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    Home > Active Ingredient News > Endocrine System > Urinary tract stones, osteoporosis, body pain, difficulty walking, who is the "culprit" and who is the "helper"?

    Urinary tract stones, osteoporosis, body pain, difficulty walking, who is the "culprit" and who is the "helper"?

    • Last Update: 2022-01-25
    • Source: Internet
    • Author: User
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    *Only for medical professionals to read and refer to the 45th article related to the prevention and treatment of osteoporosis published by Director Bian Pingda of Zhejiang Provincial People's Hospital in the medical community
    .

     When encountering some more complicated or rare cases in the outpatient clinic, doctors often recommend hospitalization.
    This is because the "culprit" of the patient's discomfort cannot be found quickly in the outpatient clinic due to the limitation of consultation time

    .

    When a doctor sees a doctor, it is actually a process of finding the "culprit".
    If the "culprit" cannot be found and corresponding measures are taken, it is often difficult for the patient's discomfort to be effectively relieved

    .

     About a year ago, Aunt Wu, who was in her 60s and emaciated (body mass index (BMI) was only 14kg/m2), came to the outpatient clinic.
    She developed multiple kidney stones when she was in her 30s.
    He underwent several surgeries, including traditional open nephrolithotomy and flexible ureteroscopic lithotripsy

    .

    About 3 years ago, the pain in the waist, ribs and limbs began to appear, accompanied by obvious tenderness, and gradually increased
    .

    About 2 years ago, he began to experience loss of appetite, weight loss, and lower limbs weakness.
    He walked like a duck and mainly relied on walkers

    .

    Outpatient urology B-ultrasound showed multiple stones in both kidneys [the larger long diameter is about 20 mm (right), 18 mm (left)]; dual-energy X-ray absorptiometry showed osteoporosis (bone density of the left femoral neck) The T value was -3.
    7, -3.
    5 for the total hip, -3.
    6 for the lumbar spine)

    .

    The patient's blood biochemistry (see screenshot 1) showed decreased serum potassium, serum calcium, and serum phosphorus, and increased creatinine (205 μmol/L).
    Calculated by the Cockcroft-Gault formula, his glomerular filtration rate was only 12.
    26 mL/min.

    .

    Figure 1 The patient's blood biochemical report (part) The patient's bone metabolism markers showed that the special sequence of type I collagen carboxy-terminal peptide beta and the total type I collagen amino-terminal propeptide were significantly increased, and the parathyroid hormone was increased (see Figure 2)
    .

     Figure 2 Is the patient's bone metabolism marker report due to hyperparathyroidism? Clinically, when encountering a large number of urinary tract stones with osteoporosis, most physicians will think of "primary hyperparathyroidism"
    .

    However, the patient's blood calcium was low; thyroid B-ultrasound showed a low echo at the rear of the left thyroid lobe (no parathyroid hyperplasia or adenoma was seen); parathyroid radionuclide scan showed that the radiation distribution in the middle of the left thyroid lobe was slightly more concentrated than that in the right lobe ( No hyperfunctioning parathyroid tissue was seen), so it is not supported
    .

    It seems that secondary hyperparathyroidism should be considered! The patient suffered from renal insufficiency induced by long-term multiple kidney stones (unknown cause), insufficient synthesis of 1,25 dihydroxyvitamin D in the body, and reduced calcium absorption in the intestine
    .

    Hypocalcemia can stimulate the parathyroid gland to secrete parathyroid hormone, and the increase of parathyroid hormone, on the one hand, accelerates bone resorption, induces osteoporosis and bone and joint pain, on the other hand, promotes the decomposition of protein in muscles, and the appearance of muscle Atrophy, pain and muscle weakness [1]
    .

    Therefore, active vitamin D preparations (calcitriol capsules) are given, which can rapidly increase serum 1,25 dihydroxyvitamin D levels, promote intestinal absorption of calcium, and increase blood calcium, which can feedback inhibit parathyroidism The glands secrete parathyroid hormone [1]
    .

    The patient has osteoporosis, but the glomerular filtration rate is lower than 30 ml/min, so the RANKL inhibitor denosumab (60 mg, subcutaneous injection) is selected [2]
    .

