Excess Parathyroid Hormone Research Articles

Normocalcemic Primary Hyperparathyroidism: Need for a Standardized Clinical Approach.

Since normocalcemic primary hyperparathyroidism (NHPT) was first defined at the Third International Workshop on the Management of Asymptomatic Primary Hyperparathyroidism in 2008, many papers have been published describing its prevalence and possible complications. Guidelines for the management of this condition are still lacking, and making the diagnosis requires fulfillment of strict criteria. Recent studies have shown that intermittent oscillations of serum calcium just below and slightly above the normal limits are very frequent, therefore challenging the assumption that serum calcium must be consistently normal to make the diagnosis. There is debate if these variations in serum calcium outside the normal range should be included under the rubric of NHPT or, rather, a milder form of classical primary hyperparathyroidism. Innovative approaches to define NHPT have been proposed that still need to be validated in prospective studies. Non-classical complications, especially cardiovascular complications, have been associated with NHPT, indicating that hyperparathyroidism may be a cardiovascular risk factor. New associations between parathyroid hormone (PTH) and several other comorbidities have also been reported from observational studies, suggesting that excessive PTH secretion might cause tissue dysfunction independent of serum calcium. Heterogeneous studies using different definitions of NHPT, however, make it difficult to draw definitive conclusions regarding the role of PTH excess when complications other than osteoporosis or kidney stones are described. This review will focus on clinical aspects and suggest an approach to NHPT.

Efficacy of ultrasonography and Tc-99m MIBI SPECT/CT in preoperative localization of parathyroid adenomas causing primary hyperthyroidism

BackgroundPrimary hyperparathyroidism (PHPT) results from an excess of parathyroid hormone (PTH) produced from an overactive parathyroid gland. The study aimed to explore the sonographic features of parathyroid adenomas and assess the diagnostic performance of ultrasonography (US) and Tc-99m MIBI SPECT/CT for preoperative localization of parathyroid adenomas.MethodsA total of 107 patients were enrolled in this retrospective study who had PHPT and underwent parathyroidectomy. Of the 107 patients, 97 performed US and Tc-99m MIBI SPECT/CT examinations for preoperative localization of parathyroid nodules. The sensitivity and accuracy of each modality were calculated.ResultsIn this study, residual parathyroid sign and polar vascular sign were identified as characteristic US features of parathyroid adenomas. These manifestations were closely related to the size of the abnormal parathyroid lesions. Among the 108 parathyroid nodules from 97 patients with PHPT, the sensitivity and accuracy of US for locating the parathyroid nodules were significantly higher than those of Tc-99m MIBI SPECT/CT (93.0% vs. 63.0% and 88.0% vs. 63.0% respectively; χ2 = 26.224, 18.227 respectively, P < 0.001). The differences between US + Tc-99m MIBI SPECT/CT and Tc-99m MIBI SPECT/CT-alone were statistically significant (χ2 = 33.410, 21.587 respectively, P < 0.001), yet there were no significant differences in the sensitivity or accuracy between US + Tc-99m MIBI SPECT/CT and US-alone (χ2 = 0.866, 0.187 respectively, P = 0.352 and 0.665).ConclusionsUS shows significantly better sensitivity and accuracy for localization of parathyroid adenomas than Tc-99m MIBI SPECT/CT. However, US combined with Tc-99m MIBI SPECT/CT is of great clinical value in the preoperative localization of parathyroid nodules in patients with PHPT.

Independent effects of secondary hyperparathyroidism and hyperphosphataemia on chronic kidney disease progression and cardiovascular events: an analysis from the NEFRONA cohort.

