Coexistence of Osteomalacia in Osteoporotic Hip Fractures in More Than 50 Years Age Group

IntroductionOsteomalacia is a hitherto common orthopaedic condition and is commonly coexists with osteoporosis. However, the identification of osteomalacia always slips under the radar and more emphasis is given to diagnosis and management of osteoporosis. Identification of osteomalacia is equally relevant as management of the osteoporotic fractures is different with or without osteomalaciaMethodsThis was a prospective study design that included patients 50 years or above of either sex presented with proximal femur fractures. Osteoporosis was identified by DEXA scan of hip and lumbar spine. Metabolic tests including serum calcium, phosphorus, ALP and vitamin D levels were done. Histopathological diagnosis of osteomalacia was performed on bony tissues that were taken during surgery from a site adjacent to the fracture and histological examination was performed on non-decalcified paraffin sections using special stains.ResultsA total of 45 patients was included in study. Mean age was 68.7 years (53–85 years). Abnormal values of serum calcium, phosphorus, ALP, vitamin D were noted in 44.4%, 22.2%, 53.3% and 48.9% patients, respectively. On histopathology, 73.17% patients showed osteomalacia. No significant correlation was found between serum biochemical markers and histopathology except with serum Vitamin D (p value − 0.004).ConclusionThe majority of patients with osteoporotic hip fractures had coexisting osteomalacia. Abnormal biochemical values were not significantly associated with osteomalacia. Hence, histopathology remains the gold standard for the diagnosis of osteomalacia. Further research is needed to identify a biomarker that may enable the clinician to diagnosis and treat osteomalacia well in time.     

Serum osteocalcin has limited usefulness as a diagnostic marker for rickets

Serum alkaline phosphatase (AP), the bone fraction of which is secreted by osteoblasts, is elevated in rickets. Both normal and elevated levels of serum osteocalcin (OC), a bone-specific marker secreted by osteoblasts, have been reported in rickets. Expression of the OC gene is enhanced by 1,25-dihydroxyvitamin D (1,25(OH)₂D) in experimental models. This study assessed serum OC levels in 14 controls and 41 patients with active rickets divided into a phosphopenic (n=20) and a calciopenic (n=21) group. Phosphopenic subjects were older (9.5 versus 5.7 years, P=0.03) with higher median serum calcium level (2.35 versus 2.16 mmol/l, P=0.0002) and serum 25-hydroxyvitamin D level (15.4 versus 10.4 ng/l, P=0.003); and lower serum phosphate (0.80 versus 1.51 mmol/l, P=0.0001), serum 1,25(OH)₂D (43.0 versus 95.6 pg/ml, P=0.0001) and intact serum parathyroid hormone level (45.0 versus 141.5 ng/l, P=0.01) than calciopenic subjects. There were no differences in median serum AP (774 versus 1430 IU/l, P=0.17) and OC (14.5 versus 13.4 ng/ml, P=0.6) between the two groups. The mean OC value for the 41 rickets subjects was 15.1 ± 6.2 ng/ml and 17.4 ± 7.8 ng/ml for the 14 control subjects. In the face of markedly elevated serum AP levels in the rickets subjects, all of the serum OC values in the study fell within two standard deviations of the mean for normals. There was no association between serum OC and 1,25-(OH)₂D in either the phosphopenic or the calciopenic group. Conclusion These results show that serum osteocalcin levels are not elevated in all forms of active rickets and that, unlike serum alkaline phosphatase, serum osteocalcin cannot be used in the diagnosis of rickets. Received: 24 September 1999 / Accepted: 23 March 2000     

Antacid and sucralfate-induced hypophosphatemic osteomalacia: A case report and review of the literature

Summary A 42-year-old woman presented to our institution with a 2-week history of bone pain in the lower extremities. Her history was remarkable for duodenal ulcer and long-term treatment with a magnesium-aluminum hydroxide antacid (Maalox) and sucralfate. Initial laboratory studies showed severe hypophosphatemia and elevated alkaline phosphatase and serum 1,25-dihydroxyvitamin D levels. Bone scan showed multiple areas of increased uptake consistent with osteomalacia and microfractures. The patient recovered completely following withdrawal of antacids and sucralfate and shortterm treatment with phosphate. Although hypophosphatemia induced by aluminum-containing antacids is rare, treatment of peptic ulcer disease with a combination of two aluminum-containing agents may increase the risk of clinically significant hypophosphatemia. Awareness of this condition is important, because early recognition can prevent morbidity and lead to safe and effective treatment.     