    However, after 3 months of the above treatment, the patient's body pain was not significantly relieved during a return visit! Could it be that the diagnosis and treatment were wrong? It was the drug that caused it! When asked about the medical history, the patient had a history of chronic hepatitis B.
    He started taking adefovir dipivoxil tablets 10 years ago due to elevated alanine aminotransferase (1600U/L)

    .

    After about 3 years of continuous use, the pain in the whole body appeared and gradually increased
    .

    I went to the Provincial City University Hospital for many times, and some doctors said that the pain was caused by osteoporosis.
    I also had intravenous drip of the anti-osteoporosis drug Zoledronic acid injection, but the pain was not relieved significantly; some doctors said that this kind of pain There is no way, eat some health products and slowly nursed back to health

    .

    Later, the patient stopped taking adefovir dipivoxil on his own due to normal liver function
    .

    About 3 months after stopping taking adefovir dipivoxil tablets, the pain gradually disappeared, and the patient thought it was the effect of taking health care products
    .

    However, 5 years ago, the patient was found to be positive for hepatitis B virus-DNA, so he took adefovir dipivoxil tablets under the guidance of an infectious disease physician
    .

    Adefovir dipivoxil is the precursor of adefovir, which exerts antiviral effect after being converted into adefovir in vivo
    .

    However, in recent years, it has been found that adefovir dipivoxil can impair renal proximal tubular function, resulting in decreased reabsorption of various substances including phosphonates, thereby causing hypophosphatemia osteomalacia
    .

    Relevant literature studies have shown that the course of hypophosphatemia osteomalacia caused by the drug is slow (mostly between 13 and 48 months), with bone pain as the main manifestation, and severe cases have walking disorders, muscle atrophy, and blood phosphorus is significantly reduced.
    It is the characteristic performance of its laboratory examination [3]

    .

    Therefore, he immediately stopped taking adefovir dipivoxil tablets, switched to entecavir tablets for antiviral treatment, and continued to take calcitriol capsules
    .

    One month after the patient stopped taking adefovir dipivoxil tablets, the pain in the whole body was significantly relieved, and the pain was further relieved in 3 months, and the tenderness of the ribs disappeared
    .

    Compared with serum potassium, serum sodium and serum calcium, serum phosphorus is often overlooked by people
    .

    In fact, as a basic element, blood phosphorus plays an important role in human life activities (especially in the development and mineralization of bones)
    .

    In addition to drugs (such as adefovir dipivoxil), certain genetic diseases (such as X-linked dominant hypophosphatemic rickets/osteomalacia) and tumors (such as phosphaturic mesenchymal tumors, etc.
    ) can induce hypoglycemia Phosphatemia, which in turn leads to bone mineralization disorders [4]

    .

    Although the elderly female patient does have diseases such as osteoporosis, renal insufficiency and secondary hyperparathyroidism, and these diseases can also cause pain and muscle lesions, these diseases can only be said to be "helpers".
    The "culprit" is severe hypophosphatemia after long-term use of adefovir dipivoxil tablets!
    References: [1] Chinese Medical Association Osteoporosis and Bone Mineral Disease Branch, Chinese Medical Association Endocrine Branch Metabolic Osteopathy Group.
    Guidelines for the diagnosis and treatment of primary hyperparathyroidism [J].
    Chinese Osteoporosis Chinese Journal of Osteoporosis and Bone Mineral Diseases, 2014, 7(3): 187-109.
    [2] Chinese Medical Association Osteoporosis and Bone Mineral Disease Branch.
    Chinese expert advice on the rational use of denosumab in osteoporosis [J].
    Chinese Journal of Osteoporosis and Bone Mineral Diseases, 2010, 13(6): 499-508.
    [3] Zhai Shuyue, Xie Yanjun, Wang Bingjie, et al.
    71 cases of hypophosphatemia induced by adefovir dipivoxil Literature analysis of softening syndrome [J].
    China Pharmacovigilance, 2015, 12(5): 290-295.
    [4] National Health Commission of the People's Republic of China.
    Guidelines for the diagnosis and treatment of rare diseases (2019 edition) [J].
    People's Republic of China The official website of the National Health Commission.
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