Secondary hyperparathyroidism (SHPT) is a complication of chronic kidney disease (CKD) and is associated with changes in calcium and phosphate. These related changes have been associated with increased cardiovascular mortality and CKD progression. It is not clear whether negative outcomes linked to SHPT are confounded by such factors. The present study was designed to assess the possible independent effects of SHPT [defined as patients with excessive parathyroid hormone (PTH) levels or on treatment with PTH-reducing agents] on the risk of CKD progression and cardiovascular event (CVE) incidence in CKD patients, as well as whether hypercalcaemia and/or hyperphosphataemia act as effect modifiers. The study enrolled 2445 CKD patients without previous CVE from the National Observatory of Atherosclerosis in Nephrology (NEFRONA) cohort (Stage 3, 950; Stage 4, 612; Stage 5, 195; on dialysis, 688). Multivariate logistic and Fine and Gray regression analysis were used to determine the risk of patients suffering CKD progression or a CVE. The prevalence of SHPT in the cohort was 65.6% (CKD Stage 3, 54.7%; CKD Stage 4, 74.7%; CKD Stage 5, 71.4%; on dialysis, 68.6%). After 2 years, 301 patients presented CKD progression. During 4 years of follow-up, 203 CVEs were registered. Patients with SHPT showed a higher adjusted risk for CKD progression and CVE. Furthermore, hyperphosphataemia was shown to be an independent risk factor in both outcomes and did not modify SHPT effect. No significant interactions were detected between the presence of SHPT and hypercalcaemia or hyperphosphataemia. We conclude that SHPT and hyperphosphataemia are independently associated with CKD progression and the incidence of CVE in CKD patients.

PTH resistance

Parathyroid hormone (PTH), which is primarily regulated by extracellular calcium changes, controls calcium and phosphate homeostasis. Different diseases are derived from PTH deficiency (hypoparathyroidism), excess (hyperparathyroidism) and resistance (pseudohypoparathyroidism, PHP). Pseudohypoparathyroidism was historically classified into subtypes according to the presence or not of inherited PTH resistance associated or not with features of Albright's hereditary osteodystrophy and deep and progressive ectopic ossifications. The growing knowledge on the PTH/PTHrP signaling pathway showed that molecular defects affecting different members of this pathway determined distinct, yet clinically related disorders, leading to the proposal of a new nomenclature and classification encompassing all disorders, collectively termed inactivating PTH/PTHrP signaling disorders (iPPSD).

Tertiary hyperparathyroidism: a review.

Tertiary hyperparathyroidism (HPT III) occurs when an excess of parathyroid hormone (PTH) is secreted by parathyroid glands, usually after longstanding secondary hyperparathyroidism. Some authorities reserve the term for secondary hyperparathyroidism that persists after successful renal transplantation. Long-standing chronic kidney disease (CKD) is associated with several metabolic disturbances that lead to increased secretion of PTH, including hyperphosphatemia, calcit-riol deficiency, and hypocalcaemia. Hyperphosphatemia has a direct stimulatory effect on the parathyroid gland cell resulting in nodular hyperplasia and increased PTH secretion. Prolonged hypocalcaemia also causes parathyroid chief cell hyperplasia and excess PTH. Af-ter correction of the primary disorder CKD by renal transplant, the hypertrophied parathyroid tissue fails to resolute, enlarge over and continues to oversecrete PTH, despite serum calcium levels that are within the reference range or even elevated. They also may become resistant to calcimimetic treatment. The main indication for treatment is persistent hypercalcemia and/or an increased PTH, and the primary treatment is surgery. Three procedures are commonly performed: total parathyroidectomy with or without autotransplantation, subtotal parathyroidectomy, and limited parathyroidectomy. It is important to remove superior parts of thymus as well. The most appropriate surgical procedure, whether it be total, subtotal, or anything less than subtotal including "limited" or "focused" parathyroidectomies, continues to be unclear and controversial. Surgical complications are rare, and para-thyroidectomy appears to be a safe and feasible treatment option for HPT III.

