Parathyroid Hormone Levels In Patients Research Articles

Diagnostic challenge of the brown tumors in developing country: A case series

Introduction and importanceBrown tumors are non-neoplastic reactive tissue with osteoclasts multinucleated giant cells, and vascular and proliferative fibrous tissue. Hemorrhage results in significant bone resorption caused by hyperparathyroidism. This study provides information about the diagnosis challenge for brown tumor cases. Case descriptionWe report four cases that experience pathological fractures with moderate pain, multiple lytic lesions, severe hypercalcemia, increased ALP (Alkaline Phosphatase), and PTH (Parathyroid Hormone). Abnormal parathyroid mass was found in ultrasound. A bone scan described increasing radio uptake in various bones, a whole body scan, or parathyroid scintigraphy with 99mTc-MIBI. Eventually, in all cases, the diagnosis of the brown tumor was confirmed through histopathological examination, which showed multiple nucleated giant cells with a deposit of hemosiderin pathognomonic for the brown tumor, and the diagnosis of primary hyperparathyroidism (PHPT) was confirmed in all cases. Clinical discussionThese cases show that initial misdiagnosis of brown tumors as other bone tumors. A definitive diagnosis of brown tumors requires more than just histological confirmation. A comprehensive evaluation encompassing laboratory tests, imaging studies, clinical symptoms, and a multidisciplinary orthopedic-oncology board discussion is essential. Observations show that treating hyperparathyroidism alleviates the osteolytic lesions caused by brown tumors, despite the lack of clinical guidelines. ConclusionBased on a review of the literature and our clinical experience, we recommend screening serum calcium, phosphorus, and PTH levels in patients presenting with multiple lesions and widespread bone pain. This screening aims to rule out multiple bone lesions caused by PHPT.

The Relationship Between Anemia and Parathyroid Hormone Levels in Patients With Kidney Failure Undergoing Hemodialysis Treatment in Georgia.

Chronic kidney disease (CKD) and its associated complications, such as anemia and secondary hyperparathyroidism (SHPT), pose significant challenges to global healthcare systems. This study explores the demographic and clinical characteristics of 284 kidney failure (KF) patients undergoing hemodialysis, in an effort to shed light on the possible association between anemia and SHPT. A proven connection between the two could theoretically influence the management plans for CKD patients, with the hopes of achieving lower morbidity and/or mortality in this patient group. A retrospective, cross-sectional, real-world data analytical study was conducted at a hemodialysis center in Tbilisi, Georgia, encompassing a sample size of n = 284 patients on maintenance hemodialysis. The data analyzed was extracted from patients' medical records. According to our results, the prevalence of anemia was strikingly high at 82.04%, underlining its substantial burden within this patient population.Our analysis revealed a notable systemic association between anemia and SHPT, particularly when considering hemodialysis vintage. However, our final analysis model revealed no statistically significant association between anemia and intact parathyroid hormone (iPTH) levels. Conclusion:Our study revealed a significant systemic relationship between anemia and SHPTwhen hemodialysis duration was considered, despite initial analyses showing no direct association. Future research should focus on longitudinal and multi-center studies to better understand this relationship, aiming to enhance the care and management of CKD patients on hemodialysis.

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.

Etelcalcetide use During Maintenance Hemodialysis and Incidence of Parathyroidectomy After Kidney Transplantation

