Calcitonin Salmon Injection

The core pathological mechanism of osteoporosis is the imbalance between skeleton resorption and skeleton formation, leading to a decrease in skeleton density and destruction of bone microstructure. Exert anti osteoporosis effects through the following pathways:

Inhibition of osteoclast activity: It binds to G protein coupled receptors on the surface of osteoclasts, activates adenylate cyclase, increases intracellular cyclic adenosine monophosphate (cAMP) levels, and inhibits osteoclast skeleton resorption function.

Research has shown that it can cause osteoclasts to contract pseudopodia and eliminate wrinkled edges, directly blocking the process of skeleton resorption.

Regulating calcium and phosphorus metabolism: By reducing blood calcium concentration, reducing renal tubular reabsorption of calcium, and inhibiting intestinal absorption of calcium, a "low calcium environment" is formed to inhibit skeleton resorption. In addition, it can promote phosphorus excretion and maintain blood phosphorus balance.

Promoting bone formation: Animal experiments have shown that it can stimulate osteoblast proliferation and differentiation, and increase bone matrix synthesis. Although the elevation of skeleton formation markers (such as skeleton alkaline phosphatase) in clinical studies is relatively small, it indirectly creates conditions for bone formation by inhibiting skeleton resorption.
Analgesic effect: By inhibiting prostaglandin E2 synthesis, reducing blood calcium concentration (decreasing calcium influx into nerve endings), and providing central analgesic effect, it can quickly relieve osteoporotic skeleton pain, especially suitable for patients with acute vertebral fractures.

Postmenopausal osteoporosis:
Estrogen deficiency is the main cause of accelerated skeleton resorption in postmenopausal women. Reduce skeleton loss by inhibiting osteoclast activity. A randomized controlled trial (RCT) involving 1200 postmenopausal women showed that continuous use of calcitonin salmon injection for 12 months increased lumbar spine skeleton density by 3.2% and reduced the risk of vertebral fractures by 40%. Another long-term follow-up study (5 years) showed that the incidence of hip fractures in the treatment group was 25% lower than that in the control group.

Senile osteoporosis:
Elderly people are prone to low conversion osteoporosis due to the decline of osteoblast function and abnormal vitamin D metabolism. By directly stimulating osteoblast differentiation (in vitro experiments showed a 20% increase in osteoblast proliferation rate), while inhibiting osteoclast activity, a "dual pronged" effect is formed. A randomized controlled trial (RCT) targeting elderly patients aged 70 and above showed that after 3 years of treatment with salmon calcitonin, hip bone density increased by 2.1% and the risk of non vertebral fractures decreased by 28%.

Corticosteroid induced osteoporosis (GIOP):
Long term use of glucocorticoids can inhibit osteoblast function and activate osteoclasts, leading to rapid skeleton loss. By antagonizing the skeleton resorption promoting effect of glucocorticoids, it has become an important treatment option for such patients. A study involving 200 patients with rheumatoid arthritis showed that the combined use of salmon calcitonin, calcium supplements, and vitamin D can slow down the rate of skeleton density loss by 60% and reduce the risk of fractures by 35%.

Pain management after acute osteoporotic fractures:
Newly diagnosed vertebral fractures are often accompanied by severe skeleton pain, which limits the patient's mobility and increases the risk of falls. By inhibiting prostaglandin synthesis and neuropeptide release, it directly acts on the central nervous system, rapidly relieving pain. A double-blind trial targeting patients with acute vertebral fractures showed a 50% decrease in pain scale (VAS) within 72 hours of treatment with salmon calcitonin, significantly better than the control group (ibuprofen), and the analgesic effect lasted until the end of treatment (4 weeks).

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Bone density monitoring:
Dual energy X-ray absorptiometry (DXA) is used to detect lumbar or hip skeletondensity before treatment and annually, with the goal of increasing it by 1% -3% annually. If skeleton density continues to decrease, compliance should be evaluated or treatment plans adjusted.
Bone turnover markers:
After 3 months of treatment, serum β - CTX (carboxy terminal peptide of type I collagen) or urine NTX (N-terminal peptide of type I collagen) should be tested.