Does “Hepatic osteodystrophy” differ from peri- and postmenopausal osteoporosis? A histomorphometric study

Summary Bone remodeling activities were assayed on undecalcified sections of iliac crest biopsies obtained from patients with primary biliary cirrhosis (PBC) (n=25), postmenopausal osteoporosis (n=64), and age, sex-matched, nonosteoporotic peri- and postmenopausal subjects (n=26). Thorough semiautomated static and dynamic bone histomorphometry was carried out. Statistical analysis was performed among the age-matched groups in 10-year intervals through the ages 45 to 74. No osteomalacia or osteoporotic condition was detected in the patients with PBC. Our data have shown they did not have a mineralization defect but rather high bone turnover rates. The discrepancy of our observations to other published studies is discussed. We suggest that the osteoporotic condition attributed by others to PBC may just be the result of the concomitant aging processes.     

Nonosteomalacic osteopathy associated with chronic hypophosphatemia

Summary We studied bone histomorphometry in 19 patients with chronic hypophosphatemia related to an idiopathic renal phosphate wasting and without histological osteomalacia. Nine patients had renal lithiasis (group 1), three had radiological osteoporosis (group 2), and seven had lumbar pain (group 3). In the whole group of 19 patients, serum phosphate levels were low (24.9±2.1 mg/l), calcium in blood was normal, calcium in urine was increased, and iPTH was low. Histomorphometric data showed decreased osteoblastic surfaces with normal resorption surfaces, normal osteoid volume and calcification front. There was no correlation between serum phosphate level and histomorphometric parameters. There was no statistical difference between the data of the 3 groups of hypophosphatemic patients. We concluded that chronic hypophosphatemia in the adult doses not always lead to osteomalacia but to an unusual osteopathy characterized by an osteopenia due to an isolated decrease in bone formation. The respective importance of phosphate deficiency and of decreased iPTH level in the pathogenesis of this osteopathy is uncertain.     

Uptake of47Ca into the forearm in normal subjects and in patients with osteomalacia,primary biliary cirrhosis,and hyperparathyroidism

Summary The rate of accumulation of⁴⁷Ca in the tissues of the forearm in the 24 h following an intravenous bolus injection of 2 μCi of⁴⁷CaCl₂ was monitored using a large-volume scintillation counter and analyzed using principal component analysis. In normal subjects activity rose rapidly to a maximum value of about 2% of the administered dose between 2 and 4 h after injection, and had declined little if at all after 24 h. The first three principal components of the uptake curves accounted for a cumulative total of 99.4% of the variance of the data. The eight patients with osteomalacia had a significantly positive weighting factor for the first component, which reflected relatively rapid uptake 15 min after injection and increased total uptake at 6 h. The 6 patients with primary biliary cirrhosis but no overt bone disease had a less marked abnormality which probably represented early osteomalacia. The 3 patients with hyperparathyroidism had normal rates of uptake. Principal component analysis made it possible to quantitate differences in the rate of calcium uptake by the forearm tissues under varying physiological conditions without the need for assumptions on compartmental distribution.     

Osteomalacia inducida por adefovir en paciente con hepatitis B

Osteomalacia is defined as a defect in mineralization of the bone matrix. We describe the case of a patient with chronic hepatitis B infection in whom treatment with adefovir induced renal phosphate loss with intense and sustained hypophosphatemia which derived in symptomatic osteomalacia.