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Introduction
The WHO definition of post-menopausal osteoporosis is based on the measurement of bone mineral density (BMD) with dual X-ray absorptiometry (DXA). Low DXA-BMD of the hip as well as poor results in the trail making and chair rising tests are risk factors of equivalent magnitude for vertebral fractures (Johnell, 2004(. Consequently, more diagnostic approaches are needed to complete the diagnostic procedure. The most important method to identify spinal fractures is conventional X-ray, particularly because >50% of spinal osteo- porotic fractures are not accompanied by clinical symptoms, and hence, remain unnoticed. Nevertheless, the diagnosis of vertebral fractures is important, because the prevalence of vertebral fractures is associated with an increased risk of incident fracture (Johnell, 2004; Felsenberg, 2004).
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So far 109 hypocalcemic patients have been registered in the RIIP of Florence. Subjects had an age ranging from 6 to 71 years. Both sexes were represented (48 female and 61 males). There were 14 cases of PHPIa; 8 cases of PHPIb; 8 cases of PPHP; 57 cases of idiopathic hypoparathyroidism; 2 case of DiGeorge syndrome; 8 cases of isolated parathyroid agenesis; 9 cases of APS 1; and 3 cases of universal calcinosis (Table III). The geographical distribution of the patients was the following: 51% from the South, 39% from the Center, and 10% form the North of Italy (Fig. 1).
Thirty-nine patients (10 women and 29 men) with a mean age 40±22.4 SEM years (range 7-66) underwent genetic test to evaluate the presence of GNA S1 gene mutations. For 4 of them, blood samples for genetic analysis from relatives were made available.
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Italian Register of Primary Hypoparathyroidism
In 1996 an Italian Register of Primary Hypoparathyroidism was created in Florence and named RIIP. It is a passive register and its Central Secretariat has been established in Florence. RIIP collects clinical records both on sporadic and familial cases of primary hypoparathyroidism. Information was obtained from Italian endocrine, neurological and pediatric Centers through the compilation of a simple form, that includes the identification code of the patient, the date of birth, the diagnosis of the type of hypoparathyroidism, the presence of other associated diseases (typical or not), the data on organ and non-organ antibodies, the results of PTH infusion and genetic tests. Each subject is requested to give informed consent and at any time the patient can ask to obtain his/her clinical data deleted from the official file. The form (available on request) has been arranged to be sent by fax and e-mail (Table II).
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Posted by James
Introduction
Calcium is an important bioinorganic ion performing a variety of intra- and extra-cellular functions and playing an important role in maintaining normal physiologic processes. It is also an important component or co-factor required for the proper functioning of coagulation factors and adhesion molecules. Homeostasis of calcium and phosphorus is maintained by a combined activity of the calciotropic hormones: parathyroid hormone (PTH), Vitamin D [25 OH2D3 and 1-25 (OH)2D3], and calcitonin (CT). PTH, the product of the parathyroid glands, regulates serum calcium concentrations and bone metabolism. In turn serum calcium concentrations regulate PTH secretion by means of a calcium-sensing receptor (CaSR) on the surface of parathyroid cells. buy cheap viagra on rx-approved
The term of primary hypoparathyroidism refers to a group of inherited disorders in which the relative or absolute deficiency of PTH leads to hypocalcemia and hyperphosphatemia (Table I). These disorders may be caused by developmental defects in the parathyroid glands, by autoimmune endocrinopathies, by defects in PTH synthesis, by impaired regulation of PTH secretion, and by defective PTH action. The latter forms termed pseudo-hypoparathyroidism are unique in that PTH secretion is increased rather than deficient.
