Whether you are suffering from corticosteroid-induced osteoporosis, or you know someone who is, there are a few things you need to know. These include what the condition is, how it is treated, and the role of calcium in treating it.
Calcium vs calcitriol
Several studies have examined the effect of calcium and calcitriol on bone mineral density in patients on long-term corticosteroid therapy. These studies have shown that combining calcium and calcitriol can reduce bone loss, and maintain bone mineral density in the lumbar spine, femoral neck, and total hip.
A recent study investigated the effect of prophylactic calcium supplementation on the bone mineral density of patients on long-term corticosteroid treatment. It found that a combination of low-dose calcium plus intermittent calcitriol prevents bone loss, regardless of underlying bone histology. It also showed that this treatment is not associated with changes in renal function.
Another study examined the effects of a prophylactic 1,25-dihydroxy vitamin D3 on bone mineral density in recipients of long-term corticosteroid therapy. It found that this treatment has a favourable effect on osteocalcin concentrations. It was concluded that calcitriol should be used for vitamin D supplementation in glucocorticoid-induced bone disease.
A third study evaluated the effects of a nasal calcitonin formulation on the bone mineral density of patients on long-term oral corticosteroid therapy. This treatment is commonly prescribed in patients who are at risk for bone loss, as compared to an injected placebo. It showed that the nasal formulation is effective in reducing bone loss. However, it did not demonstrate any significant effects on radial bone density.
In addition, another study examined the effects of a single dose of calcitriol intranasally. This study found that intranasally administered calcitriol decreased the rate of bone loss at the total hip and femoral neck. It also found that this regimen decreased post-transplantation PTH levels.
In the first year of the study, two deaths occurred. These deaths were not associated with the trial medications.
Glucocorticoids (GCs) are potent inhibitors of osteoblastic and osteoclast activities. They inhibit the osteoblast cell cycle, which reduces bone turnover. They also reduce osteoblastic activity in the bone marrow. In addition, they inhibit the expression of keratinocyte growth factor (KGF), an important protein involved in keratinocyte development. They have direct catabolic effects on skeletal muscles.
Long-term use of GCs has been associated with cardiovascular disease, diabetes, and immunosuppression. They are contraindicated in patients with untreated systemic infections. They are also related to gastrointestinal events. GC therapy has been reported to cause ulcers. The risk of Cushingoid features is dependent on the dose and age of the patient.
The use of GCs in pregnancy has been associated with an increased risk of cleft palate in offspring. This is due to their catabolic effect. In addition, prolonged exposure to GCs has been linked to osteonecrosis.
In an animal model, dexamethasone has been shown to increase Ca2+ elevation in rat hippocampal neurons. Furthermore, it has been shown to inhibit TCR signalling, which results in the inhibition of the LCK/FYN pathway.
Activation of the TCR leads to the phosphorylation of kinases and differentiation. These kinases are implicated in GR-mediated immunosuppressive effects in T lymphocytes.
During the sensitization phase of a GR-mediated TLR9-mediated inflammation, IRAK1 ubiquitination is required. GR undergoes posttranslational modifications, which affect the stability of GR and the subcellular localization of GR.
The binding of a GC to the GR triggers several immune cell mechanisms. These include apoptosis, phagocytosis, and immunosuppression. In the presence of a GC, the GR resides in the cytoplasm in a complex with multiple proteins. The hydrophobic motifs in the LBD are crucial for the ligand-mediated activation of the GR.
GC-GR-mediated endoplasmic reticulum stress
Glucocorticoids (GCs) are steroid hormones secreted from the adrenal cortex. They play a significant role in many metabolic processes, including insulin production and glucose homeostasis. They also affect lipid and skeletal muscle homeostasis. However, their effects are not well understood.
Recent evidence suggests that long-term exposure to GCs may contribute to cardiometabolic disease. For example, in a recent study, patients on GC therapy for more than 12 months had increased bone resorption and decreased bone formation. Moreover, their bone density and trabecular volume decreased. Compared with patients receiving low-dose GC, the risk of fracture was two to five times higher in high-dose GC patients.
