Birger Lund

Measurement of bone mineral content (BMC) of the lumbar spine, II. Correlation between forearm BMC and lumbar spine BMC

A comparison between forearm bone mineral content (BMC) and lumbar BMC was made in post-menopausal women. Women without symptoms, women with clinical spinal osteoporosis, and women with prednisone-treated rheumatoid arthritis were studied. A conventional two-dimensional single-photon osteodensitometer was used for measurement of forearm BMC. A new two-dimensional dual-photon osteodensitometer was used for measurement of lumbar BMC. Its radioactive source was 153Gadolinium. The mean lumbar BMC was significantly reduced in women with clinical spinal osteoporosis (P < 0.001). The mean forearm of BMC of those patients was normal. Thus, forearm BMC was a poor indicator of spinal osteopenia. If forearm BMC was used to predict lumbar BMC erroneously high results were obtained in women with clinical spinal osteoporosis, and erroneously low values were obtained in prednisone-treated women with rheumatoid arthritis.

25-HYDROXYCHOLECALCIFEROL AND FRACTURES OF THE PROXIMAL FEMUR

Abstract Plasma 25-hydroxycholecalciferol (25-H.C.C.) has been measured in 67 consecutive cases of fracture of the proximal femur. The values found in these patients were not different from those in control groups at the same time of the year. Plasma 25-H.C.C. was not correlated to plasma calcium or phosphorus, the Ca×P product, or the alkaline phosphatase. X-rays showed Looser zones in only 1 patient, in whom the lowest plasma 25-H.C.C. was found. Osteomalacia is not uncommon among elderly people in Denmark, but it is more likely to depend on a decline in the renal efficiency to convert 25-H.C.C. to 1,25-dihydroxycholecalciferol than a low dietary intake of vitamin D.

Serum 1,25-DihydroxycholecalciferoI in Anephric, Haemodialyzed and Kidneytransplanted Patients

The serum levels of 25-hydroxycholecalciferol (25-OHD3) and 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] were measured simultaneously in nephrectomized patients on mai

Bone Histology and Calcium Metabolism in Patients with Nephrotic Syndrome and Normal or Reduced Renal Function

Bone histology and its relationship with calcium metabolism was evaluated in adult patients with nephrotic syndrome: 29 had normal renal function (GFR 103 +/- 4 ml/min/1.73 m2) (group 1) and 20 had renal insufficiency (GFR 31 +/- 4 ml/min/1.73 m2) (group 2). In group 1, serum PTH, 1.25-HCC and 24.25-HCC levels were normal, while 25-HCC values were reduced. Bone histology was normal in 76% of the patients, while 17% had isolated osteomalacia and 7% an associated bone resorption. Group 2 showed a higher incidence of bone resorption when compared with a matched group of patients with renal failure and no proteinuria (40% vs. 13%) and a comparable frequency of isolated mineralization defect (25% vs. 34%). PTH levels were definitely increased and serum total calcium and all the vitamin D metabolites were reduced. A significant correlation between the apparent duration of the disease and the severity of osteodystrophy was found only in group 2. In conclusion, no constant derangement of calcium metabolism and bone histology is evident in patients with nephrotic syndrome and normal renal function, while patients with persistent proteinuria are at high risk of osteodystrophy even in the early phases of renal failure.

Vitamin D metabolism and osteomalacia in patients with fractures of the proximal femur.

A high frequency of histological osteomalacia (25 per cent) was seen in patients with fractures of the proximal femur. No correlation was found between the levels of circulating 25-hydroxyvitamin D (25-OHD) or 1,25-dihydroxyvitamin D (1,25-(OH)2D) and the bone histomorphometric changes. The serum 25-OHD levels were normal, which excludes a dietary vitamin D deficiency or a reduced hepatic hydroxylation of the vitamin. The mean serum 1,25-(OD)2D concentration was significantly reduced in the whole patient group, but surprisingly the levels were normal in those with histological osteomalacia, indicating that an impaired conversion of 25-OHD to 1,25-(OH)-2D was not the primary cause of the bone disease. A reduced sensitivity to 1,25-(OH)2D might be a possible explanation for the osteomalacia.

Changes in vitamin D metabolites and bone histology in rats during recovery from rickets.

SummaryThe relative roles of 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-(OH)2D) and 24,25-dihydroxyvitamin D (24,25-(OH)2D) in bone mineralization are largely unknown. Young vitamin D depleted rats were fed increasing amounts of vitamin D and grouped radiologically in accordance with the rat line test. They ranged from severely rachitic to normal. Radiology was correlated with serum levels of 25-OHD, 1,25-(OH)2D, 24,25-(OH)2D, ionized calcium, magnesium, and phosphate, with bone histology, and with the total mineral content of the animals. Serum 1,25-(OH)2D rose in a linear fashion to supranormal values during bone healing and correlated with the radiological degree of rickets. Serum 25-OHD was below detection limit in the most rachitic and low in the radiologicall normal rats, whereas 24,25-(OH)2D was low in all groups. These two metabolites showed no correlation with the radiologic, histologic or biochemical parameters. In rachitic rats, 1,25-(OH)2D appears to play a major role in bone healing and possibly exerts a direct effect on bone cells. It cannot be ruled out, however, that the effect is mediated through a rise in serum levels of calcium and phosphorus, although signs of bone healing were seen in the presence of a subnormal calcium x phosphorus product. Initiation of mineralization can take place with unmeasurable 25-OHD, and 24,25-(OH)2D seems to be without importance.

Serum ionized calcium in renal failure — a guideline for 1α-hydroxycholecalciferol treatment

It has been demonstrated that ltr-hydroxycholecalciferol (la-OH-D3), a synthetic analogue to the naturally occurring vitamin D metabolite 1,25-dihydroxycholecalciferol (1,25-(OH)2-D3), to which it is converted after intake [3], can ameliorate uraemic bone disease [6, 8]. One effect of lg-OH-D a is to augment serum calcium, which is often subnormal in haemodialysis patients. Hypercalcaemia is easily provoked by this drug when it is given to patients with severe renal insufficiency, especially if the dose is not reduced as the uraemic bone lesions heal [6]. Since the extracellular concentration of ionized calcium is the variable which is detected by the heart, the nervous system, the striated muscles, the bone cells, and the parathyroid gland, we have tried to evaluate the usefulness of the concentration of ionized calcium in serum (s-C# +) in the selection of patients for treatment with la-OH-D a, and as a guideline for the dosage. We here present data showing that, in patients with renal insufficiency, la-OHDs more easily provokes hypercalcaemia, when the pre-treatment s-Ca z+ is normal than when it is low.