Primary Hyperparathyroidism Presenting With Atrial Fibrillation and Calcified Pericardial Effusion

Abstract Background: Primary hyperparathyroidism is the most common cause of hypercalcemia and is frequently associated with skeletal and renal complications. It affects the older population and female gender more commonly. Cardiovascular complications due to altered calcium homeostasis are not well recognised or studied but recently cases of calcification of the pericardium, myocardium, valves and dysrhythmias have been reported. Case: A 47-year old female presented to her GP with atrial fibrillation. Initial blood tests revealed an incidental hypercalcaemia; an adjusted calcium of 2.77 (normal 2.20-2.60mmol/L), raised PTH level of 14.0 (normal 1.6–6.9pmol/L), normal phosphate level and thyroid profile. 25-OH vitamin D level was low 39 (normal 50-120nmol/L). Autoantibody screens and CRP was normal. She was initiated on edoxaban, bisoprolol, and cholecalciferol and treated with a short course doxycycline for a presumed chest infection. There was no history of previous pericarditis but she had long standing hypertension and was obese with BMI of 37kg/m2. Retrospectively patient had sustained a recent wrist fracture and reported classic symptoms of hypercalcemia including fatigue, polydipsia, nocturia, constipation, depression in the endocrinology clinic. Further blood tests found a high C-terminal telopeptide (CTX) level of 0.68 (0.10-0.50ug/L) indicative of high bone turnover.24 urinary calcium/creatinine clearance ratio was 0.0189mmol/mmol (R&amp;gt;0.01 for exclusion of FHH). She was prepped for DC cardioversion and Echocardiogram demonstrated Moderate sized pericardial effusion with some organisation but good biventricular function and dilated LA. Subsequent localisation studies with SPECT CT neck revealed a 9mm parathyroid adenoma along with calcified persistent moderate pericardial effusion putting the patient at risk of pericardial constriction. Patient was referred to the parathyroid surgeon for consideration of urgent parathyroidectomy and will be followed up by the cardiologist to see the impact of normalisation of hypercalcemia on the cardiac complication. It is thought that already established calcification of pericardial effusion is unlikely to resolve but achieving normocalcemia could slow the progression of pericardial calcification and improve bone turnover makers by switching off the excess parathyroid hormone. Patient will be followed up with repeat Echocardiogram post parathyroidectomy to elucidate the effects. Conclusion:Cardiac complications of primary hyperparathyroidism are increasingly becoming more evident with the advent and use of SPECT-CT for localising parathyroid adenomas. Simple screening tests like electrocardiogram may potentially point towards a cardiovascular complication and should be considered routinely in hypercalcaemic patients. Further studies to understand the mechanism of developing cardiac complication in such patients are needed.

Treatment-Resistant Hypercalcemia Secondary to Ectopic PTH Hypersecretion From Disseminated Ovarian Cancer

