-
Frontiers in Endocrinology 2024Although active vitamin D (VD) has been used both preoperatively and postoperatively to prevent hypocalcemia risk in patients undergoing total thyroidectomy, the role of...
INTRODUCTION
Although active vitamin D (VD) has been used both preoperatively and postoperatively to prevent hypocalcemia risk in patients undergoing total thyroidectomy, the role of 1,25-dihydroxyvitamin D (1,25(OH)D) has not been examined. This study comprehensively investigated the effects of 1,25(OH)D on calcium (Ca) concentrations after total thyroidectomy.
METHODS
Serum Ca, parathyroid hormone (PTH), and 1,25(OH)D levels were measured in 82 patients with thyroid disease before and after surgery.
RESULTS
Serum Ca, PTH, and 1,25(OH)D levels decreased significantly on the morning of the first postoperative day. Notably, the decrease in 1,25(OH)D concentration was significantly lower than that of PTH concentration (10.5 ± 33.4% vs. 52.1 ± 30.1%, p<0.0001), with 28% of patients showing increases in 1,25(OH)D. The only factor predicting a postoperative 1,25(OH)D decrease was a high preoperative 1,25(OH)D concentration. Postoperative 1,25(OH)D concentrations, as well as the magnitude and rate of decrease from preoperative levels, showed strong positive correlations with preoperative 1,25(OH)D concentrations (p<0.0001 for all three variables) but not with PTH concentrations. These findings suggest that 1,25(OH)D concentrations after thyroidectomy were more strongly dependent on preoperative concentrations than on the effect of PTH decrease and were relatively preserved, possibly preventing sudden severe postoperative hypocalcemia. A high 1,25(OH)D level was the most important preoperative factor for hypocalcemia (<2 mmol/L; p<0.05) on the first postoperative day; however, only PTH decrease was statistically significant (p<0.001) when intraoperative factors were added. In the PTH >10 pg/mL group, the decrease in 1,25(OH)D levels was significantly associated with postoperative hypocalcemia (p<0.05). Similarly, in the PTH levels >15 pg/mL group, a decrease in 1,25(OH)D concentration was a significant factor, and the amount of PTH decrease was no longer significant.
CONCLUSION
1,25(OH)D plays an important role in preventing sudden, severe hypocalcemia due to decreased PTH levels after total thyroidectomy, whereas high preoperative 1,25(OH)D levels are a significant risk factor for postoperative hypocalcemia. Optimizing preoperative protocols to adjust Ca, PTH, and 1,25(OH)D levels to improve the management of patients undergoing total thyroidectomy and to prevent extreme intraoperative PTH decreases may reduce the risk of hypocalcemia.
Topics: Humans; Thyroidectomy; Female; Male; Middle Aged; Vitamin D; Prospective Studies; Calcium; Adult; Parathyroid Hormone; Hypocalcemia; Aged; Postoperative Complications; Postoperative Period; Thyroid Diseases
PubMed: 38803480
DOI: 10.3389/fendo.2024.1360464 -
Renal Failure Dec 2024Secondary hyperparathyroidism (SHPT) can progress to severe SHPT (sSHPT), which affects the survival rate and quality of life of patients. This retrospective cohort...
Secondary hyperparathyroidism (SHPT) can progress to severe SHPT (sSHPT), which affects the survival rate and quality of life of patients. This retrospective cohort study investigated risk factors for sSHPT and the association between SHPT and mortality (all-cause and infection-related) among 771 clinically stable patients (421 male patients; mean age, 51.2 years; median dialysis vintage, 28.3 months) who underwent >3 months of regular peritoneal dialysis (PD) between January 2013 and March 2021. The sSHPT and non-sSHPT groups comprised 75 (9.7%) (median progression, 35 months) and 696 patients, respectively. sSHPT was defined as a serum intact parathyroid hormone (PTH) level >800 pg/mL observed three times after active vitamin D pulse therapy. The influence of sSHPT on the prognosis of and risk factors for sSHPT progression were evaluated using logistic and Cox regression analyses. After adjusting for confounding factors, higher (each 100-pg/mL increase) baseline PTH levels (95% confidence interval (CI) 1.206-1.649, < .001), longer (each 1-year increase) dialysis vintages (95% CI 1.013-1.060, = .002), higher concomitant diabetes rates (95% CI 1.375-10.374, .010), and lower (each 1-absolute unit decrease) / values (95% CI 0.859-0.984, .015) were independent risk factors for progression to sSHPT in patients on PD. During follow-up, 211 deaths occurred (sSHPT group, = 35; non-sSHPT group, = 176). The sSHPT group had significantly higher infection-related mortality rates than the non-sSHPT group (12.0% vs. 4.3%; < .05), and sSHPT was associated with increased infection-related mortality. In conclusion, patients with sSHPT are at higher risk for death and infection-related mortality than patients without sSHPT.
