Diagnosis, treatment and prevention of glucocorticoid osteoporosis

  Characteristics of glucocorticoid osteoporosis: 1. Glucocorticoids are widely used in the treatment of many acute and chronic diseases, including rheumatoid rheumatism, various allergic diseases and organ transplantation. Glucocorticoid treatment can cause a variety of side effects, among which osteoporosis is one of the most common and serious complications, which can lead to fractures of vertebrae, ribs, hips and other parts of the body, seriously affecting patients’ quality of life and increasing economic burden.  2. Glucocorticoid-induced osteoporosis is dose- and time-dependent, and the use of prednisone at a dose of 5-7.5 mg per day for 3 months will lead to a dramatic loss of bone minerals and an increased risk of fracture, with bone loss peaking after 6 months of continuous use, and continued use will lead to a decrease in bone formation capacity and severe osteoporosis, which can lead to fracture with minor external force.  3. The fracture threshold of glucocorticoid-induced osteoporosis is lower than that of other causes of osteoporosis: a T value below -1.5 can easily lead to spine or hip fracture, which is more demanding than other causes of osteoporosis in terms of treatment and prevention.  4. High doses of glucocorticoids are prone to osteonecrosis, and the common sites are the femoral head (hip) and the humeral head (shoulder).  The pathological mechanism of glucocorticoid osteoporosis: 1. Hormones lead to a decrease in the function and activity of bone forming cells and an increase in the life span and activity of osteoclasts, ultimately leading to a greater loss of bone than bone formation; 2. Hormones lead to a decrease in the synthesis of active vitamin D, a decrease in intestinal calcium absorption and an increase in urinary calcium excretion, resulting in hypocalcemia and a decrease in the raw material for bone formation; 3. 3. Hormones inhibit pituitary-gonadal and pituitary-adrenal glands, resulting in a decrease in gonadal secretion that affects bone reconstruction and repair; 4. Hormones cause muscle atrophy and muscle weakness, and patients are at increased risk of falling and fracture.  Clinical presentation and diagnosis of glucocorticoid osteoporosis: These patients have a history of oral or intravenous use of glucocorticoids (e.g. prednisone, dexamethasone, etc.) for other diseases. Most of the symptoms of osteoporosis are insidious, and many patients do not find out the complication of osteoporosis until they receive X-ray examination. Some patients complain of low back pain, weakness, limb twitching, etc. In severe cases, skeletal pain, fractures of the low back and hip and ischemic necrosis of the femoral head may occur with minor injuries. The diagnosis mainly relies on bone density examination, and blood test is also needed to understand blood calcium, blood vitamin D level and other bone metabolism conditions.  Prevention and treatment of glucocorticoid osteoporosis: 1. General preventive measures include minimizing the dosage and course of glucocorticoids, changing the dosage form, changing the route of administration or switching to other immunosuppressive drugs, or using alternate-day therapy to preserve the feedback function of the hypothalamic-pituitary-adrenal axis under the guidance of a doctor.  2.Healthy lifestyle: avoid smoking and alcohol, reasonable exercise, high calcium and balanced nutritional diet to maintain healthy bones.  3, reasonable calcium and vitamin D supplementation: as mentioned above, glucocorticoids tend to lead to hypocalcemia, while the Chinese population generally has insufficient dietary intake of calcium (less than 400 mg/d), so it is more necessary to supplement sufficient calcium and vitamin D to meet the needs of healthy bones, it is recommended that the total intake of elemental calcium should be about 1200-1500 mg/d (including calcium in the diet), and the general vitamin D It is recommended that total elemental calcium intake should be about 1200-1500 mg/d (including dietary calcium) and general vitamin D supplementation should be 800-1000 IU/d. During the course of treatment, blood and urine calcium levels should be monitored and the dose should be adjusted to be alert to the kidney damage caused by long-term high urine calcium.  4. Patients who have been on glucocorticoid therapy for more than 3 months or less than 3 months and are at high risk of osteoporosis (e.g. history of hip fracture, low body weight, alcoholism, etc.) should be treated with anti-osteoporosis treatment based on bisphosphonates under the guidance of an osteoporosis specialist.