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Biomedical subjects

A M Parfitt

Publications and source records attributed to A M Parfitt.

At least 127 records · Page 7Linked to original sources
PubMed1988

Lack of biochemical progression or continuation of accelerated bone loss in mild asymptomatic primary hyperparathyroidism: evidence for biphasic disease course.

We studied the natural history of primary hyperparathyroidism in patients in whom the disease was discovered fortuitously by multichannel biochemical screening and who were selected for conservative management because they were asymptomatic, had no renal stone disease or radiographic osteitis fibrosa, and had serum calcium values below 3.00 mmol/L, serum creatinine levels below 133 mumol/L, and forearm bone density not more than 2.5 SD below the mean expected for age, sex, and race. One hundred and seventy-four patients meeting these criteria were encountered during a 10-yr period, of whom 80 (mean age, 61 yr) had adequate follow-up; they did not differ significantly in any initial characteristic from the remaining 94 patients. These 80 patients were followed for 1-11 yr (mean, 46 months; median, 38 months), during which there was no change, mean or individual, in any index of PTH secretion or any of its biochemical effects and no decline in forearm bone density apart from that expected from increased age. There were 4 deaths from causes unrelated to hyperparathyroidism, and the overall death rate was not increased. The data suggest that no change occurred in either the number of parathyroid cells or secretory set-point, the 2 principal determinants of basal PTH secretion. This implies a biphasic course, with a short period of disease progression followed by a long period of disease stability. Our data support the decision to withhold surgical intervention in such patients, but to establish this as the correct policy for all asymptomatic patients will require a controlled clinical trial.

Aged↗
PubMed1988

Bone mass, skin color and body size among black and white women.

We investigated the relationship between bone mass and two variables, skin color and body size, that may contribute to the higher prevalence of osteoporosis among white than among black populations. From a sample of 36 black and 99 white women were obtained measurements of height, weight, skin color (Photovolt 670 reflectometer) and radial bone mineral content (BMC) and bone width (BW) (single photon absorptiometry). There was no significant correlation between skin reflectance and age-adjusted BMC in either population. Multiple regression models of BMC and BMC/BW on age, weight/height and skin reflectance yielded significant correlations ranging from 0.62 to 0.77, but the partial coefficients for skin reflectance were not significant. BMC and age were negatively correlated in both groups, with a significantly steeper slope for the whites. Weight was positively correlated with BMC in both populations, but differences in weight did not explain the differences in bone mass between the blacks and whites.

Adult↗
PubMed1988

Bone remodeling.

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Aging↗
PubMed1987

Trabecular bone architecture in the pathogenesis and prevention of fracture.

Rapid loss of trabecular bone (as after menopause) occurs by complete removal of some structural elements, leaving those that remain more widely separated and less well connected. The most likely cellular mechanism is an increase in the number of resorption cavities deep enough to lead to focal perforation of trabecular plates, either as a non-specific consequence of increased remodeling activation, or as a specific consequence (direct or indirect) of estrogen deficiency. Disruption of the connections between structural elements produces a disproportionate loss of strength, for which the increased thickness of the remaining trabeculae can only partly compensate. Consequently, the most biomechanically significant component of trabecular bone loss occurs rapidly and irreversibly. This emphasizes the importance of prevention, but no treatment except estrogen replacement is of proven efficacy in preventing estrogen-dependent bone loss. For adequate repair of structural damage after it has been allowed to occur, adding bone to existing surfaces may be insufficient, and it may be necessary to devise some means of forming new bone directly in the bone marrow cavity in order to re-establish normal connectivity.

Bone and Bones↗
PubMed1987

Procollagen type I carboxy-terminal extension peptide in serum as a marker of collagen biosynthesis in bone. Correlation with Iliac bone formation rates and comparison with total alkaline phosphatase.