Etelcalcetide is an i.v. calcimimetic agent, effectively reducing parathyroid hormone levels in patients on maintenance hemodialysis (HD). The clinical impact of discontinuing etelcalcetide at the time of kidney transplantation is unknown. We retrospectively reviewed all patients on HD meeting predefined criteria who received a kidney transplant at our institution between January 1, 2015, and December 12, 2022. The incidence of parathyroidectomy and the evolution of calcium, phosphate, and intact parathyroid hormone (iPTH) levels after transplantation was analyzed according to the type of calcimimetic treatment before transplantation (cinacalcet vs. etelcalcetide vs. none). Overall, 372 patients (aged 53 years; interquartile range [IQR]: 42-62 years) were included. At the time of transplantation, 35, 75, and 262 patients were under etelcalcetide, cinacalcet, or no calcimimetic, respectively. After 1064 (IQR: 367-1658) days, the incidences of parathyroidectomy in the etelcalcetide, cinacalcet, no calcimimetic groups were 29%, 12%, and 1%, respectively (P< 0.001). Etelcalcetide was associated with an increased incidence of parathyroidectomy after adjustment for age, sex, and HD vintage (hazard ratio [HR]: 97.0, 95% confidence interval [CI]: 19.1-493.9, P< 0.001). The incidence of parathyroidectomy was related to etelcalcetide dosage (6/11 [54.6%] in patients with≥ 10 mg vs. 4/24 [16.7%] in patients with< 10 mg, P= 0.02). Moreover, peak calcium levels were higher (P< 0.001) and parathyroidectomy was performed earlier (median 80 vs. 480 days, P< 0.001) in the etelcalcetide compared with the cinacalcet group. Long-term graft function, graft loss, and mortality were similar. Etelcalcetide use during maintenance HD is associated with an increased incidence of early parathyroidectomy after transplantation compared to cinacalcet or no calcimimetic.

A study of Vitamin D and parathyroid hormone levels in patients with prostatic cancer

Background: Vitamin D, a key nutrient in the body, has been linked to a decrease in prostate cancer (PCa) morbidity and mortality rates. The study concluded that any compensation mechanism may no longer be adequate for patients with PCa, and further research is needed to understand the mechanisms underlying the relationship between serum Vitamin D and parathyroid hormone (PTH) homeostasis. The findings will help determine cancer prevalence and trends in India and support public health initiatives to control cancer. Aims and Objectives: The aim is to assess the mean values of Vitamin D and PTH in patients with PCa and also to compare these levels with that of healthy controls (non-PCa). Materials and Methods: One hundred participants in the outpatient department of the Department of Biochemistry were assigned as control subjects, and another 100 participants were participants with PCa. 5 mL of fasting venous blood were drawn into red top vials using a disposable syringe and needle in an aseptic manner. PTH and serum Vitamin D were estimated. Results: When comparing PCa patients to healthy controls, the observed Vitamin D level was significantly lower in the former group. Furthermore, a notable distinction in Vitamin D levels was noted between the two groups. Furthermore, we found that PCa patients had higher PTH values than healthy controls. When we compared the PTH values of the two groups, we found a substantial difference. Conclusion: The authors conclude from the study that with alterations in the study parameters in patients with PCa, any compensation mechanism may become insufficient.

Correlation of serum ferritin with parathyroid hormone level in patients with transfusion-dependent thalassemia

Introduction: Thalassemia is a rare hereditary condition that causes hemoglobin synthesis deficiency. Recurrent blood transfusion in transfusion-dependent thalassemia (TDT) individuals results in iron overload and deposition in body tissues, leading to endocrine malfunctions, including parathyroid. This study aimed to determine the correlation between the level of serum ferritin and parathyroid hormone level in TDT patients. Methods: A cross-sectional study was conducted among adult TDT patients receiving blood transfusions at Dr. Soetomo General Academic Hospital, Surabaya, Indonesia from January to June 2023. Serum ferritin was measured using an enzyme-linked fluorescence assay (ELFA), while parathyroid hormone was quantified using an enzyme-linked immunosorbent assay (ELISA). The Spearman correlation analysis was used to identify the correlation between the level of serum ferritin with parathyroid hormone. Results: A total of 46 TDT patients were enrolled in the study, with a median age of 25 years old and represented predominantly by males (56.5%). The median levels of serum ferritin and parathyroid hormone were 5,672.90 ng/mL (min-max: 596.80–24,014.58 ng/mL) and 29.80 pg/mL (min-max: 10.61–97.01 pg/mL), respectively. The Spearman correlation analysis suggested a statistically insignificant negative correlation between serum ferritin and parathyroid hormone in TDT patients (r = -0.166; p=0.270). Conclusion: Serum ferritin was inversely, but not significantly, correlated with parathyroid hormone in TDT patients, suggesting that impaired parathyroid function might be associated with the increment of plasma iron.

