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Abstract: A 42-year-old middle-aged male gradually developed generalized skeletal pain, and his height was getting shorter and shorter when he was clearly not yet old and did not have a hunchback. After examination, it turned out to be secondary hyperparathyroidism, resulting in severe osteoporosis. Finally, after standardized surgery + medication, the patient’s generalized skeletal pain was relieved, his condition was controlled, and all indicators improved.
Basic information】Male, 42 years old
Disease Type】Secondary hyperparathyroidism
Hospital】Beijing Hospital
Date of Consultation】June 2021
Treatment plan】Medication (osteopontin injection, zoledronic acid injection, human albumin, folic acid tablets, polysaccharide iron complex capsules) + surgery (subtotal parathyroidectomy)
Treatment period】2 weeks of inpatient treatment and regular outpatient follow-up
Treatment effect] The disease has been controlled and all indicators are improving
I. Initial consultation
The patient began to have generalized weakness and pain 4 years ago, mainly in the lower back and hip, and gradually developed into generalized bone pain, which was still tolerable, accompanied by heart fatigue and tightness of breath after activity. 2 years ago, he began to have a significant decrease in height and loose teeth. The patient had a 12-year history of gout and a 9-year history of uremia, which was treated with regular hemodialysis. more than 10 years ago, elevated blood pressure was detected and is now controlled with oral antihypertensive drugs. physical examination: stable vital signs, clear consciousness, no yellow staining of skin and sclera, and no enlargement of superficial lymph nodes throughout the body. Barrel chest and bilateral ribs did not show bead-like changes. There was no abnormal abdominal examination, no developmental deformity in the limbs, no movement, and no edema in the lower limbs. He was admitted to the hospital with “bone pain investigation”.
Treatment history
Since the patient was mainly admitted with skeletal-related symptoms, the admission examination mainly focused on some indicators related to bone metabolism. Routine blood tests showed moderate anemia, blood calcium: 2.81 mmol/L, blood phosphorus: 1.74 mmol/L, PTH: 3247.56 pg/ml, serum alkaline phosphatase: 1438.1 U/L, blood creatinine: 801.2 μmol/L, uric acid: 461 μmol/L. Ultrasound of the neck showed bilateral lobe nodules of the thyroid gland, nodular goiter; thyroid gland Bilateral deep lobe nodules, parathyroid hyperplasia. Thoracic CT: enlarged heart, enlarged atria, micropericardial effusion, calcification of thoracic aorta, right and left coronary arteries, aortic valve and mitral valve. Bone destruction of multiple thoracic vertebrae, swelling and thickening of the surrounding soft tissues, and bone destruction of the sternum (see the figure below). The abdominal x-ray: lumbar vertebrae and pelvic bones were unevenly hypodense; multiple foci of calcification in the vascularized areas of the abdominal aorta and pelvic floor. parathyroid nuclide imaging suggested hyperparathyroidism. The initial diagnosis was secondary hyperthyroidism, chronic renal insufficiency, CKD stage 5, gouty nephropathy, and renal anemia.
After admission, the patient was given treatment with osteotriol injection, folic acid tablets and polysaccharide iron complex capsules to supplement hematopoietic material. Regular hemodialysis treatment was continued. Thyroid surgery was requested to evaluate the condition and further treatment with subtotal parathyroidectomy was performed. Preoperative treatment was intravenous infusion of zoledronic acid injection and infusion of human blood albumin. Intraoperatively, all detected parathyroid tissue was excised and three parathyroid glands were removed if possible, while one parathyroid gland was preserved. Heparin-free hemodialysis was performed on the next day of surgery, and heparin-free hemodialysis was performed for 1 week after surgery.
(Chest CT)
(Parathyroid nuclide imaging)
III. Treatment results
The patient’s vital signs, pronunciation and swallowing, as well as incisional blood leakage, subcutaneous hematoma and drainage were closely observed after surgery. Postoperatively, the patient did not show symptoms of laryngeal nerve injury such as hoarseness and choking, and there was no postoperative anterior cervical hematoma formation. Postoperatively, intravenous calcium gluconate was administered according to the blood free calcium/total calcium level to keep it at a normal level. The patient had an uneventful surgery and good postoperative recovery. One week after surgery, the patient was rechecked: blood calcium: 1.98 mmol/L, blood phosphorus: 1.37 mmol/L, iPTH: 102.11 pg/ml, and hyperthyroidism was basically controlled, and the patient was discharged after 2 weeks of comprehensive hospitalization. Follow-up outpatient follow-up blood free calcium levels were maintained in the normal stable range, and the patient’s symptoms were significantly improved.
IV. Notes
We are glad that the patient’s condition has improved, and we suggest that the patient should be reviewed every month to monitor the changes of parathyroid hormone and bone metabolic indexes, including blood calcium and blood phosphorus, and adjust the drug dosage according to the results. However, even though it is possible that the patient’s parathyroid hormone may rise again and secondary hyperparathyroidism may recur, as long as good control of blood calcium and blood phosphorus is achieved, bone pain symptoms can be effectively controlled and quality of life can be improved. In addition, since this patient has severe osteoporosis, it is important to prevent fractures caused by traumatic injuries such as falls in daily life to improve the survival and quality of life of long-term dialysis patients.
V. Personal insight
Chronic renal failure-induced hypocalcemia stimulates the parathyroid glands for a long time, causing hyperplasia and excessive secretion of parathyroid hormone leading to secondary hyperparathyroidism. In this case, the patient neglected to monitor parathyroid hormone levels and bone metabolic indexes during long-term hemodialysis, so that he developed relatively severe secondary hyperparathyroidism, resulting in bone destruction, significant bone pain, and height loss. Fortunately, the patient was a middle-aged male with good compensatory capacity, no traumatic injuries such as falls in daily life, and no events such as fractures yet, which would otherwise have seriously affected the patient’s quality of survival. This case reminds us that for patients with renal insufficiency on long-term dialysis, we should pay attention to patients’ bone health and regularly monitor blood calcium and phosphorus, parathyroid hormone and other indicators.