Eight of nine newborn infants with severe persistent pulmonary hypertension of the newborn (PPHN), and a predicted mortality of 100%, and one infant with a predicted mortality >94% based on alveolar-arterial oxygen tension difference ((A-a)Do2) were treated with magnesium sulphate (MgSO4) as a life saving therapy after they failed to improve with conventional treatment. At high serum concentrations magnesium is a potent vasodilator, muscle relaxant, and sedative. 1 Previous studies showed that magnesium can prevent and reduce hypoxia induced pulmonary hypertension. 1719 Eight infants with severe PPHN and a predicted mortality of 100% and one infant with a predicted mortality >94% based on (A-a)Do2 criteria were treated with magnesium sulphate (MgSO4) as a life saving therapy after they failed to improve with conventional treatment when extracorporeal oxygenation and oscillatory ventilation were not available.Methods and subjects In our unit, newborn infants with PPHN are treated by conventional methods.' 20 Nine infants with a clinical and laboratory picture consistent with PPHN'-3 20 failed to improve with conventional management after a period ranging from 15 to 92 hours (tables 1 and 2). Congenital heart disease was excluded in all infants by echocardiography. (A-a)Do2 was greater than 84-3 kPa (630 mm Hg) in eight of nine infants, and was 82-1 kPa (616 mm Hg) in one infant (table 3). By published criteria all were considered candidates for extracorporeal membrane oxygenation.6 12 (A-a)Do2 was calculated using the following formulas:

SUMMARY Seven infants with persistent neonatal hyperinsulinism were treated in Dhahran Health Centre from 1983 to 1986. The insulin:glucose ratio (serum insulin concentration pmolIl) divided by the blood glucose concentration (mmolI1) ranged from 12 to 636, mean (SD) 177 (201). To control hypoglycaemia, diazoxide (12-24 mg/kg/day) was given in a continuous intravenous glucose infusion (12-22 mg/kg/min) on 11 separate occasions, four infants twice each and three infants once each. An increase of more than one standard deviation in the heart and respiratory rates, together with other symptoms of heart failure, was considered to be evidence of diazoxide toxicity. Cardiorespiratory failure (toxicity) occurred on eight of the 11 occasions (73%) in seven infants. The average daily fluid intake, weight change, respiratory rate and heart rate before treatment were similar whether or not the infant developed toxicity. A diazoxide toxicity index was obtained by multiplying the dose of diazoxide by the insulin:glucose ratio to relate the diazoxide dose to the severity of the disease. In all instances when the toxicity index was more than 1533 (mean (SD) 3732 (2741)) cardiac toxicity developed. In contrast, infants with a toxicity index of less than 675 (mean (SD) 364 (270)

A case of histologically documented renal amyloidosis occurring in a boy who had juvenile rheumatoid arthritis is presented. The presenting problem was massive proteinuria resulting in nephrotic syndrome. Secondary amyloidosis is a serious complication of juvenile rheumatoid arthritis and it indicates very poor prognosis.

Since its description in Japan in 1967, Kawasaki disease has been reported from several parts of the world but has been reported only once in an Arab child and never from the African continent. We report a typical case of Kawasaki disease in an Arab child in Africa who later developed coronary and several peripheral aneurysms.

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