Serum Parathyroid Hormone Levels In Patients Research Articles

Self-assembled nanobody-DNA nanomachine conjugate for parathyroid glands intraoperative imaging and parathyroid hormone detection

During thyroidectomy, inadvertent parathyroid damage commonly occurs owing to the varying location of the parathyroid glands and their similarity to adipose tissue, lymph nodes, and thyroid nodules. Therefore, in this study, we aimed to develop a novel self-assembled nanobody-DNA nanomachine conjugate probe (PTH-Nb-HCR) for precisely identifying the parathyroid glands and monitoring parathyroid hormone (PTH) levels in patient blood. The probe consists of two components: the first component is the nanobody (Nb)-nucleic acid conjugate PTH-Nb-Trigger, acting as a recognition unit for PTH and capable of initiating the hybridization chain reaction (HCR), whereas the second component comprises the HCR hairpin probes HP1-FAM (with a modified FAM signal molecule at the 5′ end) and HP2. The assembly of the PTH-Nb-HCR fluorescent probe takes only 20 min. Using the probe, the serum PTH level was quantitatively detected in the 0.1–1000 pg/mL range, and the parathyroid glands were rapidly distinguished from adipose, lymphoid, and thyroid tissues within 5 min. We also used this probe for imaging parathyroid glands with hyperparathyroidism. Considering the strong correlation between fluorescence intensity and preoperative serum PTH levels in patients, we anticipate the use of this probe to distinguish normal and hyperfunctional tissues during hyperparathyroidism surgery.

PTH Predicts the in-Hospital MACE After Primary Percutaneous Coronary Intervention for Acute ST-Segment Elevation Myocardial Infarction.

To investigate the correlation between serum parathyroid hormone (PTH) levels and in-hospital major adverse cardiovascular events (MACE) in patients with acute ST-segment elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (PCI), and establish a risk prediction model based on parameters such as PTH for in-hospital MACE. This observational retrospective study consecutively enrolled 340 patients who underwent primary PCI for STEMI between January 2016 and December 2020, divided into a MACE group (n=92) and a control group (n=248). The least absolute shrinkage and selection operator (LASSO) and logistic regression analyses were used to determine the risk factors for MACE after primary PCI. The rms package in R-studio statistical software was used to construct a nomogram, to detect the line chart C-index, and to draw a calibration curve. The decision curve analysis (DCA) method was used to evaluate the clinical application value and net benefit. Correlation analysis revealed that PTH level positively correlated with the occurrence of in-hospital MACE. Receiver operating characteristic curve analyses revealed that PTH had a good predictive value for in-hospital MACE. Multivariate logistic regression analysis indicated that Killip class II-IV, and FBG were independently associated with in-hospital MACE after primary PCI. A nomogram model was constructed using the above parameters. The model C-index was 0.894 and the calibration curve indicated that the model was well calibrated. The DCA curve suggested that the nomogram model was better than TIMI score model in terms of net clinical benefit. Serum PTH levels in patients with STEMI are associated with in-hospital MACE after primary PCI, and the nomogram risk prediction model based on PTH demonstrated good predictive ability with obvious clinical practical value.

Abstract 11631: A Critical Role of Parathyroid Hormone in the Development of Pulmonary Hypertension

Background: Pulmonary hypertension (PH) is characterized by increased pulmonary artery pressure and develops right heart failure. Parathyroid hormone (PTH) is secreted from parathyroid gland and play a critical role in calcium homeostasis. Recent studies have suggested that PTH also acts on the cardiovascular system and affects cardiovascular prognosis. We hypothesized that PTH would play a role in the pathogenesis of PH. Object: This study aimed to investigate the effect of PTH on pulmonary hemodynamics. Method: We measured serum PTH levels in patients who were suspected of PH and underwent right heart catheter examination. We used two types of PH animal models, hypoxia (Hx)-induced PH mouse model and Sugen/hypoxia (SuHx)-induced PH rat model. Hx mice were administered PTH daily for 3 weeks. SuHx rats underwent parathyroidectomy, after which they received SuHx treatment for 10weeks. We measured physical data and right ventricular systolic pressure (RVSP) in these models. We cultured pulmonary artery smooth muscle cell (PASMC) treated with PTH to analyze cell signaling, proliferation and migration. Result: We enrolled 20 participants. PTH concentration was significantly correlated with mean pulmonary artery pressure and pulmonary vascular resistance. PTH treatment exacerbated right ventricular hypertrophy and increased RVSP (33.6mmHg vs. 48.2mmHg) in Hx mice compared with non-treated Hx mice(Figure). Conversely, parathyroidectomy significantly attenuated right ventricular hypertrophy and reduced RVSP (54.2mmHg vs. 29.3mmHg) in SuHx rats compared with sham-operated SuHx rats. PTH promoted migration and proliferation through ERK signaling in PASMC. Conclusion: Our clinical and experimental data demonstrated a critical role of PTH in the development of PH and suggested that PTH would be a novel therapeutic target for PH treatment.