Background: Hypercalcemia of malignancy (HCM) can present secondary to hypersecretion of parathyroid hormone (PTH)-related protein (PTHrP) from malignant tumors, but rare cases of HCM have also been documented due to inappropriate PTH secretion from ectopic neoplasms. Here, we report an unusual case of HCM due to hypersecretion of PTH from a disseminated mucinous ovarian adenocarcinoma. Case Presentation: A 45-year-old female presented with confusion, constipation, fatigue, and abdominal pain two weeks after total abdominal hysterectomy with bilateral salpingo-oophorectomy and suboptimal debulking of a newly discovered left ovarian mucinous adenocarcinoma with metastasis to the bladder, parametrium, vagina, right ovary, and rectosigmoid. Subsequent CT revealed numerous bilateral pulmonary nodules, hilar adenopathy, liver lesions, and abdominal adenopathy. On exam, she was tachycardic and hypertensive with diaphoresis, dry mucous membranes, respiratory distress, guarded abdominal tenderness, and altered mental status. Her labs were significant for a serum calcium of 21.7 mg/dL, creatinine of 1.93 mg/dL, ferritin of 2,379 ng/mL, leukocytosis of 21.9 bil/L, PTH of 1,061 pg/mL, and PTHrP of 29 pmol/L. Ectopic PTH secretion was highly suspected after negative parathyroid ultrasound. Pamidronate (60 mg IV), calcitonin (200 U IM), and fluid resuscitation were unable to normalize her serum calcium, resulting in the need for dialysis and subsequent continuous renal replacement therapy. Further intervention with denosumab (120 mg SQ), etelcalcetide (5 mg IV), and cinacalcet (60 mg PO) was also attempted. Serum calcium began to decline, but repeat PTH resulted greater than 2,500 pg/mL. Unfortunately, the patient died just one week into her hospital course from septic shock and multi-organ system failure. Discussion: Hypercalcemia of malignancy typically arises from tumor secretion of PTHrP, cytokine release from osteolytic metastases, or tumor production of calcitriol. In cases of hypercalcemia due to excess PTH secretion, primary parathyroid etiologies are typically considered while ectopic PTH-secreting tumors are rare. PTH staining of biopsy specimens and total body sestamibi scan may prove useful in the early detection and treatment of these tumors, but HCM offers a poor prognosis with mean survival of 2 to 3 months and in-hospital mortality of 6.8%. Currently, there are only three cases in the reported literature of ectopic PTH-induced hypercalcemia related to ovarian cancer. To our knowledge, this is the fourth reported case. Conclusion: Ectopic PTH-secreting tumors carry a poor prognosis and should be considered in cancer patients presenting with PTH-associated hypercalcemia. Biopsy staining for PTH and total body sestamibi scan may assist in the early detection of these tumors, but current treatment strategies offer suboptimal outcomes.

Primary Hyperparathyroidism: A Narrative Review of Diagnosis and Medical Management.

Primary hyperparathyroidism (PHPT) is the most common cause of hypercalcemia in the outpatient setting. Symptomatic presentation includes non-specific signs and symptoms of hypercalcemia, skeletal fragility, nephrolithiasis and nephrocalcinosis. The majority of individuals present at an asymptomatic stage following routine biochemical screening, without any signs or symptoms of calcium or parathyroid hormone (PTH) excess or target organ damage. Indications for surgery have recently been revised as published in recent guidelines and consensus statements. Parathyroidectomy is advised in patients younger than 50 years old and in the presence of either significant hypercalcemia, impaired renal function, renal stones or osteoporosis. Surgery is always appropriate in suitable surgical candidates, however, medical management may be considered in those with mild asymptomatic disease, contraindications to surgery or failed previous surgical intervention. We summarized the optimal medical interventions available in the care of PHPT patients not undergoing parathyroidectomy. Calcium and vitamin D intake should be optimized. Antiresorptive therapy may be used for skeletal protection in patients with an increased fracture risk. Cinacalcet, a calcimimetic agent, has been shown to effectively lower serum calcium and PTH levels. The effect of medical treatment on the reduction in fracture risk is unknown and should be the focus of future research.