We measured iliac bone formation rates on all surfaces after double tetracycline labeling, serum levels of type 1 procollagen carboxy-terminal extension peptide (pColl-I-C), and serum levels of total alkaline phosphatase activity (TAP) in four normal subjects and in 44 patients with various forms of metabolic bone disease. In three patients with enzymatic evidence of liver disease both biochemical serum markers were disproportionately raised. In a patient with idiopathic axial osteosclerosis serum pColl-I-C was selectively increased by more than ten-fold. In the remaining 44 subjects pColl-I-C and TAP levels correlated significantly with each other (r = 0.70) and both showed the same directional changes and broadly similar correlations with iliac bone formation rate expressed in different ways. In general, pColl-I-C levels correlated better with cancellous bone formation rates and TAP levels cortical bone formation rates. There was a modest improvement in prediction of bone formation rate with multiple regression using both markers. In 15 patients with typical uncomplicated postmenopausal osteoporosis, neither biochemical marker, singly or jointly, correlated significantly with any expression of bone formation rate. Disadvantages to the use of pColl-I-C as a marker include a significant contribution to the serum level from type 1 collagen biosynthesis in tissues other than bone, and (probably) variable metabolic clearance. For both biochemical markers the most consistently high correlations (r = 0.77-0.79) were found with total bone formation rate for the entire biopsy core volume, which is the best estimate available from a biopsy of formation rate at the bone organ level of organization in vivo. The core volume as a referent also allows the amount of bone formed on cortical, endocortical, and cancellous surfaces to be compared. Measurement of serum pColl-I-C levels merits further study as a noninvasive index of bone metabolism. Differences between normal and abnormal subjects in the relationships between a variety of biochemical markers and a variety of histologic indices have the potential for providing insight into the pathogenesis of osteoporosis.

Adolescent↗
PubMed1987

Hypophosphatemic osteomalacia and adult Fanconi syndrome due to light-chain nephropathy. Another form of oncogenous osteomalacia.

Two patients, one with myeloma (Patient 1) and the other with probable chronic lymphocytic leukemia (Patient 2), had reduced renal tubular phosphate reabsorption in the absence of hyperparathyroidism together with other features of the Fanconi syndrome, as consequences of the nephropathy associated with light-chain proteinuria. Both patients had hypophosphatemic osteomalacia, demonstrated for the first time in this condition by iliac bone histomorphometry after in vivo double tetracycline labeling, despite absence of bone pain or Looser zones. Neither patient was vitamin D-depleted, but plasma calcitriol level was normal in Patient 1 and low in Patient 2; only the latter patient had severe muscle weakness. Complete histologic correction of osteomalacia was achieved by treatment in accordance with the biochemical defects--oral phosphate therapy alone in Patient 1 and combined with calcitriol in Patient 2. Both patients are now symptom-free, five and three years after the initial diagnosis of bone disease and hematogenous malignancy. Thirteen previous instances of the same form of osteomalacia were reviewed; in most cases, the Fanconi syndrome developed before its probable cause became apparent. The Fanconi syndrome has also been reported in two cases of osteomalacia due to mesenchymal tumor, but not in osteomalacia associated with prostatic carcinoma. Light-chain nephropathy and consequent renal tubular dysfunction appears to be a third form of oncogenous osteomalacia.

Aged↗
PubMed1987

Metabolic bone disease in asymptomatic men after partial gastrectomy with Billroth II anastomosis.

We sought to determine whether gastric surgery might be associated with metabolic bone disease in a well-characterized population, and if so to explore its etiology. Sixteen asymptomatic middle-aged men who had had partial gastrectomy with Billroth II anastomosis but no other risk factors for metabolic bone disease were compared with unoperated healthy controls. Studies included a dietary survey, biochemical tests of bone and mineral metabolism, radiographs of the spine, determinations of bone mineral content, and bone histomorphometry. The gastric surgery subjects exhibited frequent vertebral fractures and an unusual constellation of bone abnormalities characterized by decreased bone mineral content and hyperosteoidosis without evidence of osteomalacia. Although serum immunoreactive parathyroid hormone and 25-hydroxyvitamin D levels were not different, 1,25-dihydroxyvitamin D levels were significantly higher (p = 0.037), and 24,25-dihydroxyvitamin D levels were significantly lower (p less than 0.0001) in subjects than in controls. Partial gastrectomy with Billroth II anastomosis may be associated with asymptomatic but clinically important metabolic bone disease. The pathophysiology is uncertain, but appears to involve alterations in vitamin D metabolism.

