Ca&Bone

[Disturbance of bone development in experimental hepatic cirrhosis in growing rats]

FERENCZ Viktória és munkatársai

JUNE 20, 2005

Ca&Bone - 2005;8(02)

[INTRODUCTION -The pathomechanism of hepatic osteopathy is not fully understood.We investigated how bone parameters change in growing rats with experimentally induced fatty liver, liver cirrhosis and hepatocellular carcinoma. METHODS - Liver disease was induced by administration of CCl4 and phenobarbital (PB) following a single injection of diethylnitrosamine (DEN) in 55 Fischer 344 rats.Animals were sacrificed and their femur removed at week 8 or 16. Bone mineral content (BMC), femoral length, cortical index (ratio of cortical thickness and total diameter at the diaphysis) and ultimate bending load (Fmax) of femora were determined. Results of animals treated with DEN+PB+CCl4 (group DPC, n=21) were compared to untreated animals (n=14) and to a second control group treated only with DEN+PB (group DP, n=20). RESULTS - Fatty liver and cirrhosis developed in each animal in the DPC group (n=21) at week 8 and in a subgroup of these animals (n=11) hepatocellular carcinoma also appeared by week 16. No changes in bone parameters were observed in this group at week 8, but lower BMD, femoral length, cortical index and Fmax values were found at week 16 compared to the untreated controls or to the DP group (p<0.05 for both). In the DP group no fatty liver or cirrhosis was observed at any time. Femoral length and Fmax values were higher in the DP group at week 8 compared to the untreated controls (p<0.05 for both).At week 16, however, no difference could be detected. CONCLUSION - Experimentally induced liver cirrhosis and hepatocellular carcinoma are associated with growth inhibition and reduced bone mineral content, cortical index and mechanical resistance in growing rats.]

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[INTRODUCTION - Smoking is associated with a decreased bone mass and increased risk of osteoporotic fractures.The aim of this study was to investigate the impact of current tobacco smoking to bone mineral density (BMD) in Hungarian females. PATIENTS AND METHODS - We measured BMD in 43 (25-72 yrs) smoker and 43 age- and BMI-matched non-smoker women by dual X-ray absorptiometry (Prodigy, GE Lunar) at the lumbar spine and proximal femur and by single photon absorptiometry at the radius midshaft of the non-dominant side (NK 364, Gamma). RESULTS - Osteoporosis (T-score at any measured site below - 2.5) was found to be more common among smokers compared to non smokers (63.6% vs 36.4%, χ2-test p=0.009). Among premenopausal women no difference was found in BMD between the two groups, whereas postmenopausal smoker women tended to have a lower BMD value compared to those who didn’t smoke. In postmenopausal women a decrease of borderline significance was found in lumbar BMD (0.977 vs 1.04; p=0.06). CONCLUSION - Our observation suggests that there is only a slight decrease in bone mass due to smoking, however, added to menopausal bone loss this effect can be a significant contributor to the increased fracture risk of involutional age.]

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[INTRODUCTION - Parathyroid hormone (PTH) excretion is increased both in primary hyperparathyroidism (pHPT) and in pseudohypoparathyroidism type Ia (PHP Ia). Pseudo-pseudohypoparathyroidism (P-PHP) is considered to be the normocalcemic form of pseudohypoparathyroidism type Ia. Our aim was to assess bone mineral content and bone quality as well as to determine whether these parameters are related to PTH levels in the above mentioned disorders. PATIENTS AND METHOD - 10 patients with pseudopseudohypoparathyroidism (P-PHP, age: 41.6 ±5.4 ys) were compared to 10 patients with primary hyperparathyroidism (pHPT) and to 10 healthy subjects, matched for age and gender. Moreover, nine patients with pseudohypoparathyroidism type Ia (PHP, age: 34.2 ±5.43 ys) were compared to nine age- and gender-matched patients with primary hyperparathyroidism and to nine healthy controls, respectively.The occurrence of previous bone fractures was recorded and bone mass was measured (by dual photon absorptiometry on the axial bones and by single photon absorptiometry on the forearm). Quantitative ultrasound (QUS) examination was performed both on the calcaneus by broadband ultrasound attenuation (BUA, dB/MHz) and speed of sound (SOS, m/s) measurements and on the proximal phalanges by amplitude-dependent speed of sound (AdSOS, m/s) measurements. In addition, some laboratory parameters of calcium metabolism were tested. RESULTS - No difference was found between PHP Ia and pHPT in bone mass.The lowest value was observed at the radius. Among the QUS parameters, pathologically low AdSOS was found at the phalanges in PHP Ia and it was lower than in pHPT patients, whereas at the calcaneus BUA showed a similar tendency. Bone mass did not significantly differ between P-PHP and healthy controls, it was decreased, however, at the forearm in the patients. Pathological AdSOS was found in P-PHP, which was lower than in pHPT. SOS at the calcaneus was lower in P-PHP than in pHPT, though it was not considered pathological. Laboratory results were typical for the diseases and the radiological examinations confirmed the diagnosis. Bone fractures occurred in three and two patients with PHP Ia and P-PHP, respectively, while no fractures were recorded in the pHPT and healthy groups. CONCLUSION - Bone loss among patients with PHP Ia is considered to be the impact of PTH excess on bone tissue.The deterioration of bone quality and architecture may play a role in the development of bone fractures.]

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