Renal excretion function in primary hyperparathyroidism: cardio-renal syndrome

Background. Primary hyperparathyroidism (PHPT) is an endocrine disease, due to the formation of excess parathyroid hormone secretion and a disturbance of phosphorus-calcium metabolism. PHPT is associated with reduced renal function and related increased mortality, therefore renal function impairment defined as a glomerular filtration rate (GFR) less than 60 mL/ min/1.73 m 2 is considered as an indication for surgical treatment. Some patients with PHPT have secondary cardio-renal syndrome (type 5), which is characterized by the presence of combined renal and cardiac pathology. THE AIM: Evaluate the GFR in patients with mild and symptomatic PHPT and its changes after parathyroidectomy and on medical treatment. Patients and methods : A cross-sectional comparative and prospective study was conducted on 100 patients with confirmed PHPT. A clinical and laboratory examination was performed at 6, 12, and/or 24 months and included an assessment of the PHPT complications as well as expression of cardio-renal syndrome according to the selected management tactics. Changes in GFR were evaluated in 29 patients after surgical treatment and in 27 patients on conservative management. Glomerular filtration rate was calculated by the Modification of Diet in Renal Disease Study (MDRD) formula. The chronic kidney disease (CKD) stage was estimated accordingly to current recommendations. Results: We included 100 patients (10 men and 90 women) with PHPT: 33 with mild and 67 with symptomatic PHPT. The median age was 57 years [51;61]. Mean GFR was 84,1 [73,3; 97,9] ml/ min/1,73 m 2 . Prevalence of CKD 3-4 in patients with PHPT was recorded at 11 %. Patient management tactics were determined in accordance with international recommendations. In the long-term period after surgery, we observed the decrease of GFR in patients with mild form within the limits of CKD 1-2 (p=0,013, W-test). No significant changes in GFR were noted during medical management and monitoring. Summary, the cardio-renal syndrome (CKD of any stage and cardiovascular pathology) was revealed in 26 % of patients. Arterial hypertension was registered in 40 %. Conclusions : We found a high frequency of renal function impairment in patients with PHPT, including patients with a mild form of the disease. We did not observe any significant improvement in renal filtration function, after surgical treatment and remission of PHPT. The safety of conservative tactics has been confirmed. The high frequency of cardiovascular pathology in patients with PHPT is beyond doubt and requires prospective studies in the larger cohorts of patients.

MiR-129 Blocks Secondary Hyperparathyroidism-Inducing Fgf23/αKlotho Signaling in Mice with Chronic Kidney Disease

BackgroundSecondary hyperparathyroidism, a condition of excess parathyroid hormone (PTH, Pth) production, is often seen in chronic kidney disease (CKD) patients with elevated fibroblast growth factor 23 (FGF23, Fgf23). Elevated FGF23 levels stimulate secondary hyperparathyroidism-associated parathyroid αKlotho signaling. As overexpression of rationally selected microRNAs can suppress target gene activation, we hypothesized that microRNA-based suppression of parathyroid FGF23/αKlotho axis activity may be a potential strategy to combat secondary hyperparathyroidism. MethodsIn vitro luciferase assays and human parathyroid adenoma cell experiments were used to determine miR-129-1-3p's effects on αKlotho expression in vitro. We also studied the effects of parathyroid-specific miR-129-1 overexpression (miR-129Ox) in CKD and non-CKD mice and parathyroid tissue cultures derived therefrom. ResultsmiR-129-1-3p directly targets the αKlotho mRNA strand in human parathyroid cells. miR-129Ox CKD mice and control CKD mice displayed comparable serum levels of calcium, phosphate, Fgf23, and 1,25-dihydroxyvitamin D (1,25(OH)2D). However, miR-129Ox CKD mice displayed reduced parathyroid αKlotho expression and lower circulating Pth levels. In vitro culture of miR-129Ox CKD murine parathyroid tissue showed suppressed responses to Fgf23, with decreased Pth secretion and diminished cell proliferation after four days. ConclusionsmiR-129 negatively regulates pro-proliferative, Pth-inducing Fgf23/α​Klotho signaling in the parathyroid glands of CKD mice.

Osteitis Fibrosa Cystica.

ABSTRACTOsteitis fibrosa cystica is a rare presentation of both primary and secondary hyperparathyroidism. In this perspective, we provide a historical backdrop to this form of parathyroid disease and contend that this clinical presentation of excess parathyroid hormone, particularly in primary hyperparathyroidism, is still seen today. In view of its rarity and the way it typically presents, the diagnosis of metastatic cancer is often the first diagnostic impression. © 2020 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.

Mineralização vascular associada a distúrbio mineral ósseo em paciente com doença renal crônica - relato de caso

A doença renal crônica (DRC) é uma afecção comum na rotina clínica de animais de companhia e sua presença está associada há alterações polissistêmicas, como distúrbios minerais ósseos relacionados a ação de toxinas urêmicas como o paratormônio (PTH). O desequilíbrio da homeostasia causada pelo excesso do PTH pode cursar com repercussões clínicas como osteodistrofia fibrosa, calcificações teciduais e progressão da doença renal. Objetiva-se com o presente trabalho, descrever o caso de um paciente canino de quatro anos de idade, portador de DRC associada a distúrbio mineral ósseo com repercussões como osteodistrofia fibrosa e alterações cardiovasculares como hipertensão arterial sistêmica, hipertrofia concêntrica do ventrículo esquerdo e calcificações vasculares.

