Evidence for Secondary Hyperparathyroidism in the Osteomalacia Associated With Chronic Liver Disease

Dibble, J. B.; Sheridan, Peter J.; Hampshire, Robert C.; Hardy, G. J.; Losowsky, M. S.

doi:10.1111/j.1365-2265.1981.tb00677.x

Cited by 33 publications

(12 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Dibble et al (13) and Cuthbert et al (14) have drawn attention to the secondary hyperparathyroidism in untreated patients with PBC who had florid osteomalacia with very low serum 25OHD concentrations.…”

Section: Discussionmentioning

confidence: 98%

Hyperparathyroidism and Low Serum Osteocalcin Despite Vitamin D Replacement in Primary Biliary Cirrhosis

Fonseca¹,

Epstein

Gill³

et al. 1987

The Journal of Clinical Endocrinology & Metabolism

View full text Add to dashboard Cite

Thirty-six patients with primary biliary cirrhosis (PBC) receiving calcium and calciferol supplements (100,000 IU monthly by im injection) were investigated for their calcium, vitamin D, PTH, and osteocalcin status. The corrected plasma calcium concentrations in PBC patients were significantly greater than those in normal subjects. While the mean serum 25-hydroxycholecalciferol and 1,25-dihydroxyvitamin D concentrations in these patients were similar to those in normal subjects, the mean serum PTH concentration was significantly greater, and it was supranormal in 11 patients. Three patients had elevated corrected calcium concentrations; 1 of them had a concomitant increase in ionized calcium and a supranormal PTH level, and another had a high normal PTH. Ionized calcium concentrations were normal in the rest. Serum osteocalcin concentrations were significantly lower in the patients compared with those in normal subjects. These results indicate that PTH concentrations are frequently elevated in PBC patients despite adequate vitamin D supplementation and normal or even supranormal plasma calcium concentrations. Nonsuppression of PTH concentrations and autonomy of PTH secretion suggest that vitamin D deficiency and secondary hyperparathyroidism in such patients probably occur much earlier in the natural history of this disease than is currently realized. Persistent nonsuppressible hypersecretion of PTH probably contributes to the bone disease of primary biliary cirrhosis. The low osteocalcin concentrations probably reflect diminished osteoblastic activity, which may also contribute to osteopenia in these patients.

show abstract

Section: Discussionmentioning

confidence: 98%

Hyperparathyroidism and Low Serum Osteocalcin Despite Vitamin D Replacement in Primary Biliary Cirrhosis

Fonseca¹,

Epstein

Gill³

et al. 1987

The Journal of Clinical Endocrinology & Metabolism

View full text Add to dashboard Cite

show abstract

“…21 82 decreased tubular phosphate reabsorption,8 86 increased urinary cyclic AMP excretion82 and histological evidence of osteitis fibrosa.2182 It is important to note, however, that low serum 250HD levels are also well documented in patients with no histological evidence of osteomalacia.1718 20 47 69 70 Whether this reflects insufficient duration of vitamin D deficiency for the development of osteomalacia or the need for additional pathogenetic factors is unknown. OH)2D3.88 Precipitation of calcium salts by unabsorbed fats within the intestinal lumen may also contribute to calcium malabsorption.90Finally, malabsorption of phosphate has been reported in chronic liverThe first quantitative study of cortical osteoporosis in chronic liver disease was reported by Paterson and Losowsky, who carried out metacarpal thickness measurements in 38 patients with a variety of liver diseases.…”

mentioning

confidence: 99%

Hepatic osteodystrophy: vitamin D metabolism in patients with liver disease.

Compston¹

1986

Gut

118

View full text Add to dashboard Cite

The current interest in hepatic osteodystrophy was stimulated by the discovery in 1969 that vitamin D undergoes 25-hydroxylation in the liver.'It has subsequently been shown that the metabolite thus formed, 25-hydroxyvitamin D (250HD) is the major circulating metabolite of vitamin D; the major active metabolite, 1,25-dihydroxyvitamin D3 is formed by lahydroxylation of 250HD, this step occurring almost exclusively in the kidney.2 Although diet was formerly believed to be the major source of vitamin D in man it has been shown, both in the UK and North America, that endogenous skin synthesis is quantitatively the most important source,3 4 cholecalciferol (vitamin D3) being produced from the precursor 7-dehydrocholesterol in the presence of ultraviolet irradiation.5After the demonstration that 25-hydroxylation occurred in the liver many groups, both in Europe and North America reported low serum or plasma 250HD concentrations in patients with chronic cholestatic, alcoholic and other forms of liver disease.f22 The pathogenesis of this vitamin D deficiency aroused considerable controversy. Whilst impaired hepatic metabolism of vitamin D was an obvious possibility, -other causes such as reduced exposure to ultraviolet irradiation, low dietary vitamin D intake, impaired cutaneous synthesis of vitamin D3 caused by jaundice and malabsorption of vitamin D also required investigation. Hepatic production of vitamin DHepatic production of vitamin D in man has been studied mainly by measurement of the serum 250HD response to vitamin D adnministration, using either unlabelled or radioactive vitamin D. The former studies have often involved administration of pharmacological doses of vitamin D and the results obtained may thus not be of physiological significance although they are relevant when considered in the light of vitamin D therapy. Radiolabelled vitamin D studies, in most of which the vitamin is injected as an intravenous bolus, have also to be interpreted with some caution as both the rate of delivery of the vitamin to the circulation and the form in which it is delivered are unphysiological. The appearance of 250HD in plasma after vitamin D administration reflects hepatic uptake and hydroxylation of the vitamin together with hepatic release and metabolism of the metabolite, so that these investigations do not directly measure 25-hydroxylation of 250HD. In addition, changes in serum 250HD levels after oral vitamin D will be affected by absorption of the vitamin from the intestine.Early evidence for impaired hepatic production of 250HD in liver 1073 on 12 May 2018 by guest. Protected by copyright.

show abstract

“…However, secondary hyperparathyroidism is also associated with chronic liver disease. 37 Haagsma et a136 suggested that the pre-existing bone disease in liver transplant recipients was a major factor in the development of bone disease but in their patients another major factor may have been the postoperative dose of corticosteroid immunosuppression as they were treated with 200 mg of prednisolone/day reducing to 40 mg/day after one month and 20 mg/day at one yearhigh doses of corticosteroids compared with current regimens.…”

mentioning

confidence: 99%