Topics: Humans; Male; Hyperparathyroidism, Secondary; Middle Aged; Retrospective Studies; Female; Peritoneal Dialysis; Prognosis; Risk Factors; Parathyroid Hormone; Adult; Kidney Failure, Chronic; Disease Progression; Proportional Hazards Models
PubMed: 38803195
DOI: 10.1080/0886022X.2024.2356022 -
AACE Clinical Case Reports 2024Although common in adults, primary hyperparathyroidism (PHPT) is a rare condition in children with the most common etiology being solitary parathyroid adenoma (PTA). The...
BACKGROUND/OBJECTIVE
Although common in adults, primary hyperparathyroidism (PHPT) is a rare condition in children with the most common etiology being solitary parathyroid adenoma (PTA). The typical presentation is symptomatic hypercalcemia. Management of PHTP secondary to PTA requires excision of the adenoma.
CASE REPORT
A 13-year-old adolescent boy presented because of orbital cellulitis and was noted to have hypercalcemia. Despite this, the patient was curiously asymptomatic. Further investigations yielded an elevated parathyroid hormone (PTH) level and a normal urine calcium-to-creatinine ratio making the most likely cause of hypercalcemia PHTP secondary to PTA. Imaging demonstrated PTA. The patient underwent parathyroidectomy with the pathology demonstrating PTA. Postoperatively, the PTH levels were undetectable; hence, the patient was treated with calcitriol and calcium supplementation for 1 month and 4 months, respectively. Genetic work-up for multiple endocrine neoplasia 1 and rearranged during transfection mutations was negative.
DISCUSSION
Solitary PTA is the most common cause of PHPT. Adenomas are mostly sporadic or may be a manifestation of an inheritable syndrome, such as multiple endocrine neoplasia. Although symptomatic disease is more common in children, our patient denied any hypercalcemia symptoms. The distinguishing biochemical feature of PHPT because of PTA is high or inappropriately normal PTH level in the context of high-normal or elevated serum calcium levels. Urinary calcium excretion is usually normal or high. PTAs are localized by ultrasound and Tc-99m-Sestamibi scintigraphy. Management includes parathyroidectomy and monitoring for postoperative hypocalcemia.
CONCLUSION
In a child or adolescent presenting with hypercalcemia and elevated PTH levels, it is important to consider PHPT secondary to PTA, because an early diagnosis will aid in preventing complications from hypercalcemia.
PubMed: 38799050
DOI: 10.1016/j.aace.2024.02.008 -
AACE Clinical Case Reports 2024Severe dysphagia is a rare presenting symptom of primary hyperparathyroidism, whereas the most common hypercalcemia-related causes include gastrointestinal symptoms,...
BACKGROUND/OBJECTIVE
Severe dysphagia is a rare presenting symptom of primary hyperparathyroidism, whereas the most common hypercalcemia-related causes include gastrointestinal symptoms, such as anorexia, constipation, and pancreatitis. This case presentation aimed to describe swallowing difficulty as a leading symptom of hypercalcemia.
CASE REPORT
A 62-year-old man experienced vomiting, dysphagia bordering with aphagia, and 20-kg weight loss in a 2-month period. The parathyroid hormone and serum calcium levels were 102 pmol/L (reference range, 1.8-7.9 pmol/L) and 4.12 mmol/L (reference range, 2.14-2.53 mmol/L), respectively. Ultrasound-guided exploration of the neck revealed a large, rounded hypoechoic mass inferior to the left thyroid lobe, which contained parathyroid tissue on fine-needle aspiration cytology examination. Contrast-enhanced neck computed tomography revealed a mass measuring 3.6 × 2.6 × 2.5 cm behind the left thyroid lobe, alongside massive ventral spondylophytes of the cervical spine at the level of the postcricoid segment of the hypopharynx. Magnetic resonance imaging confirmed ventral tissue displacement due to spondylophyte size and location. Surgical exploration of the left side of the neck was performed, and the left lower parathyroid gland weighing 9.07 g was excised. Pathohistologic findings verified a parathyroid gland adenoma. The postoperative values showed parathyroid hormone and serum calcium levels at 4.54 pmol/L and 2.25 mmol/L, respectively.