Relationship between Parathyroid Hormone Level and Early Remodeling Heart Failure after Acute Myocardial Infarction

Background: Previous studies have indicated that parathyroid hormone (PTH) has been linked to post-myocardial infarction (MI) development. The aim of this cross-sectional study was to evaluate the relationship between PTH level and heart failure due to post infarction remodeling during the first 72 hours of hospitalization. Methods: Seventy patients with a diagnosis of acute MI (age ≥18 years, 22 females and 48 males) were enrolled. Patients were admitted to the Imam Raza Educational, Research and Treatment Center, Mashhad University of Medical Sciences, Iran between July 2014 to September 2015. We measured PTH and vitamin D level. Blood samples were taken after 24 hours and 72 hours. Results: During the first 72 hours, the PTH level significantly increased in patients with Post-MI heart failure. 68% of the subjects had an inappropriate vitamin D level at the time of admission. Mean levels of vitamin D and PTH increased compared with the baselines (95% CI, 0.15 to 10.03, P: 0.044), (95% CI, 6.5 to 24.8, P:0.001) respectively. Conclusion: Acute elevations of serum PTH levels increased early remodeling heart failure after MI. Serum vitamin D status was independent of high serum PTH level. Based on the current evidence, PTH excess may be a risk factor for heart failure, so early treatment and omitting risk factors are the most effective strategies for the patients with acute myocardial infarction. J Pharm Care 2020; 8(1): 11-15.

Use of denosumab to treat refractory hypercalcemia in a peritoneal dialysis patient with immobilization and tertiary hyperparathyroidism

Hypercalcemia due to excess parathyroid hormone (PTH) production is a common condition among patients with end-stage renal disease (ESRD), often referred to as tertiary hyperparathyroidism. There are limited effective medical treatment options currently available for such patients. Denosumab is a monoclonal antibody that inhibits osteoclast activation, thereby reducing calcium release from bones. Denosumab has been used to treat medically-refractory hypercalcemia in non-ESRD patients with hyperparathyroidism. Denosumab has also been used to treat non-PTH-mediated hypercalcemia in patients with advanced chronic kidney disease and ESRD. In this case report, we describe the use of denosumab to successfully treat a case of medically refractory hypercalcemia due to immobilization in a patient on peritoneal dialysis with severe underlying tertiary hyperparathyroidism. In spite of persistently elevated PTH, hypercalcemia quickly resolved after a single dose of denosumab. The patient subsequently developed temporary hypocalcemia requiring medical intervention. Our case report, which is the first described use of denosumab for treatment of hypercalcemia in the setting of tertiary hyperparathyroidism in a peritoneal dialysis patient, adds to the body of literature suggesting denosumab is a useful therapeutic agent in patients with ESRD. Issues with post-treatment electrolyte management and other therapeutic considerations are also discussed.

Coincident Bilateral Atraumatic Hip Fracture in a Young Patient with Renal Osteodystrophy

Bilateral, coincident, atraumatic hip fracture is extremely uncommon and usually occurs secondary to seizures, trauma and metabolic disease including renal osteodystrophy. One of the major types, secondary hyperparathyroidism is associated with high bone turnover due to excess parathyroid hormone and usually seen in a chronic dialysis patient. We reported a 20-year-old woman with end stage renal failure and renal osteodystrophy. She sustained atraumatic right subtrochanteric fracture and left neck of femur fracture (Garden 1), then underwent bilateral long proximal femoral nail. Renal osteodystrophy causes pathological fracture by affecting calcium metabolism that stimulates bone resorptions and leads to osteoporotic bone. The aim of this case report is to discuss the approach and management done to the patient presented to our center. Bilateral long proximal femoral nail (PFN) was chosen, taking into account the patient’s premorbid, age, fracture pattern and potential complications. Careful multidisciplinary team approach led by the orthopaedic surgeon, nephrologist and physical therapist is vital for the patient to achieve good outcome postoperatively, thus reducing morbidity and mortality.