Biochemical markers and FokI and TaqI vitamin D receptor genes polymorphism in rheumatoid arthritis

BackgroundPrevious studies have reported the role of genes in different metabolic processes in the human body, and any variation in gene polymorphisms could lead to disturbances in these processes and different diseases.ObjectiveThis study aimed to compare vitamin D receptor (VDR) FokI and TaqI genotypes in terms of parathyroid hormone (PTH) and some biomarkers of inflammation and susceptibility to rheumatoid arthritis (RA) disease.MethodsThis study included 100 patients with rheumatoid arthritis (RA). Genotyping was performed by polymerase chain reaction (PCR) and examined by specific restriction enzymes using restriction fragment length polymorphism (RFLP). Serum intact PTH, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), rheumatoid factor (RF), and anti-cyclic citrullinated peptide antibodies (ACCPs) levels were measured.ResultsAn increased PTH level (> 65 pg/ml) was found in 8% of patients. No significant differences among FokI and TaqI vitamin D receptor genes polymorphism regarding positive and negative RF or ACCPs were found. A significant difference was found among FokI (p = 0.009) and none in TaqI genotypes regarding intact parathyroid hormone level categories. No significant correlation was found between the serum intact PTH level and ESR or CRP levels (P = 0.13 and 0.28, respectively). The parathyroid hormone level was not a good predictor for RF or ACCPs (P = 0.5 and 0.06, respectively).ConclusionThe FokI gene may play a role in controlling PTH levels in patients with RA. There was no significant correlation found between the serum intact PTH level and RA severity according to ESR and CRP inflammatory biomarkers. There are no differences between VDR genes FokI and TaqI polymorphism in terms of RA susceptibility (for RF and ACCPs).

Estimation of serum levels of Parathyroid hormone, Vitamin D, Calcium and Phosphorus to study their association with age, gender, disease duration, and severity of chronic plaque psoriasis: Results of a case control study

: Psoriasis is a chronic inflammatory disease characterized by rapid turnover of epidermal keratinocytes; presenting clinically as erythema, induration, and scaling Parathyroid hormone (PTH) is secreted by parathyroid glands and its elevated levels may be seen in psoriasis and several other disorders of keratinization. PTH/PTH-related peptide receptors are present in dermal fibroblasts &amp; regulate proliferation and maturation of fibroblasts and keratinocytes. Release of PTH is under the feedback regulation of serum Ca2+, Vit.D and PO: To assess the Parathyroid hormone levels in patients of Psoriasis along with Vitamin D, Serum Calcium and Serum Phosphorus levels.: Out of the 50 cases aged between 18 and 91 years majority of patients i.e 22 (44%) were in the age group of 18-40 years followed by 20 (40%) patients in 41-60 years age group. Eight (16%) patients were above &amp;#62;60 years. 32 (64%) patients who had psoriasis for less than ≤60 months while 18 (36%) patients had psoriasis for more than &amp;#62;60 months Serum PTH (normal 10–65pg/ml), Vitamin D(normal 20-50(ng/ml), calcium (normal 9-11mg/dl and phosphorus (normal 2.5-4.5mg/dl) levels were measured after overnight fasting. : A total of 50 psoriasis patients along with 50 non-psoriatic age and sex matched controls were recruited for the study. There were 28 males and 22 females in the patient group aged between 18 and 91 years (mean±SD 43.52±16.23 years). The mean age of controls was 47.12±16.29 years with 19(38%) subjects in 18-40 years age group and 21(42%) in 41-60 years age group. Amongst the cases, there were 10(20%) patients who had abnormal PTH levels (six had elevated levels of PTH and four patients with low PTH levels) while 40(80%) had normal levels (mean±SD 47.97±25.46 pg/ml). : The interpretation of our observation remains complex and any conclusion for the significance of these biochemical abnormalities remain conjectural. Moreover, association of psoriasis with abnormal biochemical parameters remains debatable in view of limited number of studies whether abnormal biochemical parameters can serve as markers of severity and their correction can lead to improvement in the disease needs confirmation with more well designed experimental and prospective clinical studies.