Parathyroid hormone affects right heart hemodynamics and exacerbates pulmonary hypertension

Abstract Background Pulmonary hypertension (PH) is characterized by increased pulmonary artery pressure and develops right heart failure. Parathyroid hormone (PTH) is secreted from parathyroid gland and regulates a calcium homeostasis. Recent studies have suggested that PTH also acts on the cardiovascular system and affects cardiovascular prognosis. We hypothesized that PTH would play a role in the pathogenesis of PH. Purpose This study aimed to investigate the effect of PTH on pulmonary hemodynamics. Method We measured serum PTH levels in patients who were suspected of PH and underwent right heart catheter examination. We used two types of PH animal models, hypoxia (Hx)-induced PH mouse model and Sugen/hypoxia (SuHx)-induced PH rat model. Hx mice were administered PTH daily for 3 weeks. SuHx rats underwent parathyroidectomy, after which they received SuHx treatment for 10weeks. We measured physical data and right ventricular systolic pressure (RVSP) in these models. We cultured pulmonary artery smooth muscle cell (PASMC) treated with PTH to analyze cell signaling, proliferation and migration. Result We enrolled 20 participants. PTH concentration was significantly correlated with mean pulmonary artery pressure (r=0.58, p=0.006) as well as with pulmonary vascular resistance (r=0.61, p=0.04). Receiver operating characteristic curve displayed a cut-off PTH level of 48.0pg/ml that offered optimal differentiation between patients with and without PH (100% sensitivity, 73% specificity). PTH treatment exacerbated right ventricular hypertrophy and increased RVSP (33.6mmHg vs. 48.2mmHg) in Hx mice compared with non-treated Hx mice (Figure 1). Conversely, parathyroidectomy significantly attenuated right ventricular hypertrophy and reduced RVSP (54.2mmHg vs. 29.3mmHg) in SuHx rats compared with sham-operated SuHx rats. PTH promoted migration and proliferation through ERK signaling in PASMC. Conclusion Our clinical and experimental data demonstrated a critical role of PTH in the development of PH and suggested that PTH would be a novel therapeutic target for PH treatment. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Grant-in-Aid for Young Scientists Figure 1. PTH treatment exacerbated RVSP

Serum parathyroid hormone levels in patients with chronic right heart failure.

Parathyroid hormone (PTH) is a novel cardiovascular biomarker which is particularly useful for detection and assessment of heart failure (HF). However, previous studies examining PTH in heart failure have primarily focused on left HF; thus, the relationship between PTH and right HF remains unclear. The aim of the present study was to evaluate the serum PTH levels in patients with chronic right HF. A total of 154 patients with chronic right HF were enrolled in the present study. A binary logistic regression analysis model was used to assess the independent predictive value of PTH levels in chronic right HF. Partial correlative analysis was used to demonstrate the relevance of PTH levels on the parameters of assessment of right heart function. A multiple linear regression analysis model was used to evaluate the independent factors of PTH levels in patients with right HF. The results showed that the serum PTH levels in the right HF group were significantly higher compared with the control group. After adjusting for predictors of right HF, serum PTH levels were associated with right HF with an odds ratio of 1.066 (95% confidence interval: 1.030-1.102, P<0.001. Serum PTH levels were independently correlated with plasma N-terminal pro-B-type natriuretic peptide levels, right ventricular end-diastolic diameter and severity of lower extremity edema (all P<0.05). Therefore, based on the results of the present study, PTH may be a useful biomarker for detection and assessment of right HF.

