Hypervitaminosis A

Rothman, Phillip E.; Leon, Eddie E.

doi:10.1148/51.3.368

Cited by 43 publications

(2 citation statements)

References 2 publications

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“…The differentiation from hypervitaminosis A deserves, however, special consideration since some of the cases described in early reports as infantile cortical hyperostosis are now recognized as cases of hypervitaminosis A (6,14). Excessive intake of vitamin A may produce periosteal proliferation resulting in cortical overgrowth,strikingly similar to those observed in patients with infantile cortical hyperostosis (15,11). Characteristically this condition occurs after one year of age in contrast to infantile cortical hyperostosis which is encountered during the first half year of life or even in utero (1).…”

Section: Discussionmentioning

confidence: 93%

Infantile Cortical Hyperostosis

Meadors¹,

Weens²

1954

Acta Radiologica

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Section: Discussionmentioning

confidence: 93%

Infantile Cortical Hyperostosis

Meadors¹,

Weens²

1954

Acta Radiologica

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“…In fact, the incidence of this complication of prostaglandin therapy is high, with radiographic changes occurring in 62% of all infants receiving PGE1 infusion for more than 60 days (14). Other conditions that can cause cortical bone lesions in children less than 2 years of age, and may thus mimic infantile cortical hyperostosis, include trauma (15), hypervitaminosis A (16), hyperphosphatemia (17), and infection (18). Sporadic cases of infantile cortical hyperostosis not associated with PGE1 or PGE2 infusion appear to be on the decline, but the reason(s) for the diminished frequency of these bone abnormalities remain(s) uncertain (8).…”

Section: Introductionmentioning

confidence: 99%

A Novel Col1A1 Mutation in Infantile Cortical Hyperostosis (Caffey Disease) Expands the Spectrum of Collagen-Related Disorders

Gensure

Mäkitie

Barclay

et al. 2005

Journal of Investigative Medicine

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Background: Alendronate has been widely used in the treatment of patient with osteoporosis; several studies have demonstrated the long-term efficacy and safety of alendronate (Fosamax) in patient with osteoporosis. Secondary hyperparathyroidism has been described in patient with chronic renal failure due to stimulation of parathyroid cells by stimuli such as hyperphosphatemia, hypocalcemia and calcitriol deficiency, leading to parathyroid gland hyperplasia. Case Report: We describe a patient who developed secondary hyperparathyroidism despite elevated levels of vitamin D, and normal renal function, while on alendronate, vitamin D and calcium for severe osteoporosis. In August 1998 a 43 year old female was referred to our endocrine clinic for severe osteoporosis. She was found to have normal PTH, serum calcium, phosphorus, urinary calcium excretion, and creatinine clearance. Her 25-hydroxyvitamin D [25-(OH)vitD] level was 16.4 ng/mL. She was started on alendronate 70 mg/w, vitamin D 50,000 IU/w, and calcium 2 g/d. She responded well to this treatment with improvement in her bone mineral density and vitamin D level. In June 2002 she developed secondary hyperparathyroidism, (PTH = 176 pg/mL, calcium of 8.8 mg/dL, normal ionized calcium, 25(OH)vitD = 45.1 ng/mL, 24 h urinary calcium = 240 mg/d). The patient eventually underwent neck exploration in 2004, during which 3 1/5 hyperplastic parathyroid glands were excised. Subsequently the PTH level returned to normal. Discussion: Secondary hyperparathyroidism has classically been described in patients with renal failure or severe vitamin D deficiency due to constant stimulation of parathyroid cells by hyperphosphatemia, hypocalcemia and calcitriol deficiency, leading to parathyroid gland hyperplasia. Skeletal resistance to the calcemic action of PTH is another factor that appears to contribute to the genesis of secondary hyperparathyroidism in chronic renal failure. Recently several studies have demonstrated that alendronate impairs the ability of PTH to increase bone mineral density in osteoporotic patients, possibly by reducing the impact of PTH on bone formation. The present case demonstrates the occurrence of parathyroid hyperplasia and secondary hyperparathyroidism, despite absence of conventional etiologic factors. We propose the possibility of long-term alendronate therapy and skeletal resistance to the effect of PTH as a mechanism of hyperparathyroidism in this patient.

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Local Depilatory Action of Some Unsaturated Compounds

Flesch¹

1952

Arch Dermatol

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Hypervitaminosis A

Cited by 43 publications

References 2 publications

Infantile Cortical Hyperostosis

Infantile Cortical Hyperostosis

A Novel Col1A1 Mutation in Infantile Cortical Hyperostosis (Caffey Disease) Expands the Spectrum of Collagen-Related Disorders

Local Depilatory Action of Some Unsaturated Compounds

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