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.

PSAT216 Turner Syndrome and Congenital Hypoparathyroidism

Abstract Background Patients with Turner syndrome may have multiple associated metabolic comorbidities, some of which are rare. We present a case report with Turner syndrome and congenital hypoparathyroidism. Clinical Case A 30-year-old Caucasian female with Turner syndrome and primary ovarian insufficiency was referred for evaluation of osteopenia and elevated TSH. On her initial visit, the patient was asymptomatic, physical exam was significant only for short stature. The DEXA scan showed a T-score of -2 at the lumbar spine and -1.8 at the femoral neck. TSH was elevated at 4.81 (0.5–5.0 mIU/L), with normal serum levels of free T3 and free T4 consistent with subclinical hypothyroidism. Patient previously underwent aortic root imaging with no evidence of dilatation. Her only home medication was a combination oral contraceptive tablet (Yaz; drospirenone and ethinyl estradiol) for primary amenorrhea. The patient was started on calcium 500 mg daily and vitamin D3 400 IU. On her next visit, patient's calcium was 8.7 mg/dL (8.6–10.6 mg/dL), phosphorus 4.4 mg/dL (3–4.3 mg/dL), albumin 3.9 g/dL (3.4–5.4 g/dL), 25-hydroxy vitamin D 63.2 ng/dL (30-100 ng/dL), 24-hour urine calcium 93 mg/day (100-300 mg/day), and PTH 20 pg/mL (15–65 pg/mL) suggestive of hypoparathyroidism. There have only been a few case reports of congenital hypoparathyroidism in patients with Turner syndrome. (1) The patient was started on calcitriol 0.25 mcg daily and her calcium was increased to 500 mg twice daily. Repeat serum calcium was 9.1 and 25-hydroxy vitamin D 75.6 ng/dL showing that the patient responded appropriately to calcium and calcitriol supplementation. In the absence of a history of neck surgery or autoimmune diseases, the etiology behind hypoparathyroidism in this patient with Turner syndrome appears to be secondary to genetic mutation. Conclusion We highlight the importance of measuring parathyroid hormone level in patients with Turner syndrome who exhibit symptoms or signs of osteopenia as part of diagnostic workup. Reference (1) Suzuki Y, Watanabe H, Haeno S, Omori T, Hiramatsu R, Asada M, Tanaka F, Maeda T, Okada M, Suzuki T, et al. Primary hypoparathyroidism in Turner's syndrome. Intern Med. 1995 Nov;34(11): 1071-3. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

The 1,24,25(OH)3D3 metabolite in clinical and experimental CKD: Impact of calcitriol treatment

Calcitriol, and other vitamin D receptor activators, remain a primary treatment for elevated parathyroid hormone levels in patients with end stage kidney disease. The objective of this study was to assess the 24-hydroxylation-mediated metabolism of 25(OH)D3 and 1,25(OH)2D3 in rats with experimental kidney disease treated with calcitriol and in a cross-sectional analysis of patients requiring hemodialysis. Methods: Animals were stratified by creatinine into a time control group or calcitriol (20 ng/kg/day) for 3 weeks following CKD induction using a dietary adenine model (0.25% adenine). Hemodialysis patients were recruited and demographic data including calcitriol prescription was obtained by chart review and participant interview. Vitamin D metabolites were assessed using LC-MS/MS. In the rat model, 1,25(OH)2D3 levels increased substantially in calcitriol-treated rats yet there was no increase in its primary metabolite: 1,24,25(OH)2D3. A lower ratio of 1,24,25(OH)2D3:1,25(OH)2D3 (1,25-VMR) was associated with increased calcium levels in calcitriol treated rats. In hemodialysis patients (N = 86), the level of 1,25(OH)2D3 was substantially higher in calcitriol-treated patients yet there was no difference between groups in 1,24,25(OH)3D3, resulting in a marked decrease in the 1,25-VMR in calcitriol treated patients. In hemodialysis patients treated with calcitriol, 1,25(OH)2D3 and a lower ratio between 1,24,25(OH)3D3 and 1,25(OH)2D3 were associated with higher serum calcium levels. Impaired metabolism of exogenous calcitriol may contribute to the adverse effects associated with this treatment. A better understanding of the uniquely dysfunctional catabolic vitamin D profile in CKD may guide more effective treatment strategies.