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In PHPT, a hypersecretion of PTH from a benign solitary parathyroid adenoma (80%) or multiglandular parathyroid hy- perplasia (15%) produces excessive bone resorption. Under normal circumstances, an increase in circulating ionized calcium is followed by a rapid decrease in PTH secretion. In PHPT with adenoma, this feedback control is impaired, resulting in hypersecretion of PTH. In PHPT caused by hyperplasia, the sensitivity to circulating calcium is relatively intact but the number of parathyroid cells is increased, enhancing PTH secretion. In either case, the PTH excess increases the number of active osteoclasts on the bone surface, stimulating bone resorption. The resulting rise in serum calcium increases the renal filtered load of calcium, causing hypercalciuria. Although PTH augments renal tubular reabsorption of calcium, hypercalciuria ensues from the greatly increased filtered load of calcium and from a suppressive effect of hypercalcemia on calcium reab- sorption. Cheap canadian drugs canadian medshop 247
PTH also induces the renal 25-hydroxyvitamin D3-1a-hydroxy- lase; thus, serum 1,25(OH)2D3 concentration is often high in PHPT. The enhanced 1,25(OH)2D3 synthesis stimulates osteo- clastic bone resorption and, more importantly, raises intestinal calcium absorption. These effects further increase the circulating concentration of calcium and contribute to hypercalciuria. Thus, hypercalciuria of PHPT is primarily resorptive and secondarily absorptive in origin.
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High Animal Protein Diet. A high animal protein diet has long been known to cause hypercalciuria. Several mechanisms have been invoked. It may partly be due to enhanced bone loss (see Resorptive Hypercalciuria). Hypercalciuria of dietary acid excess does not appear to be intestinal in origin since there is no change in intestinal calcium absorption. High dietary protein intake causes glomerular hyperfiltration, which causes increased filtered load of calcium. The hypercalciuria, however, is above and beyond that of an increased filtered load to the kidney, indicating that a high dietary protein intake also causes a direct inhibition of calcium reabsorption in the kidneys. The possibility that hypercalciuria of animal protein excess is due to an acid-mediated renal calcium leak is supported by studies to be described below. Dietary Acid Load. On a daily basis, the normal Western diet generates about 1 mEq/kg of acid in adult human beings. The kidney is responsible for clearing the systemic acid load. However, there is a gradual reduction in overall renal function with age, which reduces the ability of the kidneys to excrete acid. When combined with a continued intake of animal proteins (contain acid-generating components such as methionine or cystine), a slight but significant acidemia may persist in the elderly. Even in younger individuals, overindulgence of animal proteins, can produce a degree of systemic acidity. The ensuing metabolic acidosis or acid load can produce marked hyper- calciuria. mycanadianhealthcare com discount drugs online
In a recent clinical study, a high protein-low carbohydrate weight reducing diet increased net acid excretion by 54 mEq/day and reduced urinary pH by 0.5 unit. While urinary calcium increased by 90 mg/day, intestinal calcium absorption was not altered and changes in bone markers were unremarkable. In another study, an animal model of animal protein excess was produced in rats by feeding a high casein diet. Compared with a low casein diet, urinary calcium was 3-4 fold greater on a high casein diet that was high in acid ash content. In a preliminary study (unpublished observations, Preisig et al.), the neutralization of the acid load by co-administration of potassium citrate completely abrogated the rise in urinary calcium from the high casein diet.
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Although the active transcellular reabsorption of calcium in the distal nephron accounts for only about 20% of total reabsorbed calcium, it is the major target for regulation by key factors implicated in the development of hypercalciuria.
Luminal pH. Using patch-clamp electrophysiological recording of recombinant EcaC1 channels expressed in cultured cells, low extracellular pH directly inhibited ECaC1 channel activity with an apparent pK of 6.55 which is within the physiologic range of luminal pH of the distal nephron. The direct inhibition occurred as a result of extracellular proton titration of glutamate- 522 (rabbit ECaC1) in an extracellular loop. The ECaC1 activity was inhibited by 16% for a drop in extracellular pH of 0.4. canadian healthcare shop com we care about you health
1.25(OH)oD33 and Estrogen. 1,25(OH)2D3 stimulates calcium reabsorption via genomic mechanisms analogous to classical steroid hormones. It increases the mRNA levels of both cal- bindin-D28K and the Na+/Ca2+ exchanger in a time frame that requires a genomic mechanism. While not expressed as high a level as calbindin-D28K, calbindin-D9K is also expressed in the kidney and upregulated at the mRNA level by 1, 25(OH)2D3. Recently, 1,25(OH)2D3 was shown to regulate the expression of ECaC2 in the kidney (24). 1,25(OH)2D3 may also influence calcium reabsorption by altering the expression levels of the PTH receptor and 25-hydroxyvitamin D3- 2 4 – h y- droxylase.
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