Besides its role in glucose metabolism, GCs also influence the physiology of adipose tissue. They stimulate the release of free fatty acids from adipose tissues in circulation. This increases the amount of fat in the body. This can contribute to insulin resistance in adipose tissue, which is one of the major causes of diabetes. GCs have also been shown to reduce the apoptosis of mature osteoclasts.
GR is a transcription factor that is able to bind to GCs. GCs then translocate to the nucleus and activate target genes. They also inhibit a number of other proteins. GC-GR complexes repress genes, including those that control bone remodelling. In addition, they also repress inflammatory genes.
GCs can cause endoplasmic reticulum stress. This stress induces structural plasticity in neurons and neuropsychiatric disorders. GCs affect the neurotransmission of glucose and glutamate. They may also affect pancreatic endocrine function.
GC-GR complexes have also been implicated in hepatic steatosis. In mice, adipose-specific deletion of GR (GRa) has been found to be protective against hepatic steatosis. Moreover, the pharmacological blockade of GR has been shown to prevent the progression of diabetes.
Anabolic steroids have also been tested in GCOP
Generally speaking, anabolic steroids are used to enhance the performance of an athlete. However, there are many adverse side effects of using them. In fact, misuse of anabolic steroids can lead to serious health problems.
If you are an amateur athlete, you should discuss your use of steroids with your healthcare provider. They can help you understand the dangers of steroid abuse and suggest safe ways to increase your strength.
The use of steroids is prohibited by most professional sports organizations. The National Collegiate Athletic Association tests players for illicit use once a year. Major League Baseball and the NFL also test players.
Law enforcement officers, who are known for their strength and physical prowess, are also prone to steroid use. Some of them may be clean weightlifters, but many use illegal substances to boost their performance.
In some cases, the use of steroids can cause permanent changes to the male reproductive system. In some cases, these changes can be reversed.
There is also evidence that anabolic steroids can cause heart disease. In addition, they can cause cancer. They can also affect the liver and blood vessels.
Anabolic steroids are classified as class C drugs, meaning that they have limited medical uses. However, they are also highly addictive drugs. Users of anabolic steroids tend to take more of the drug to achieve the same effects.
Designer drugs are a particularly dangerous category of anabolic steroids. These drugs are manufactured specifically for athletes. Until now, these drugs have not been tested for safety or effectiveness by the FDA.
Many professional athletes and bodybuilders use anabolic steroids. These are synthetic compounds that imitate the male sex hormone testosterone. They can be taken in capsule form, or in injectable liquids.
Glucocorticoid-induced osteoporosis treatment is a serious problem that occurs as a result of the long-term use of exogenous glucocorticoids. It is characterized by a loss of bone mass and a reduction in the number of new bone formations. Glucocorticoids have been used to treat a wide range of diseases.
The long-term use of high-dose corticosteroids can lead to bone loss, including a higher risk of fracture. This is particularly true for postmenopausal women who take oral corticosteroids. In addition, underlying conditions can contribute to a patient’s increased risk of fracture.
The use of bisphosphonates has shown promise for the prevention of bone loss in patients starting corticosteroid therapy. They have also been shown to reduce the incidence of non-vertebral fractures. However, their effectiveness has not been rigorously tested. Similarly, they have not been used for the treatment of symptomatic vertebral fractures.
Glucocorticoid-induced osteoporosis is a relatively unrecognized complication of chronic glucocorticoid therapy. The best preventive measure is to avoid systemic steroids and to utilize local steroid preparations, if possible.
Clinical fracture risk is assessed using a series of clinical evaluations, including evaluation for malnutrition, falls, muscle strength, and history of glucocorticoid use. The patient’s height, deformity, and family history of hip or lumbar fractures are also considered. If the risk of fracture increases, fracture prophylaxis should be instituted.
The decision to initiate intervention depends on the anticipated duration of the therapy. If the patient has a T-score less than minus 1 per cent, or if the Z-score is negative, then instituting a therapy is recommended. In contrast, if the T-score is greater than minus one per cent, or the Z-score is positive, there is no consensus on the appropriate threshold for intervention.
Additional info on LINK