This study shows the high prevalence of marginal vitamin D nutrition in women in Saudi Arabia, which may predispose babies to rickets during infancy. In a country endowed with plentiful sunshine, the exclusion of sunshine by thick dark veils and bad housing probably contribute to this marginal state of vitamin D nutrition.The two major sources of vitamin D in the body are the diet and the skin. Dietary vitamin D is obtained from animal sources, and hence vegetarian diets are notorious for the lack of this vitamin.' The synthesis of vitamin D in the skin depends on exposure to ultraviolet rays from the sun2-4; the lack of sunshine in a country such as the UK can curtail exposure of the skin to the sun to an extent that people on vegetarian diets-for example, Asian immigrants in the UK-may develop a deficiency of vitamin D.5-8 This deficiency may be corrected spontaneously during the summer.9 It is, however, difficult to conceive of vitamin D deficiency in a setting where most people are non-vegetarian and where there is plentiful sunshine. It was therefore surprising that rickets was found frequently in preschool children in Saudi Arabia.In view of this finding we embarked on a study of vitamin D state in that section of the population of Saudi Arabia most vulnerable to lack of vitamin D-that is, the pregnant women and their newly delivered babies. Since the demands of vitamin D

The existence of nutritional deficiency rickets among infants in sunny Riyadh was confirmed radiologically. Most of the rachitic infants were breast-fed, some received unsupplemented infant feeding formulae, and all live in an environment that is devoid of sunlight. Their mean age at the time of onset was 10.5 months. 25-Hydroxyvitamin D (25OHD) levels were found to be low in mothers of the rachitic infants. This maternal deficiency as a factor in pathogenesis of rickets in the infant is discussed. Proposals are made to prevent the occurrence of rickets on this scale.

One hundred and twenty percutaneous renal biopsies performed in 104 patients aged 1 month to 15 years were analysed. Ultrasound examination was used for localization of the kidneys. Adequate renal tissue was obtained in 103 biopsies, with an overall success rate of 85.8%. The most frequent complication was gross haematuria, which occurred in 32 biopsies, but only 5 children required blood transfusion. Nineteen patients developed perirenal haematoma; 2 of these were symptomatic. Arteriovenous fistula was diagnosed in 2 patients. One patient died secondary to intestinal perforation. Serious complications were noted in patients with chronic renal failure. The success and complication rates in 10 patients less than 1 year of age were comparable with the rest of the group. The frequency of serious complications on renal biopsy in the present study was slightly higher than in the more developed countries.

We need to look out for cardiomyopathy among infants with hypocalcemia. For prevention maternal supplementation during pregnancy and lactation with up to 2000 units of vitamin D and 400 units for their infants.

Blood coagulation and platelet aggregation were assessed in children with nephrotic syndrome who were divided into the following groups: (1) relapse without treatment: (2) relapse on steroids; (3) early remission; (4) late remission and (5) steroid resistant. The renal histological findings were also recorded. Plasma anti-thrombin III (ATIII) levels were markedly reduced in groups 1 and 2, below normal in group 3 and were normal in groups 4 and 5. There was significant urinary loss of ATIII in groups 1 and 2 as well as in group 5. Plasma fibrinogen fluctuations exhibited the expected negative correlations with plasma ATIII. Reptilase time showed significant prolongation in groups 1, 2 and 3, and was near normal in groups 4 and 5. Platelet aggregation in response to arachidonic acid exhibited aggregation followed by disaggregation in groups 1, 2, 4 and 5, and was normal in group 3. Hyperaggregation in response to decreasing doses of ADP was noted in all patient groups as well as controls with no relationship to serum albumin levels. Aggregation responses to collagen and ristocetin were normal. It is concluded that: 1. The fluctuations in ATIII levels in childhood nephrotic syndrome are determined by the response to steroids and not by the renal histology per se. 2. An acquired fibrin polymerization defect (dysfibrinogenaemia) and an abnormality of the prostaglandin pathway of platelet activation, both reversible, are yet other haemostatic abnormalities in childhood nephrosis. 3. The discrepancies in the literature on haemostatic parameters, specially ATIII in childhood nephrosis, would not have arisen if their fluctuation in relation to steroid therapy as well as the renal histological features of nephrotic syndrome had been documented simultaneously.

Congenital rickets is the term given to fetus born with clinical features of rickets, but those born with biochemical evidence of rickets without obvious clinical features still can be considered occult congenital rickets. Some of the affected babies with this disease have the intrauterine rachitic environment, but a calcium trans-placental pump prevents the fetus from having clinical features of rickets. They may present with hypocalcemia few days after birth or later with more florid features of rickets. Congenital rickets cases born with florid features reported over the last 40 years are few and can be divided into two groups. The first due to severe maternal osteomalacia in which their bones were so decalcified to have enough calcium to be pumped to their fetus. Another group in which newborn babies were hypocalcemic due to other maternal diseases as malabsorption, celiac disease, pre-eclampsia, and prematurity. All inherited rickets cases per se, or as part of other syndromes can be considered congenital rickets. Most cases seen in our region are due to maternal vitamin D deficiency with symptoms becoming obvious when the infants are breastfed, or may present with hypocalcemic convulsions or craniotabes. This is a review of congenital rickets with the aim of shedding light on this potentially acute disease that needs more attention and awareness in the neonatal period to avoid rare serious complications as cardiomyopathy or myelofibrosis and the complications of hypocalcemic convulsions. Congenital rickets cases seen simulate a tip of an ice-burg and its prevention is an important issue, especially with the tremendous urbanization with tall buildings living in sun-deprived flats as the commonest type of residence leading to the increasing incidence of maternal osteomalacia and rickets.

Rickets among breast-fed infants is seen in Riyadh, Saudi Arabia. This study was carried out to elucidate the relationship between protein-calorie malnutrition (PCM) and rickets, since a positive correlation has been reported from other areas of the Middle East and India. Children with active rickets were assessed nutritionally, clinically and anthropometrically and were compared to nonrachitic children. The protein-calorie nutritional status of rachitic and nonrachitic children did not show a statistically significant difference. Only 31% of the rachitic children in this study were malnourished in contrast to more than 70% in three other reports. Malnutrition was more marked after the first year of life, especially among breastfed infants who received no nutritional supplement. Nutritional rickets in Riyadh usually occurs as an isolated disease entity related to environmental deprivation of sunlight among infants with no dietary vitamin D supplementation. The PCM that may occur in some of the rachitic children is merely coincidental.

Plasma antithrombin III (AT III) and fibrinogen were measured in 25 Saudi children with nephrotic syndrome during both relapse and remission. During relapse the mean AT III level was 46.6% (range 7–84%) and mean fibrinogen was 992 mg/dl (range 413–1,433), while during remission, AT III levels increased remarkably to a mean value of 120.6% (range 81–160) and plasma fibrinogen dropped to a mean level of 431 mg/dl (range 230–693). In 10 of these patients AT III was measured simultaneously in urine. During relapse urine AT III levels were of the same magnitude as plasma AT III, while during remission no AT III was detected in urine. These findings confirm the hypercoagulable state during the relapse of nephrotic syndrome and the quick recovery during remission. None of our patients showed any clinical evidence of thromboembolism. Loss of AT III in urine during relapse and/or its consumption is the probable cause of low AT III during relapse while excessive production of AT III by liver probably accounts for the high levels in remission.