Changes in Serum Alkaline Phosphatase, Calcium, and Parathyroid Hormone with Different Doses of Iodine Therapy:.

Background: Despite the benefits of radioactive iodine (RAI) therapy as an adjunctive treatment for thyroid cancer, it can be associated with several side effects. The main purpose of this study was to determine the changes in serum alkaline phosphatase (ALP), calcium (Ca), and parathyroid hormone (PTH) at different doses of RAI therapy among patients who were referred to the nuclear medicine department of Namazi Hospital, Shiraz. Materials and Methods: This cross-sectional study was conducted on 60 patients with papillary thyroid cancer who underwent RAI therapy at different doses of 100, 150, and 200 mCi. The ALP, Ca, and PTH levels of patients were measured before and 60 days after RAI therapy. Results: Our study revealed that RAI therapy at all doses significantly increased ALP level in comparison with baseline amounts (P≤0.05). However, changes in PTH and Ca levels were not significant among patients who received different doses of RAI (P˃0.05). Conclusion: RAI therapy could affect important hormones and enzymes such as ALP and PTH. This issue can be considered in diagnostic and therapeutic prescriptions of RAI for the treatment of thyroid cancer.[GMJ.2022;11:e2397].

Full-length versus intact PTH concentrations in pseudohypoparathyroidism type 1 and primary hyperparathyroidism: clinical evaluation of immunoassays in individuals from China.

PurposeThe application of the third-generation parathyroid hormone (PTH) assay [PTH(1–84) assay] for evaluating PTH levels in patients with pseudohypoparathyroidism type-1 (PHP1) is less popular than the second-generation assay. Therefore, we aimed at examining the conformity between the PTH(1–84) assay and the intact PTH (iPTH) assay, specifically examining their performance in individuals with PHP1 versus individuals with primary hyperparathyroidism (PHPT), compared to healthy controls.MethodsPTH(1–84) and iPTH assay were performed in patients with PHP1, patients with PHPT, and healthy volunteers. ∆PTH%, PTH(1–84)/iPTH (3rd/2nd ratio), iPTH/upper limit of normal (ULN), and PTH (1–84)/ULN of each group were calculated for comparison. Linear regression, Kappa conformity test, and Bland–Altman analysis of ∆PTH/mean of iPTH and PTH(1–84) (percent bias) plotted against the mean of iPTH and PTH(1–84) were performed to determine the conformance of PTH(1–84) assay with iPTH assay.ResultsA total of 54 patients with PHP1, 127 patients with PHPT, and 65 healthy volunteers were enrolled in this study. All the three groups showed strong linear relationship between iPTH and PTH (1–84) (r2 = 0.9661, 0.7733, and 0.9575, respectively). No significant differences were noted in 3rd/2nd ratio (median 0.76 vs. 0.72) between the PHP1 and PHPT groups (p > 0.05). Conformity examination showed the Kappa value was 0.778 and 0.395 for PHP1 and PHPT groups respectively. No difference in the Kappa values was found between PHP1A and PHP1B subgroups. Bland–Altman plot demonstrated that the proportion of data points that were plotted within mean ± 1.96 SD in PHP1, PHPT and normal control groups were 96.3%, 93.7%, and 98.5%, respectively. The mean percent bias of the three groups were 26.1%, 31.2%, and 17.0%, respectively. The range of mean ± 1.96 SD of percent bias of the three groups were 2.2%–50.0%, −14.3%–76.6%, and 6.7%–27.2%, respectively.ConclusionAlthough iPTH and PTH(1–84) values were both lower in the present PHP1 cohort than in the PHPT cohort, there appear to be differences in the relative agreement between both immunoassays, and in the relationship between the two values, especially in comparison to healthy controls. Whether these differences are due to differential accumulation of C-terminal fragments or other factors requires further study.

