3. Von Noorden GK, Crawford ML. The sensitive period. Trans Ophthalmol Soc UK 1979;99:442-6. 4. Robb R. Children's ophthalmologic problems. Hospital Pract April 1977:107-15. 5. Merlob P, Sivan Y, Reisner SH. Anthropomorphic measurements of the newborn infant. Birth Defects 1984;20(7):8-14. 6. Neweomb R. The causes of blindness in children: a review of the literature. J Am Optom Assoc April 1977:48(4). 7. Francois J. Surgical results of congenital cataract: the Belgian experience. Ophthalmic Forum 1984;2(3):126-8. 8. Brown C, Hanna C. Use of dilute drugs for routine cycloplegia and mydriasis. Am J Ophthalmol 1978;86:820-4. 9. Palmer E. Drug toxicity in pediatric ophthalmology. J Toxicol Cutan Ocul Toxicol 1982;1(3):181-210. 10. Palmer EA. How safe are ocular drugs in pediatrics? Ophthalmology 1986;93:1038-40. 11. Caputo AR, Sehnitzer RE. Systemic response to mydriatic eyedrops in neonates: mydriatics in neonates. J Pediatr Ophthalmol Strabismus 1978;15:109-22.
An 86-year-old woman with a history of treated hyperthyroidism and a 20-year history of untreated primary hyperparathyroidism developed generalized bone pain and a pseudofracture of the midshaft of the left femur. Laboratory examinations revealed elevated serum calcium, alkaline phosphatase, and C-terminal parathyroid hormone levels. Serum inorganic phosphate was below normal and 25-hydroxyvitamin D levels were low-normal. An undecalcified transiliac bone biopsy specimen following tetracycline double labeling revealed osteomalacia and osteitis fibrosa. Following treatment with vitamin D and phosphate, the serum inorganic phosphate level rose to normal. There was a decrease in bone pain, and the pseudofracture healed. However, the serum calcium, alkaline phosphatase, and C-terminal parathyroid hormone levels remained elevated. Longstanding primary hyperparathyroidism causes chronic hypophosphatemia and may lead to osteomalacia. Osteomalacia and its consequences may be part of the spectrum of bone disease seen in patients with longstanding primary hyperparathyroidism.
Because of the importance of estrogen in osteoporosis, the effects of decreased estrogen production using sensitive measurements of bone mineral metabolism were studied in oophorectomized rats. Serum levels of ionized calcium, bone gla protein (BGP), vitamin D metabolites (25-hydroxyvitamin D and 1,25-dihydroxyvitamin D), and estradiol were measured before and serially for 6 weeks after oophorectomy in the rat. In addition, static and dynamic indices of bone histomorphometry were determined after double tetracycline labeling. Fifty Sprague- Dawley female rats (-250 g) were studied. Twenty-five rats underwent oophorectomy (0), while the remaining rats were sham operated. Estrogen deficiency was noted in the O group within a week after surgery (estradiol, 2.45 ± 0.78 vs. 27.9 ± 4.15 pg/ml; P < 0.05). Serum ionized calcium levels, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and PTH levels did not differ between the two groups during the length of the study. Serum BGP levels were the same in both groups until the second week postoophorectomy, after which BGP remained significantly elevated in the 0 animals (121.7 ± 5.95 us. 76.7 ± 3.87; P < 0.001). Bone histomorphometry revealed increased osteoid volume (4.4 ± 0.9% vs. 2.3 ± 0.7%), osteoblast surface (26.5 ± 2.4% vs. 3.2 ± 1.2%), tetracycline surface (18.9 ± 4.1% vs. 6.8 ± 2.2%), as well as osteoclast surface (8.2 ± 1.4% vs. 2.5 ± 2%) in all O animals compared with those in the sham-operated group. These data indicate that oophorectomy and decreased estrogen result in increased bone turnover with elevated BGP levels. The marked BGP elevation within 2 weeks postoophorectomy suggests that estrogen withdrawal results in rapid altered bone mineral metabolism. The lack of concomitant increase in circulating PTH levels suggests that other factors may be mediating the bone loss following surgical oophorectomy. (Endocrinology122: 624–630,1988)
Local factors, such as interleukin-1, may mediate the accelerated bone remodeling in the acute estrogen-deficient rat. Cyclosporin A (CsA), which in vitro inhibits some of these local factors, was administered to oophorectomized (OX) rats in an attempt to modify this high turnover state. Three groups of 15 rats were studied. Group A was sham operated, group B was OX, and group C was OX and received CsA (15 mg/kg per day) by gavage commencing 4 days postoophorectomy for 28 days. Estradiol levels were determined to confirm oophorectomy. Blood was sampled on days -7, 0, 7, 14, 21, and 28 for ionized calcium (Ca2+), 1,25-(OH)2-vitamin D, PTH, and bone gla protein (BGP). Rats received tetracycline hydrochloride for bone histomorphometric labeling. All results were compared to group A. Body weight was increased in group B (p less than 0.003) but not in group C. There was no difference in Ca2+ or PTH between the groups. BGP levels were higher in group B by day 28 (p less than 0.005); BGP levels were increased in group C from days 7-28 (p less than 0.002). 1,25-(OH)2-vitamin D was significantly increased in group C (p less than 0.0001) but not in group B. Tibial bone histomorphometry revealed increased measurements of bone formation and osteoclast number without a loss of bone volume (BV/TV) in group B. Group C showed a dramatic increase in bone turnover with significant loss of BV/TV (p less than 0.001). In conclusion, CsA in the OX rat resulted in unexpected enhanced bone remodeling with high BGP levels and severe bone resorption.(ABSTRACT TRUNCATED AT 250 WORDS)