DISCUSSION
The pathophysiology of dysphagia in hypercalcemia is not fully elucidated. In this case, the patient's improvement after surgery implies a plausible connection between hypercalcemia and dysphagia, suggesting a causal relationship.
CONCLUSION
Although aphagia is not a typical presenting symptom of parathyroid adenoma, it should be noted in the differential diagnosis.
PubMed: 38799048
DOI: 10.1016/j.aace.2024.02.004 -
Asia Pacific Journal of Clinical... Jun 2024A comprehensive nutritional management is necessary for favourable outcomes in patients with chronic kidney disease (CKD). We aimed to assess the changes in nutritional...
BACKGROUND AND OBJECTIVES
A comprehensive nutritional management is necessary for favourable outcomes in patients with chronic kidney disease (CKD). We aimed to assess the changes in nutritional status and disease progression with nutritional management where renal replacement therapy (RRT) was not in place.
METHODS AND STUDY DESIGN
A quasi-experiment intervention was conducted on 70 CKD patients at stages 3-5 from July to December 2022. Participants were excluded if they underwent RRT, including dialy-sis (hemodialysis or peritoneal dialysis), or kidney transplantation. The nutritional regimen covered nutrition-al counseling, samples of the dietary menu, and supplement products. We evaluated nutritional status using Subjective Global Assessment (SGA) scale and sub-clinical blood test at T0 (hospital admission) and T1 (two weeks after the admission or 24 hours before the discharge).
RESULTS
After the intervention, the number of patients classified as malnutrition or at risk of malnourished reduced significantly (65.7% to 54.3% and 25.7% and 5.7%, respectively). The serum concentration of urea, creatinine and parathyroid hormone decreased remarkably, especially in patients receiving nutritional management. In the intervention group, the dietary pattern provided increased intakes of calcium and iron at T1, while phosphorus, sodium and potassium decreased after follow-up. Nausea/vomiting, loss of appetite, tiredness and sleep disorders were improved in the intervention compared to the control group.
CONCLUSIONS
Nutritional therapy enhanced the nutritional sta-tus, and quality of dietary and renal function in CKD patients without RRT. Applying nutrition education and treatment at an early stage can slow CKD progression, which should be applicable elsewhere in Vietnam.
Topics: Humans; Renal Insufficiency, Chronic; Male; Female; Vietnam; Middle Aged; Nutritional Status; Malnutrition; Aged; Adult; Nutrition Therapy
PubMed: 38794977
DOI: 10.6133/apjcn.202406_33(2).0004 -
Medicina (Kaunas, Lithuania) May 2024Secondary hyperparathyroidism (SHPT) poses a common condition among patients with chronic kidney disease (CKD) due to the chronic stimulation of the parathyroid glands...
Secondary hyperparathyroidism (SHPT) poses a common condition among patients with chronic kidney disease (CKD) due to the chronic stimulation of the parathyroid glands as a result of persistently low calcium levels. As a first option for medical treatment, vitamin D receptor analogs (VDRAs) and calcimimetic agents are generally used. Apart from cinacalcet, which is orally taken, in recent years, another calcimimetic agent, etelcalcetide, is being administered intravenously during dialysis. In a 5-year retrospective study between 2018 and 2023, 52 patients undergoing dialysis were studied. The aim of this study is to highlight the possible effects and/or benefits that intravenously administered calcimimetic agents have on CKD patients. A total of 34 patients (65.4%) received cinacalcet and etelcalcetide while parathormone (PTH) and calcium serum levels were monitored on a monthly basis. A total of 29 out of 33 patients (87.9%) that received treatment with etelcalcetide showed a significant decrease in PTH levels, which rose up to 57% compared to the initial values. None of the included patients needed to undergo parathyroidectomy (PTx) due to either extremely high and persistent PTH levels or severe side effects of the medications. It is generally strongly advised that parathyroidectomies should be performed by an expert surgical team. In recent years, a significant decrease in parathyroidectomies has been recorded globally, a fact that is mainly linked to the constantly wider use of new calcimimetic agents. This decrease in parathyroidectomies has resulted in an important decrease in complications occurring in cervical surgeries (e.g., perioperative hemorrhage and nerve damage). Despite the fact that these surgical complications cannot be easily compared to the pharmaceutical side effects, the recorded decrease in parathyroidectomies is considered to be notable, especially in cases of relapse where a difficult reoperation would be considered based on previously published guidelines.