The complex role of post-operative magnesium on the long term serum calcium and parathyroid hormone levels in patients undergoing total and near-total thyroidectomy.

To assess the role of hypomagnesaemia in the development of permanent hypocalcaemia following thyroidectomy. The prospective cohort study was conducted from April 3, 2017, to January 2, 2020, at Surgical Unit 1, Benazir Bhutto Hospital, Rawalpindi, Pakistan, and comprised of patients of both genders undergoing total and near total thyroidectomy. Post-operative calcium and magnesium levels were noted, and the patients were followed up after 6 months and fasting serum calcium, magnesium and parathyroid hormone levels were checked. Signs and symptoms of hypocalcaemia were noted. Data was analysed using SPSS 22. Out of the 62 patients followed up, 57 (91.9%) were females and 5 (8.1%) males. The overall mean age was 38.5 ± 12.1 years Post-operative hypomagnesaemia was seen in 6(9.8%) patients and none developed follow-up hypocalcaemia. Post-operative magnesium levels were significantly negatively correlated with follow-up parathyroid hormone level (p=0.006). Fall in magnesium post-operatively and follow-up magnesium were positively correlated with follow-up parathyroid hormone (p<0.05). Permanent hypocalcaemia was seen in 7(11.4%) patients and it was significantly associated with pre-operative and post-operative calcium levels, post-operative symptoms of hypocalcaemia and readmission for hypocalcaemia after discharge (p<0.05). Follow-up hypomagnesaemia was significantly associated with follow-up hypocalcaemia (p=0.024) and follow-up symptoms of hypocalcaemia (p=0.031). Acute development of mild hypomagnesaemia post-operatively may be beneficial in early positive feedback for parathyroid hormone secretion. Hypomagnesemia 6 months after surgery may be involved in PTH organ resistance. The complex role of hypomagnesemia on PTH levels must be further explored.

Evaluation of changes in minerals like calcium, phosphorus and parathormone levels in ESRD patients on haemodialysis: A case control study

Chronic kidney disease (CKD) is an international public health problem affecting about 5–10% of the population. KDOQI guidelines highlight the importance of measuring the parathyroid hormone levels annually once diagnosed with CKD. If the levels are maintained within the target range, then the various complications can be prevented by adequate treatment. 1. To measure the levels of Calcium, Phosphorus, Alkaline phosphatase and parathyroid hormone levels in patients with stage 4 kidney disease. 2. To compare these biochemical parameters with healthy controls. 50 CKD patients visiting dialysis unit were included in the study. Patients with congenital renal disorders were excluded. A written informed consent was taken from all patients. The personal details of patients were documented. Clinical history, personal &amp; family history was taken in detail from each patient. 50 Healthy individuals were included as controls in the study. Statistically significant increase in levels of Calcium, Phosphorus, Alkaline phosphatase, Uric acid and parathyroid hormones were seen in CKD patients as compared to controls. The levels of parathormone, calcium &amp; phosphorus are used as surrogate markers of disease progression. Alteration in minerals like calcium and Phosphorus occurs early in the course of disease and are responsible for various cardiovascular manifestations and bone osteodystrophy. The ultimate goals of treating secondary hyperparathyroidism are to normalize mineral metabolism, prevent bone disease and prevent extra skeletal manifestations of the altered biochemical processes.

