In Suleimania Children's Hospital, Riyadh, Saudi Arabia, 110 diabetic children were diagnosed and followed over a 5-year period (1985-1989). Seventy-five percent (82/110) were of Saudi origin and 54% (59/110) female. Their parents were often related, 31% (34/110) being first degree cousins, and 12% (13/110) second degree cousins. First degree family history was positive for Type 1 diabetes in 28% (31/110). Among these cases, siblings accounted for 26%, fathers 2%, and mothers none. Family history was also positive for Type 2 diabetes in 35% (38/110) and for both Type 1 diabetes and Type 2 diabetes in 14% (15/110). Mean age at onset was 5.9 years (7 months to 12 years). Thirty percent (33/110) of the patients were under 3 years of age on admission. The most common clinical presentation was diabetic ketoacidosis, seen in 67% of the patients (74/110).

The incidence of congenital adrenal hyperplasia in Saudi Arabia and the frequency of the carrier rate are not well known. Both figures should be high, considering the commonness of first-degree consanguinity in this part of the world. We present 25 cases of congenital adrenal hyperplasia, most of them due to a defect of the 21 hydroxylase enzyme, diagnosed and followed over three years at Suleimania Children's Hospital in Riyadh. There were ten boys and 15 girls exhibiting all degrees of masculinization, mostly Grade III (53%) and Grade IV and V (13.3% each). The degree of masculinization of the external genitalia in the girls (46XX) was sufficiently pronounced in seven patients to lead to sex identity errors at birth. This aggravated the psychological reactions in the families, particularly before the surgical correction. The frequency of neonatal deaths in the patients' families related to a similar disorder was high (12%). The mean age at onset of the salt-losing crises in affected infants was 9 days in females and 25 days in males and this was the most common clinical presentation of the disorder (80%). Systematic neonatal screening and intrauterine diagnosis in at risk families must be done to provide hormonal intervention and thus prevent the formation of ambiguous genitalia and avoid the resulting plastic surgery that must be performed in female patients. Congenital adrenal hyperplasia is common in Riyadh, where marriages between first-degree relatives are frequent. As everywhere, and particularly under the local sociocultural conditions, discussion is focused on the genetic sex which isnot always easy to determine, depending on the degree of masculinization of otherwise genetically defined females. The surgical correction and the psychological consequences in the affected families also contribute to the problems. Intrauterine and neonatal screening are therefore important. Likewise, intrauterine treatment may prevent genital abnormalities and the neonatal deaths caused by salt-losing crises. The etiology, medical and surgical treatment, and follow-up of clinical, radiological, and biological features are discussed, along with the problems of neonatal and intrauterine screening. Patients and MethodsCongenital adrenal hyperplasia was diagnosed in 25 patients who were followed up at the Suleimania Children's Hospital in Riyadh over a period of three years. Nationality and supposed sex as well as family history were recorded. The age of onset and clinical presentation, particularly the presence or absence of a salt-losing syndrome,

Despite the fact that much of Saudi Arabia is sunny throughout most of the year, vitamin D deficiency rickets is not rare. Different factors are responsible for this phenomenon, especially nutritional, social, and maternal vitamin D deficiency. We identified 500 cases of rickets out of a total of 27,236 hospital admissions, and followed at Suleimania Children's Hospital in Riyadh over three years (1986 to 1988). Eighty-one percent of the patients were Saudi (mean age, 8.2 months), which is significantly lower than that usually observed. Most of the patients had nonspecific findings at onset, indirectly related to the vitamin D deficiency, particularly recurrent chest infections (66%) and hypocalcemic convulsions (17.2%). The young age at onset, which was 39.2% in patients younger than six months at onset and 14.2% in those younger than three months, is unusual compared with ages cited in the literature, and this most probably relates to maternal vitamin D deficiency. Subclinical forms of rickets, detected by the screening, also seem to be common. We conclude that rickets is a major health problem in Saudi Arabia and more attention needs to be paid to its detection, treatment, and prevention.A Abanamy, H Salman, M cheriyan, M Shuja, S Siddrani, Vitamin D Deficiency Rickets in Riyadh. 1991; 11(1): 35-39 Vitamin D deficiency rickets is due to dietary factors and poor sunlight exposure. The incidence of vitamin D rickets is therefore usually low in sunny countries, but in Riyadh it is not rare.We evaluated the factors associated with the development of rickets in our community, and discuss the preventive measures that should be adopted. Patients and MethodsRickets was diagnosed in 500 patients (out of a total of 27,236 admissions) and patients were followed at Suleimania Children's Hospital in Riyadh over a period of three years (1986 to 1988).Diagnosis was based on clinical (widened wrists and rosary rickets), radiological (rosary rickets, widening, cupping, fraying of distal ends of the ulna and radius), and biological (high alkaline phosphatase activity) findings. Furthermore, 1213 breastfed Saudi children below two years of age, seen in the outpatient clinic for nonspecific

No abstract

Sera from 162 Saudi Arab children were examined for autoantibodies to thyroid microsomes, thyroglobulin pancreatic islet cells, gastric parietal cells, and adrenocortical cells. The subjects included a control group (n = 76) and 86 children below 14 years with Type 1 diabetes. Antithyroid antibodies were detected in 8.1% of the diabetic group and in none of the control group. Parietal cell antibodies were found in 9.3% of the diabetic group and 4.4% of the control group; 14.6% of diabetic children and 2.2% of control children were positive for islet antibodies. However, 56.3% (9/16) of those who were tested at onset of diabetes had positive islet antibodies. In none of the children could we detect adrenocortical cell antibodies.