Topics: Humans; Hyperparathyroidism, Secondary; Retrospective Studies; Male; Female; Middle Aged; Cinacalcet; Aged; Calcimimetic Agents; Parathyroidectomy; Renal Dialysis; Peptides; Parathyroid Hormone; Renal Insufficiency, Chronic; Calcium; Adult
PubMed: 38792994
DOI: 10.3390/medicina60050812 -
Life (Basel, Switzerland) May 2024Tumoral calcinosis is an extremely rare genetic disease caused by mutations in three genes, GALNT3, FGF23, and KL, which disrupt phosphorus metabolism. The hallmark of...
A Sole Case of the FGF23 Gene Mutation c.202A>G (p.Thr68Ala) Associated with Multiple Severe Vascular Aneurysms and a Hyperphosphatemic Variant of Tumoral Calcinosis-A Case Report.
Tumoral calcinosis is an extremely rare genetic disease caused by mutations in three genes, GALNT3, FGF23, and KL, which disrupt phosphorus metabolism. The hallmark of this condition is the formation of tumors in the soft tissues around the joints. Other phenotypic features of tumoral calcinosis are dental involvement and brain and vascular calcifications. The clinical case reported herein presents for the first time to the scientific community the c.202A>G (p.Thr68Ala) mutation of the FGF23 gene, associated with a hyperphosphatemic variant of tumoral calcinosis and multiple severe vascular aneurysms. A female patient underwent multiple surgeries for tumor formations in her soft tissues that first appeared at the age of 12 months. On this occurrence, the patient was found to have hyperphosphatemia, low phosphate clearance, increased tubular reabsorption with normal levels of total and ionized calcium, vitamin D3, and parathyroid hormone, and no effect of treatment with sevelamer hydrochloride and a low-phosphate diet. At the age of 39, the patient underwent imaging studies due to edema and a pulsating formation in the neck area, which revealed multiple vascular aneurysms with thrombosis, for which she received operative and interventional treatment. In this connection, and because of the established phosphorus metabolism disturbance, a genetic disease was suspected. The sequence analysis and deletion/duplication testing of the 358 genes performed on this occasion revealed that the woman was homozygous for a variant of the c.202A>G (p.Thr68Ala) mutation of the FGF23 gene. The established mutation is not present in population databases. The presented clinical case is the first and only one in the world to demonstrate the role of this type of FGF23 gene mutation in the development of a hyperphosphatemic variant of tumoral calcinosis characterized by aggressive formation of multiple vascular aneurysms.
PubMed: 38792634
DOI: 10.3390/life14050613 -
International Journal of Molecular... May 2024Chronic kidney disease (CKD) is associated with significant reductions in lean body mass and in the mass of various tissues, including skeletal muscle, which causes... (Review)
Review
Chronic kidney disease (CKD) is associated with significant reductions in lean body mass and in the mass of various tissues, including skeletal muscle, which causes fatigue and contributes to high mortality rates. In CKD, the cellular protein turnover is imbalanced, with protein degradation outweighing protein synthesis, leading to a loss of protein and cell mass, which impairs tissue function. As CKD itself, skeletal muscle wasting, or sarcopenia, can have various origins and causes, and both CKD and sarcopenia share common risk factors, such as diabetes, obesity, and age. While these pathologies together with reduced physical performance and malnutrition contribute to muscle loss, they cannot explain all features of CKD-associated sarcopenia. Metabolic acidosis, systemic inflammation, insulin resistance and the accumulation of uremic toxins have been identified as additional factors that occur in CKD and that can contribute to sarcopenia. Here, we discuss the elevation of systemic phosphate levels, also called hyperphosphatemia, and the imbalance in the endocrine regulators of phosphate metabolism as another CKD-associated pathology that can directly and indirectly harm skeletal muscle tissue. To identify causes, affected cell types, and the mechanisms of sarcopenia and thereby novel targets for therapeutic interventions, it is important to first characterize the precise pathologic changes on molecular, cellular, and histologic levels, and to do so in CKD patients as well as in animal models of CKD, which we describe here in detail. We also discuss the currently known pathomechanisms and therapeutic approaches of CKD-associated sarcopenia, as well as the effects of hyperphosphatemia and the novel drug targets it could provide to protect skeletal muscle in CKD.
