|03-12-2008, 04:38 AM||#11|
رد: الكالسيوم القاتل
الكورتيزونات قد تستخدم فى علاج Hypercalcemia والتى نتجت عن تسمم بفيتامين د
hypercalcemia caused by vitamin D toxicity
وكذلك قد يستخدم فى بعض حالات Thyrotoxic hypercalcemia
كمان هى بتعمل decreased absorption of calcium, and Cause hypercalciuria
يعني بتزود خروج الكالسيوم
|03-12-2008, 04:46 AM||#12|
رد: الكالسيوم القاتل
يعنى تأثيرات الكالسيوم الضارة على العظام تتضمن:
|03-12-2008, 04:50 AM||#13|
رد: الكالسيوم القاتل
لمزيد من المعلومات
Since this kind of osteoporosis is so difficult and so devastating, I am frequently asked about it, and many of my patients have this form of osteoporosis. I have been intending to write a more comprehensive page about this, with better evidence tables, but in the meantime will give a sketch about this disease.
Corticosteroids cause osteoporosis and fractures in a high percentage of patients. There is a dose-dependent effect, which is difficult to define because of varying durations at each dose. The beneficial effects of steroids on the underlying disease may partially offset the detrimental effects on bone. Because the effects are so variable and can be clinically severe, patients embarking on long-term steroid treatment should have bone density monitored, and measures taken to try to preserve bone.
Corticosteroids have several adverse effects on bone metabolism.
Bone density should be measured in patients who are expected to remain on corticosteroids. The same lab tests that are used for "ordinary" osteoporosis are indicated for steroid-induced osteoporosis. In males it is very important to remember to check the testosterone level. Females should be asked about amenorrhea (which is probably a better indication of estrogen deficiency than estrogen levels). Measurement of LH or FSH will not be helpful in this situation, since the hypogonadism is usually hypogonadotropic, and thus low estrogen will not be associated with high FSH the way it is in a postmenopausal woman.
A 24-hour urine calcium is indicated, because often these patients have hypercalciuria. I usually check a urine N-telopeptide, too, to get an idea of how much of the hyercalciuria is due to bone resorption. Low urine calcium is also seen, especially if patients have any other reason for malabsorption. Vigorous treatment with calcium and vitamin D is too frequently undertaken without checking the urine calcium, and this could worsen hypercalciuria.
In patients with markedly low bone density, prevalent fractures, or high doses of steroids I usually also check a PTH and 25-hydroxyvitamin D level. In less severe cases I will just check these if the serum calcium or alkaline phosphatase is abnormal.
Xrays of the spine are especially important in patients taking long-term corticosteroids, because sometimes the fractures are not clinically obvious, and if they are present the patient will need maximal therapy. Therapy
The physiology of corticosteroid-induced osteoporosis is different than postmenopausal osteoporosis, so treatment cannot be expected to have the same results. For example, anti-resorptive therapy does not result in the same degree of increase in bone mass as in postmenopausal osteoporosis.
Treatment/prevention of steroid-induced osteoporosis should begin with adequate calcium intake of 1000 to 1500 mg/day. Greater amounts are unlikely to be beneficial. If the patient already has hypercalciuria, low-dose thiazides (12 mg/day) will reduce the hypercalciuria and allow more calcium intake.
The use of vitamin D in corticosteroid-treated osteoporosis is debated, and there is still not enough data to make strong recommendations. The most recent studies do not show a difference in bone density with active vitamin D metabolites or high doses of ergocalciferol. However, patients should receive some vitamin D to prevent deficiency (1000 units/day). In those cases with low urine calcium or clinical malabsorption or renal insufficiency the more potent vitamin D should be used (such as calcitriol at 0.25 mcg/day as a beginning dose).
Gonadal steroids (estrogen in women and testosterone in men) should be replaced as appropriate unless there are contraindications.
Anti-resorptive therapy can prevent some of the bone loss. Calcitonin nasal spray (one puff = 200 units/day) or bisphosphonates (I prefer alendronate 5mg/day) have been used. Recent clinical trials using etidronate or alendronate have shown benefits after one year; long-term studies are still needed. These studies really don't have enough power to measure fracture prevention, and the only beneficial effect on fractures has been seen in postmenopausal women not taking estrogen. The magnitude of change in bone density is definitely lower than in studies of postmenopausal women taking these drugs; this makes sense, because the anti-resorping medications do not help with the osteoblasts which are inhibited by the corticosteroids. These therapies should not be used in patients with low serum calcium, and adequate dietary intake should be assured before they are started. Also avoid them in patients with reflux esophagitis, patients who are bedridden and can't be upright after taking the medication, and patients with renal insufficiency.
I don't use bisphosphonates in premenopausal women unless they are at serious risk of fractures - - - especially if they think they may wish to become pregnant in the future. There isn't enough data yet on other treatments such as growth hormone or fluoride. Some recent studies suggest that PTH might improve spine bone density, but in other situations PTH increases the spine at the expense of the total body or the hip, so PTH cannot be recommended at this time. Besides, if patients can't absorb calcium very well, secondary hyperparathryoidism could be making the bone disease worse.
نقلاً عن : http://courses.washington.edu/bonephys/opsteroid.html
|03-12-2008, 09:59 AM||#15|
رد: الكالسيوم القاتل
شكرا ليك دكتور محمد دكتوره sucess
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شكرا الك كتير علا المعلومات وربنا يزيدك علم كمان وكمان يا رب
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