Bone Loss Correlated with Parathyroid Hormone Levels in Adult Celiac Patients.

BACKGROUND: Celiac disease (CD) is a gluten-sensitive enteropathy with intestinal and extra-intestinal presentations in genetically predisposed cases. Musculoskeletal problems are one of the most common extra-intestinal manifestations in adult patients with CD. In the present study, we evaluated parathyroid hormone (PTH) levels in men and premenopausal women with CD who had osteoporosis and osteopenia. METHODS: This was a cross-sectional study of 387adult patients with CD who were referred to the Mashhad Celiac Disease Center between 2014 and 2019. We excluded bone loss confounding factors, including cases with endocrine disorders, corticosteroid consumption, smoking, and age of more than 55 years. Factors such as intestinal pathology, bone mineral density (BMD), serum level of anti-tTG, serum vitamin D, and PTH levels were also assessed at the time of diagnosis. RESULTS: Femoral osteopenia was found in 140 (36.2%) patients, and osteoporosis was observed in 55 (14%) patients. Spinal osteopenia and osteoporosis were observed in 127 (33%) and 63 (16.4%) patients, respectively. High levels of PTH were detected in 72/193 (27.2%) of the patients with CD. There was a significant difference between PTH levels in patients with osteopenia, osteoporosis, and normal BMD (P=0.0001). CONCLUSION: This study showed a correlation between low BMD and PTH levels in patients with CD, which suggests autoimmune endocrine disorder as a cause of osteopenia and osteoporosis.

Use of intraoperative parathyroid hormone measurements during parathyroidectomy to predict postoperative parathyroid hormone levels in patients with renal hyperparathyroidism: meta-analysis.

BackgroundSeveral studies have reported on the use of intraoperative parathyroid hormone (ioPTH) measurements during parathyroidectomy (PTX) for renal hyperparathyroidism (rHPT), but there is no consensus on whether it is helpful and, if so, what protocol should be used. Therefore, the literature was systematically reviewed to assess a correlation between ioPTH and early postoperative parathyroid hormone (PTH) levels in patients undergoing PTX for rHPT, separately for those on dialysis and those with a functioning renal transplant.MethodsA systematic literature search was performed in electronic databases. Quality assessment was performed using the Quality In Prognosis Studies tool. Mean ioPTH values were calculated at different time points and correlated to the postoperative PTH levels within 1 month. Fixed-effect and random-effects models were performed to assess the mean ioPTH levels at 10 or 20 min after resection (T10 and T20). Stratified analyses were performed for patients on dialysis and those with a functioning renal transplant.ResultsOf the 3087 records screened, 14 studies were included, including some 1177 patients; 1091 were on dialysis and 86 had a functioning kidney transplant. Risk of bias was moderate for most studies. For patients on dialysis, T10 and T20 mean ioPTH levels were 32.1 (95 per cent c.i. 24.3 to 39.9) pmol/l and 15.4 (95 per cent c.i. 7.8 to 22.9) pmol/l) in the random effects meta-analysis. Between individual studies, ioPTH ranged from 4.0–65.1 pmol/l at T10 and 8.6–25.7 pmol/l at T20. T10 and T20 ioPTH were 9.6 and 4.1 times the postoperative PTH—after T20 ioPTH stabilized in those on dialysis. In patients with a functioning renal transplant, ioPTH levels seemed to plateau after 10 min and measured 2.6 times the postoperative PTH.ConclusionThere is a strong correlation between ioPTH and early postoperative PTH levels, indicating that ioPTH is potentially a useful instrument during PTX in patients with rHPT. For patients on dialysis, at T20 ioPTH levels have stabilized and are approximately four times the postoperative PTH. Therefore, it is recommended to use ioPTH 20 min after resection in patients on dialysis, which might be longer than necessary for those with a kidney transplant.

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.