MANDIBLE BROWN TUMOR ASSOCIATED WITH HYPERPARATHYROIDISM SECONDARY TO CHRONIC RENAL INSUFFICIENCY: CASE REPORT

Chronic renal disease decreases serum calcium level contributing to excess parathyroid hormone (PTH) synthesis. As more PTH is available, a significant change in osteoclastic activity can lead to bone focal well-defined lytic lesions known as brown tumor. We report a case of a 30-year-old female patient referred to our clinic with a chief complaint of a painful swelling of the left mandible and difficulty chewing. Her medical history included systemic lupus erythematosus, hypertension, and chronic kidney disease (was on hemodialysis for the past 9 years). Complementary computed tomography and scintigraphy examinations helped the diagnosis of brown tumor and parathyroid hyperplasia. The patient is currently undergoing dental treatment for the removal of infectious foci prior to kidney transplantation and awaits bone mineral recovery after parathyroidectomy before osteoplasty in the mandible can be surgically performed. Chronic renal disease decreases serum calcium level contributing to excess parathyroid hormone (PTH) synthesis. As more PTH is available, a significant change in osteoclastic activity can lead to bone focal well-defined lytic lesions known as brown tumor. We report a case of a 30-year-old female patient referred to our clinic with a chief complaint of a painful swelling of the left mandible and difficulty chewing. Her medical history included systemic lupus erythematosus, hypertension, and chronic kidney disease (was on hemodialysis for the past 9 years). Complementary computed tomography and scintigraphy examinations helped the diagnosis of brown tumor and parathyroid hyperplasia. The patient is currently undergoing dental treatment for the removal of infectious foci prior to kidney transplantation and awaits bone mineral recovery after parathyroidectomy before osteoplasty in the mandible can be surgically performed.

Mental Effects of Excess Parathyroid Hormone in Hemodialysis Patients: A Possible Role for Parathyroid 2 Hormone Receptor?

Depression as measured by the kidney disease quality of life (KDQOL) form is known to be an independent risk factor for mortality dialysis patients. Excess parathyroid hormone (PTH) has long been associated with neuropsychiatric disturbances. Those psychiatric complications are currently attributed to hypercalcemia with very little evidence; however, with the discovery of the parathyroid hormone 2 receptor (PTH2R) in the brain which can be activated by PTH, PTH2R might indicate a direct effect of PTH. As secondary and tertiary hyperparathyroidism is common in dialysis patients where the serum calcium is low or normal, we chose to investigate a possible relationship between PTH levels and depression in dialysis patients. This was a matched pair observational study with 10 patients with intact PTH values above 1000 pg/mL who were matched with 10 patients who had PTH values less than 400 pg/mL for the presence of diabetes, years on dialysis, duration of dialysis time, Kt/V, hemoglobin, and 25 OH vitamin D levels, as well as intravenous iron and erythropoietin administration. The Kidney Disease Quality of Life questionnaire (KDQOL-36) scores and patient Health Questionnaire scores were analyzed during that time. All variables underwent tests for normality and matched pair t-test. All subscales of the KDQOL-36 were worse in the high PTH group with the effect on daily life reaching P = 0.01 and the burden of disease and symptoms both reaching P = 0.02. PTH and PTH2R may be appropriate targets for investigations to improve the quality of life in hemodialysis patients.

Two cases of spontaneous remission of primary hyperparathyroidism due to auto-infarction: different management and their outcomes.