Relação entre o Paratormônio e Depressão na insuficiência cardíaca

Depression has been found to be a predictor of rehospitalization and mortality in heart failure (HF). Parathyroid hormone (PTH) is a novel promising biomarker that can predict hospitalization, functional status and mortality in HF. We aimed to investigate the association of depression with serum PTH levels in patients with systolic HF. A total of consecutive 100 outpatients with systolic HF having left ventricular ejection fraction (LVEF) < 40%, were prospectively studied. All patients underwent laboratory tests, including brain natriuretic peptide (BNP) and PTH analyses. The patients were asked to complete the Beck Depression Inventory- II (BDI). Fifty-one patients (51%) were shown to have poor BDI score (BDIS > 18). Patients with poor BDI score had significantly higher PTH levels compared to those with good BDIS (133 ± 46 pg/ml vs. 71 ± 26 pg/ml, p < 0.001). In multivariable logistic regression model, PTH level (Odds ratio (OR) = 1.035, p = 0.003), LVEF (OR = 0.854, p = 0.004), NYHA functional class III/IV (OR = 28.022, p = 0.005), C-reactive protein (CRP) (OR = 1.088, p = 0.020), and presence of pretibial edema (OR = 12.341, p = 0.033) were found to be independent predictors of moderate to severe depression after adjustment of other potential confounders. Systolic HF patients with moderate to severe depression had higher serum levels of PTH and CRP, poor functional status and lower LVEF. The association of depression with such parameters might explain the contribution of depression to hospitalization and mortality in HF.

Suppressive effect of calcium on parathyroid hormone release in adynamic renal osteodystrophy and secondary hyperparathyroidism

Serum parathyroid hormone (PTH) levels are markedly lower in patients with the adynamic lesion (AD) of renal osteodystrophy than in those with secondary hyperparathyroidism (2 degrees HPT), but serum PTH values are often moderately elevated in AD when compared to subjects with normal renal and parathyroid gland function (NL). To study the inhibitory effect of calcium on PTH release in AD and in 2 degrees HPT, the response to two-hour intravenous calcium infusions was examined in 6 patients with AD, in 31 patients with 2 degrees HPT and in 20 NL. Basal serum PTH levels were 88 +/- 51, 536 +/- 395, and 26 +/- 6 pg/ml, respectively, in AD, 2 degrees HPT and NL, whereas basal ionized calcium levels did not differ. When expressed as a percentage of pre-infusion values, PTH levels at the end of two-hour calcium infusions were higher both in AD (23.2 +/- 5.6%) and in 2 degrees HPT (27.8 +/- 12.3%) than in NL, (11.9 +/- 5.8%, P < 0.001). Both the amplitude of suppression (%) and the rate of decline (min-1) in serum PTH were less in AD and 2 degrees HPT than in NL, P < 0.05 for each parameter; corresponding values for each group, with 95% confidence intervals, were 77% (73 to 82) and 0.039 min-1 (0.030 to 0.048) in AD, 72% (68 to 76) and 0.031 min-1 (0.025 to 0.036) in 2 degrees HPT and 87% (84 to 89) and 0.070 min-1 (0.058 to 0.089) in NL. Neither variable differed between AD and 2 degrees HPT. Basal and nadir serum PTH levels were highly correlated: r = 0.95 and P < 0.05 in AD; r = 0.90 and P < 0.01 in 2 degrees HPT; r = 0.75 and P < 0.01 in NL. The slope of this relationship was less, however, both in AD and in 2 degrees HPT than in NL, P < 0.05 by analysis of co-variance. Thus, serum PTH levels fell below 20% of pre-infusion values in fewer subjects with AD (1 of 6) or 2 degrees HPT (9 of 31) than in NL (17 of 20) (chi 2 = 17.81, P < 0.005). The results indicate that the inhibitory effect of calcium on PTH release in vivo does not differ in AD and 2 degrees HPT despite marked differences in basal serum PTH levels. Variations in functional parathyroid gland mass rather than disturbances in calcium-sensing by the parathyroids probably account not only for the lower basal serum PTH levels in patients with AD compared to those with 2 degrees HPT, but also for the moderately elevated serum PTH values commonly seen in patients with AD.