGH) therapy, namely GH deficiency, Turner syndrome, short stature related to birth size small for gestational age (SGA), and idiopathic short stature are discussed with recommendations described for best practice. Finally, two key components of short stature management, namely transitional care for the transfer of patients from pediatric to adult endocrinology services and adherence to recommended therapy with hGH, have been addressed with current practice outlines and recommendations presented.

The autosomal recessive form of persistent hyperinsulinemic hypoglycemia of infancy (PHHI) is associated with mutations in either ABCC8 or KCNJ11 genes. In the present study, we describe the clinical features and results of genetic analysis of 13 Saudi Arabian patients with PHHI. Clinically, most patients presented with infantile seizures and/or developmental delay, with a subset of patients who were also found to have abnormal brain imaging and electrophysiological studies. Interestingly no coding pathogenic mutations were identified in these two genes by direct sequencing. However, two splice variants were identified in ABCC8 gene in two patients, and a large deletion of exons 1-22 of the ABCC8 gene was identified in three patients. Our data shows that large deletions in ABCC8 gene are the common genetic mechanism in the Saudi population.