Topics: Humans; Renal Insufficiency, Chronic; Muscle, Skeletal; Animals; Sarcopenia
PubMed: 38791164
DOI: 10.3390/ijms25105117 -
Veterinary Journal (London, England :... Jun 2024The pathogenesis of increased serum phosphate concentration and proteinuria in dogs with spontaneous hyperadrenocorticism (HAC) is unclear. A potential link between...
The pathogenesis of increased serum phosphate concentration and proteinuria in dogs with spontaneous hyperadrenocorticism (HAC) is unclear. A potential link between proteinuria and calcium/phosphate metabolism has never been studied in dogs with HAC. The aims of the study were: (1) To evaluate calcium/phosphate metabolism in dogs with spontaneous HAC and compare to healthy dogs as well as to dogs with non-HAC illness; (2) to look for associations between markers of calcium/phosphate metabolism and biomarkers of kidney disease in dogs with HAC. Fifty-four dogs were included in the study, classified as HAC (n=27), non-HAC disease (n=17), and healthy (n=10). Serum calcium, phosphate, 25(OH)Vitamin D, 1,25(OH)Vitamin D, plasma intact parathyroid hormone concentration (iPTH), FGF23, and urinary fractional excretion of calcium and phosphate were evaluated in all dogs at diagnosis and compared between each group. The correlation between these variables and urine protein-to-creatinine ratio (UPC) and urinary N-acetylglucosaminidase-to-creatinine ratio (uNAG/C) was evaluated in the HAC group. Medians [range] of serum phosphate concentration, urinary fractional excretion of calcium (FE(Ca)), and iPTH were significantly higher in dogs with HAC than in dogs with non-HAC illness (P<0.01) and healthy dogs (P<0.01). Increased 1,25(OH)Vitamin D/25(OH)Vitamin D was also observed (P<0.001). In HAC group, UPC was significantly negatively correlated with 25(OH)Vitamin D (r(s): -0.54; P<0.01). Urinary NAG/C was significantly positively correlated with serum phosphate (r(s): 0.46; P=0.019). Increased serum phosphate, urinary excretion of calcium, and hyperparathyroidism were observed in dogs with HAC. Vitamin D metabolism may be shifted towards increased 1-alpha hydroxylation.
Topics: Animals; Dogs; Dog Diseases; Biomarkers; Male; Phosphates; Female; Calcium; Adrenocortical Hyperfunction; Kidney Diseases; Parathyroid Hormone; Vitamin D; Proteinuria; Fibroblast Growth Factor-23
PubMed: 38788995
DOI: 10.1016/j.tvjl.2024.106146 -
Dentistry Journal May 2024Familial isolated hypoparathyroidism is a rare genetic disorder due to no or low production of the parathyroid hormone, disturbing calcium and phosphate regulation. The...
OBJECTIVE
Familial isolated hypoparathyroidism is a rare genetic disorder due to no or low production of the parathyroid hormone, disturbing calcium and phosphate regulation. The resulting hypocalcemia may lead to dental abnormalities, such as enamel hypoplasia. The aim of this paper was to describe the full-mouth rehabilitation of a 15-year-old girl with chronic hypocalcemia due to a rare congenital hypoparathyroidism.
CLINICAL CONSIDERATIONS
In this patient, in the young adult dentition, conservative care was preferred. Onlays or stainless-steel crowns were performed on the posterior teeth, and direct or indirect (overlays and veneerlays) were performed on the maxillary premolars, canines, and incisors, using a digital wax-up. The mandibular incisors were bleached. The treatment clearly improved the patient's oral quality of life, with fewer sensitivities, better chewing, and aesthetic satisfaction. The difficulties were the regular monitoring and the limited compliance of the patient.
CONCLUSION
Despite no clinical feedback in the literature, generalized hypomineralized/hypoplastic teeth due to hypoparathyroidism in a young patient can be treated as amelogenesis imperfecta (generalized enamel defects) with a conservative approach for medium-term satisfactory results.
HIGHLIGHTS
This study provides new insights into the management of enamel hypoplasia caused by familial isolated hypoparathyroidism, helping to improve patient outcomes in similar cases.
PubMed: 38786528
DOI: 10.3390/dj12050130