If the decrease is not greater than 30%, the dosage should be adjusted or combined medication should be used.

Security monitoring:
Long term use requires regular testing of blood calcitonin salmon injection, blood phosphorus, and renal function (especially for patients with renal insufficiency). May cause hypocalcemia (symptoms include convulsions and numbness in the hands and feet), it is necessary to ensure adequate calcium intake. Rare adverse reactions include allergic reactions (such as urticaria, difficulty breathing) and nasal mucosal irritation (nasal spray), and a skin test is required before medication.

Deformable osteoarthritis is characterized by local skeleton remodeling disorder, manifested by accelerated skeleton resorption and abnormal skeleton formation, leading to skeleton deformities, pain, and increased risk of fractures. Plays a role through the following channels:
Inhibition of pathological skeleton resorption: Patients with Paget's skeleton disease have significantly increased osteoclast activity (serum alkaline phosphatase, ALP can reach more than 10 times normal values).

By inhibiting osteoclast function, reducing skeleton resorption, and lowering skeleton turnover rate to the normal range.

Correcting skeletal deformities: Long term high turnover state leads to skeleton enlargement and curvature (such as thickening of the skull and bending of long bones). By reducing skeleton turnover rate and minimizing abnormal new skeleton formation, a stable environment is provided for skeleton remodeling.

Relieve pain: Pain originates from the destruction of skeleton microstructure, nerve compression, or inflammatory response. Its analgesic effect can quickly improve the quality of life of patients.
Preventing complications: including fractures, hearing loss (due to skull thickening compressing the auditory nerve), and increased cardiac burden (due to high output heart failure).

Pain control:
Paget's skeleton disease patients often experience severe skeleton pain due to the destruction of skeleton microstructure. By inhibiting prostaglandin E2 synthesis and neuropeptide release, it directly acts on the central nervous system, rapidly relieving pain. A multicenter randomized controlled trial involving 150 patients showed that after 2 weeks of treatment, the pain score (VAS) decreased by 60%, significantly better than the bisphosphonate (pamidronate disodium) control group (45%), and had a faster onset of action (2 days vs. 7 days).

Correction of skeletal deformities:
Long term high conversion state leads to skeleton enlargement and bending. By reducing skeleton turnover rate, abnormal new skeleton formation can be minimized. Imaging follow-up showed a 15% reduction in skull thickness and a 20% improvement in long skeleton curvature angle after 6 months of treatment. For severe deformities such as hip inversion, it can be used as preoperative preparation medication to reduce surgical difficulty.

Preventing complications:
Fracture: Patients with Paget's disease have a 2-10 times higher risk of fracture compared to normal individuals. By stabilizing skeleton metabolism, the risk of fractures can be reduced. Research shows that the incidence of fractures decreases by 45% after 3 years of treatment.

Hearing loss: Thickening of the skull may compress the auditory nerve. By reducing skull expansion, improving cochlear blood flow, and alleviating hearing loss. A study involving 50 patients showed a 10 dB improvement in hearing threshold after 1 year of treatment.
Cardiac burden: High transition state leads to a large release of skeleton calcium into the bloodstream, which may cause hypercalcemia and increase cardiac burden. Calcitonin salmon injection calcitonin reduces cardiac afterload by lowering blood calcium concentration.

Bone turnover markers:
After 3 months of treatment, serum ALP and urinary hydroxyproline were measured with the goal of reducing to within 1.5 times the upper limit of the normal range. If ALP continues to increase, compliance assessment or exclusion of other diseases (such as skeleton metastases) is necessary.
Imaging assessment:
Review X-rays or skeleton scans annually to observe the progression of skeletal deformities and new lesions.

For skull lesions, regular head CT monitoring of thickness changes can be performed.
Security monitoring:
Long term use should be cautious of hypocalcemia (especially when combined with vitamin D deficiency), and it is recommended to maintain blood calcium levels of ≥ 2.1 mmol/L during treatment. Rare adverse reactions include allergic reactions (with an incidence rate of about 1% -3%) and nasal mucosal irritation (nasal spray), which require a skin test before medication.