4.1 Hypocalcemia and Intravenous Calcium Supplementation after t-ptx in SHPT Patients
Hypocalcemia is a common complication that can develop within 24–48 h after t-ptx, resulting in clinical symptoms including numbness and convulsions of the hands and feet, arrhythmia, epilepsy, a positive cheek reaction, severe asphyxia, and even cardiac arrest . However, only 29.82% of affected patients exhibit clinical symptoms. The primary causes of hypocalcemia following t-ptx include a sudden drop in PTH levels following parathyroidectomy, resulting in the transfer of large quantities of calcium ions from the blood into the bone and a concomitant rapid drop in serum calcium concentrations . In the present study, hypocalcemia developed in 72.7% of patients, consistent with the 29–80% incidence rate reported previously . However, there are no unified standards available to treat postoperative hypocalcemia in SHPT patients at present. Based upon several years of clinical experience, our department generally treats this condition through calcium supplementation via the intravenous infusion of 100 ml normal saline + 100 ml 10% calcium gluconate at a flow rate of 20–50 mL/h. This infusion is performed once, twice, or thrice daily when the blood calcium level is 1.8–2.0 mmol/L, 1.6–1.8 mmol/L, and < 1.6 mmol/L, respectively. Such intravenous calcium supplementation was terminated when the blood calcium level was > 2.0 mmol/L on the mornings of two consecutive days and the patients did not exhibit any symptoms of perceived hypocalcemia . The total amount of intravenous calcium supplementation in the present study was 0-3600 mL, in line with previous reports of high levels of intravenous calcium supplementation during hospitalization (0-2800 mL), with an average supplementation volume of 557.86 ± 376.20 mL . Differences among studies may be attributable to differences in sample size, operative approach, preoperative dialysis, or patient management. Our department conducted postoperative follow-up assessments for patients and found that 82.47% were able to maintain appropriate blood calcium levels by taking oral calcium tablets containing vitamin D3, while 5 patients required high concentration intravenous calcium supplementation. These findings highlight the clinical significance of operative approach selection and intravenous calcium supplementation.
4.2 Construction of a model to predict the volume of intravenous calcium supplementation in SHPT patients following t-ptx
An extensive literature search revealed that several models to predict postoperative hypocalcemia following t-ptx have been developed to date , yet no corresponding predictive tools are available to estimate the amount of postoperative intravenous calcium supplementation required by these patients . In this study, the final predictive model incorporated independent variables including gender, SF, AKP, and FT4 that were associated with the need for postoperative intravenous calcium supplementation, in contrast to variables included in other studies such as age, hemoglobin, CA, AKP, and PTH .
The developed model revealed a negative relationship between gender and the amount of intravenous calcium supplementation such that the amount of intravenous calcium administered to men was, on average, higher than that administered to women. This may be attributable to the higher number of men in this study relative to women, and to the fact that the average population age was 48 years. At this age, the rate of osteoporosis among women is roughly twice that among men, and the lower levels of postoperative blood calcium in women may suggest that men require higher levels of blood calcium to maintain sufficient calcium levels within the bone. However, this will need to be tested in future studies.
The developed model further indicated that ferritin levels had a positive impact on the amount of intravenous calcium supplementation, with higher SF levels corresponding to higher amounts of postoperative calcium administration. SF is the primary iron storage mechanism in the body and thus the main index used to evaluate iron deficiency or overload. It can also be used to evaluate malnutrition, calcium/phosphorus metabolism disorders, and the presence of micro-inflammatory states . In prior research, elevated SF levels have frequently been observed in dialysis patients and independently associated with mortality in this patient population, and a high SF environment can impact phosphorus excretion and utilization. Higher levels of phosphorus in the blood can, in turn, inhibit calcitriol formation and lower blood calcium levels . Lien et al.  reported that increases in iron ion concentrations were associated with reductions in calcium ion levels within osteoblasts. As iron ions are closely tied to the metabolism of calcium ions, it can thus impact bone metabolism. Kim et al.  determined that when SF levels are appropriately controlled, this can alleviate bone metabolism and microinflammation related to iron deficiency, thus improving patient outcomes. This evidence all supports the incorporation of SF levels in our postoperative intravenous calcium supplementation model.
In the developed model, AKP was found to positively impact the amount of postoperative intravenous calcium supplementation in this patient population, in line with prior results . Serum AKP is primarily secreted by the liver and by osteoblasts, and functions as a key enzyme that promotes bone matrix mineralization. KDIGO guidelines recommend the use of AKP levels as a metric to gauge the severity of bone mineral metabolic abnormalities in chronic kidney disease patients . Ge et al.  found AKP to be associated with osteoblast activity and to reflect the severity of postoperative hungry bone syndrome. Yang et al.  further determined that AKP can reflect bone reconstructive activity, serving as a valuable index to guide postoperative calcium supplement dosing. Tsai et al.  analyzed 62 patients that had undergone t-ptx and determined that higher AKP values were associated with a greater risk of postoperative hypocalcemia, more serious symptoms, and the need for a larger supplemental calcium dose.
The regression coefficient in the developed model indicates that GT4 levels negatively impact the amount of postoperative intravenous calcium supplementation. Laowalert et al.  previously demonstrated that FT4 can impact bone metabolism, altering the absorption and formation of bone tissue. Liangos et al.  found that patients suffering from chronic renal failure often exhibit normal or reduced FT4 levels owing to impaired pituitary thyroid functionality. As renal function deteriorates, pronounced FT4 abnormalities can develop. Abnormal FT4 metabolism can also be associated with high PTH levels and hypogonadism, with high PTH inhibiting the production of T3 from T4. As such, we can infer that FT4 may impact bone and calcium metabolism to some degree. However, research on this topic is limited, and further research will thus be critical to test this hypothesis, with the present large-scale study serving as a valuable foundation for future studies.