Bone Diseases, Metabolic↗
PubMed1987

Atypical insufficiency fractures confused with Looser zones of osteomalacia.

Six women, aged 24-67 years, had osteopenia and insufficiency fractures, which suggested a diagnosis of osteomalacia. The insufficiency fractures occurred at traditional sites for Looser zones, were multiple in number, were symmetrically distributed in three patients, and did not heal promptly. Bone mass was low, as assessed by single-energy photon absorptiometry at the midshaft of the radius. Two postmenopausal women had vertebral compression fractures. Biochemical indices and bone histomorphometric analysis excluded osteomalacia, and in vivo double tetracycline labeling in five patients revealed both high and low bone turnover states. We propose more stringent radiographic criteria for the designation of the term "Looser zone" that retains the customary association between the radiologic event and osteomalacia. This paper also outlines a diagnostic strategy for future cases of atypical insufficiency fractures and proposes reasons for their resemblance to true Looser zones.

Adult↗
PubMed1987

Bone histomorphometry in hypogonadal and eugonadal men with spinal osteoporosis.

We present iliac bone histomorphometric data after in vivo double tetracycline labeling and related biochemical data from 14 nonalcoholic men referred for evaluation of symptomatic spinal osteoporosis. Six patients had previously undiagnosed hypogonadism, and 8 had normal gonadal function and no evident etiology for osteoporosis. Bone histomorphometry revealed no differences in structural measurements or resorption indices between the 2 groups. However, compared to reference values for normal postmenopausal women, osteoblast surface, mineralizing surface, and formation rate were normal or modestly increased in the hypogonadal men and significantly reduced in the idiopathic group. There were significant corresponding differences between the 2 groups in the fasting urinary hydroxyproline to creatinine ratio, an index of bone resorption, and serum total alkaline phosphatase, an index of bone formation. Plasma 25-hydroxyvitamin D levels did not differ between the 2 groups and were above 10 ng/mL in all patients. Plasma 1,25-dihydroxyvitamin D [1,25-(OH)2D] levels were normal in the hypogonadal group and significantly reduced in the idiopathic group, but did not correlate with any histological measurements. The formation indices fell substantially in 3 of 4 hypogonadal men after 7-14 months of therapy with testosterone and a calcium supplement. We conclude the following. In vitamin D-replete hypogonadal men with osteoporosis, 1,25-(OH)2D synthesis is normal, and bone remodeling is modestly increased and correctable by hormone replacement therapy, as in normal postmenopausal women. In middle-aged men with idiopathic osteoporosis, there is impairment of 1,25-(OH)2D synthesis and of the recruitment and activity of teams of osteoblasts, as in postmenopausal osteoporosis.

Adult↗
PubMed1987

Bone and plasma calcium homeostasis.

Regulation of plasma free calcium concentration displays the following features: (1) The level in an individual varies within fairly narrow limits and is characterized by a mean (an estimate of the individual set point) and a standard deviation (an estimate of oscillation about the set point). (2) There is an intrinsic circadian oscillation that is independent of external disturbing signals. (3) Individual values (set points) are partly under genetic control with significant between-family differences. (4) Correction of errors is rather slow-it usually takes at least 12 hours to restore the basal level after experimental induction of hyper- or hypocalcemia. (5) Correction of errors can occur with normal efficiency in the absence of parathyroid hormone or calcitonin, provided the system is adequately primed with some form of vitamin D. These and other facts are best explained by a concept that locates the calcium homeostatic system at the quiescent bone surface. Across this cellular and tissue barrier exchange of calcium between blood and bone in the absence of net flux can be demonstrated by autoradiography. The distinction between the homeostatic system and the remodeling system that regulates bone mass is not absolute, since the latter can participate in short term correction of errors, and if the obligatory calcium loss (determined by the difference between the plasma calcium set point and the threshold for renal tubular reabsorption of calcium) is too high to be satisfied by net intestinal absorption, the remodeling system must make up the difference by sacrificing bone.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone Regeneration↗