“Ideal” PTH in ESA-Resistant Anemia

Background: Anemia is a nearly universal complication of End Stage Renal Disease (ESRD). Erythropoiesis-stimulating agents (ESAs) have greatly decreased transfusion dependence in the anemia of ESRD. In some cases, ESAs are not effective, indicating ESA-resistance. ESA-resistant anemia is not well characterized and can be difficult to manage. Among the most frequent causes of ESA-resistant anemia is secondary hyperparathyroidism (SHP), which can induce bone marrow remodeling and fibrosis. Treatment protocols in SHP are centered on goal calcium, phosphorus and parathyroid hormone (PTH) levels and not the biologic consequences of high PTH. The hematologic insults secondary to SHP are rarely addressed. Instead, it is common to simply increase ESA dosing, rather than address the cause of ESA-resistance. In this retrospective review, we describe a cohort of patients with ESRD and SHP and highlight in detail one patient with reversible bone marrow changes and transfusion-dependent anemia, as well as descriptive and laboratory findings of bone marrow changes in patients with anemia and ESRD referred to our center.Methods: Using the EMR, the patient's data including demographics, progress notes, laboratory values, and bone marrow findings were extracted. Subsequently, the EMR was interrogated to reveal all patients with anemia and ESRD, who had undergone a bone marrow biopsy at out center over a ten year period from 2010 to 2020, revealing 64 patients. Data including demographics, laboratory values, bone marrow findings, and medications were extracted. Data was presented descriptively.Results: A 67-year-old male with ESRD secondary to hypertension and type 2 diabetes was referred to our Hematology clinic for anemia of ESRD. He was receiving Epoetin 20,000 IU three times weekly but was still transfusion-dependent to maintain a hemoglobin of 6.3 g/dL, with a concomitant PTH of 400.5 pg/mL. Calcium and phosphorus were normal and thus his SHP was not aggressively managed. Bone marrow biopsy revealed focal areas of bone marrow remodeling and reticulin fibrosis. Fluorescence in situ hybridization studies for myelodysplastic syndrome were negative, as were thyroid studies, serum protein electrophoresis, and free light chain ratio. In conjunction with his nephrologist, treatment of his SHP was optimized. His initial regimen was calcitriol 0.25 mcg once daily and calcium acetate 667 mg three times daily. Subsequently, cinacalcet 30 mg twice daily was added and calcium acetate was replaced with sevelamer 1600 mg three times daily. Following these changes, his hemoglobin remained stable in the range of 8-9 g/dL. He was no longer transfusion-dependent, despite only a modest reduction in PTH to 311.2 pg/mL. Repeat bone marrow biopsy revealed no bone marrow remodeling or reticulin fibrosis. Bone marrow findings for all patients referred to our clinic with ESRD and anemia are summarized in Table 1. The range of PTH for patients with bony remodeling was 183-16161.9 pg/mL versus 90.8-3283 pg/mL for those without bony remodeling. The range of PTH for patients with fibrotic changes was 183-2487 pg/mL versus 90.8-16161.9 pg/mL for those without fibrotic changes. ESA dosing varied among the patients.Conclusion: SHP is an increasingly identifiable cause of ESA-resistant anemia, as demonstrated by the reversal of transfusion dependence in our patient once SHP was more adequately treated. The degree of reversible ESA-resistant anemia and transfusion dependence in the setting of a PTH elevation to 400.5 in this case is surprising. The great variability in PTH levels of patients both with and without bone marrow changes presented here indicates the relationship between SHP and anemia is intricate. A single target level for the whole dialysis population is not appropriate; neither is targeting only and the same goal calcium, phosphorus, and PTH levels for the whole dialysis population either. Based on the findings of our institutional cohort, we suggest that it is justified to deviate from “on-size-fits-all” protocols and attempt a trial of aggressive management of SHP in patients with difficult to manage ESA-resistant anemia with what is considered only modest PTH elevation. [Display omitted] DisclosuresMoe: Allena Pharmaceutical: Consultancy; Janssen: Consultancy; Alnylum: Consultancy; DIcerna: Consultancy; Tricida: Consultancy.

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