SummarySpontaneous remission of primary hyperparathyroidism (PHPT) due to necrosis and haemorrhage of parathyroid adenoma, the so-called ‘parathyroid auto-infarction’ is a very rare, but previously described phenomenon. Patients usually undergo parathyroidectomy or remain under close clinical and biochemical surveillance. We report two cases of parathyroid auto-infarction diagnosed in the same tertiary centre; one managed surgically and the other conservatively up to the present time. Case #1 was a 51-year old man with PHPT (adjusted (adj.) calcium: 3.11 mmol/L (reference range (RR): 2.20–2.60 mmol/L), parathyroid hormone (PTH) 26.9 pmol/L (RR: 1.6–6.9 pmol/L) and urine calcium excretion consistent with PHPT) referred for parathyroidectomy. Repeat biochemistry 4 weeks later at the surgical clinic showed normal adj. calcium (2.43 mmol/L) and reduced PTH. Serial ultrasound imaging demonstrated reduction in size of the parathyroid lesion from 33 to 17 mm. Twenty months later, following recurrence of hypercalcaemia, he underwent neck exploration and resection of an enlarged right inferior parathyroid gland. Histology revealed increased fibrosis and haemosiderin deposits in the parathyroid lesion in keeping with auto-infarction. Case #2 was a 54-year-old lady admitted with severe hypercalcaemia (adj. calcium: 4.58 mmol/L, PTH 51.6 pmol/L (RR: 1.6–6.9 pmol/L)) and severe vitamin D deficiency. She was treated with intravenous fluids and pamidronate and 8 days later developed symptomatic hypocalcaemia (1.88 mmol/L) with dramatic decrease of PTH (17.6 pmol/L). MRI of the neck showed a 44 mm large cystic parathyroid lesion. To date, (18 months later), she has remained normocalcaemic.Learning points:Primary hyperparathyroidism (PHPT) is characterised by excess parathyroid hormone (PTH) secretion arising mostly from one or more autonomously functioning parathyroid adenomas (up to 85%), diffuse parathyroid hyperplasia (<15%) and in 1–2% of cases from parathyroid carcinoma.PHPT and hypercalcaemia of malignancy, account for the majority of clinical presentations of hypercalcaemia.Spontaneous remission of PHPT due to necrosis, haemorrhage and infarction of parathyroid adenoma, the so-called ‘parathyroid auto-infarction’, ‘auto-parathyroidectomy’ or ‘parathyroid apoplexy’ is a very rare in clinical practice but has been previously reported in the literature.In most cases, patients with parathyroid auto-infarction undergo parathyroidectomy. Those who are managed conservatively need to remain under close clinical and biochemical surveillance long-term as in most cases PHPT recurs, sometimes several years after auto-infarction.

Role of routine frozen sections for parathyroid exploration in a resource poor setting

Removal of parathyroid is recommended for patients suffering from hypercalcemia due to excess parathyroid hormone levels. There are several causes for a hyperfunctioning parathyroid gland out of which parathyroid adenoma is the most common pathological entity. There is great variation in the number and location of parathyroid glands. Hence, intra-operative confirmation of parathyroid tissue makes it easier for the surgeon to be confident of the outcome of the procedure and assure the patient of a permanent cure. A descriptive cross sectional study was done in a cohort of 26 patients who presented with elevated total serum calcium and parathyroid hormone concentrations. Intra-operative frozen section diagnoses were correlated with routine histological studies and post-operative parathyroid hormone concentration. The majority of patients were diagnosed as having parathyroid adenoma (88.46%). Three out of 26 patients (11.53%) had parathyroid hyperplasia involving more than one gland. Sensitivity and specificity of intraoperative frozen section diagnosis was 100%. There was a statistically significant association (p In the light of the discussion on parathyroid surgery it is apparent that frozen sections play a pivotal role in resource poor settings, when facilities for novel intra-operative imaging studies such as sestamibi scan and single-photon emission computed tomography are limited. The participants of the study have been followed up during last 5 years with no evidence of residual disease or recurrence up to date.

Parathyroid hormone excess due to denosumab application and concomitant parathyroid adenoma with an atypical scintigraphic pattern- a case report

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