Significance of Elevated Parathyroid Hormone After Parathyroidectomy

ObjectiveTo review the prevalence of parathyroid hormone elevation after parathyroidectomy for primary hyperparathyroidism and to discuss possible mechanisms.MethodsA Medline search of the English-language literature published between 1990 and 2009 was performed using the search terms “elevated PTH after parathyroidectomy.” All of the identified articles reported either prospective or retrospective studies without control groups. Studies that included patients with secondary or tertiary hyperparathyroidism were not reviewed.ResultsWithin 1 week to 5 years after parathyroidectomy, 9% to 62% of patients with a normal serum calcium concentration are reported to have an elevated parathyroid hormone concentration. No evidence suggests that postoperative normocalcemic parathyroid hormone elevation is an indication of surgical failure and recurrent hypercalcemia. Preoperative findings in patients with postoperative parathyroid hormone elevation include lower vitamin D concentration, higher concentrations of bone turnover markers, and higher parathyroid hormone concentration. Potential mechanisms for parathyroid hormone elevation in the setting of normocalcemia include vitamin D deficiency, hungry bone syndrome, and parathyroid hormone resistance. Study findings suggest a possible benefit of postoperative calcium and vitamin D supplementation, but no randomized trials have been done.ConclusionElevation of parathyroid hormone commonly occurs after parathyroidectomy for primary hyperparathyroidism, although the underlying mechanism remains unclear. (Endocr Pract. 2010;16:112-117)     

A Parathyroid Hormone–Guided Calcium and Calcitriol Supplementation Protocol Reduces Hypocalcemia-Related Readmissions Following Total Thyroidectomy

ObjectiveTo determine the effect of a 4-hour postoperative serum parathyroid hormone (PTH)–guided calcium (Ca) and calcitriol supplementation protocol on the incidence of hypocalcemia and hospital readmissions in patients undergoing total thyroidectomy.MethodsThis was a single-institution, retrospective chart review of patients who underwent total thyroidectomy; 148 and 389 of the patients underwent surgery prior to and after the protocol implementation, respectively. The risk of hypocalcemia was stratified as low (PTH level of >30 pg/mL), medium (15-30 pg/mL), and high (<15 pg/mL), using serum PTH values obtained 4 hours postoperatively. Hypocalcemia was defined as a total serum Ca level of <8 mg/dL. Baseline demographic and operative characteristics and postoperative outcome were recorded for both groups. The Fisher exact test and Wilcoxon rank sum test were used to compare the characteristics of the 2 groups. A multivariate logistic regression model was applied to account for potentially confounding variables.ResultsPostoperative hypocalcemia occurred significantly less frequently in the protocol group compared with that in the preprotocol group (10.3% vs 20.9%, P = .002). The reduction in hypocalcemia in the protocol group was observed in both patients with (16.3% vs 25.6%) and without (8.4% vs 19.3%) cervical lymph node dissection. The protocol group had a significantly lower incidence of hospital readmission events than the preprotocol group (1.0% vs 4.7%, P = .013).ConclusionCompared with a historical cohort, a PTH-guided protocol for Ca and calcitriol supplementation significantly reduces the postoperative hypocalcemia and hospital readmission rates in patients undergoing total thyroidectomy.     

Hypocalcemia after Alendronate Therapy in a Patient with Celiac Disease

ObjectiveTo describe a patient with osteoporosis who was treated with alendronate and developed hypocalcemia, which ultimately led to the diagnosis of celiac sprue.MethodsWe present the clinical and laboratory findings in a patient with osteoporosis, in whom hypocalcemia developed after treatment with alendronate. This patient was subsequently diagnosed with celiac sprue. The pertinent literature regarding orally administered bisphosphonate-induced hypocalcemia is reviewed.ResultsA 79-year-old man who was diagnosed with osteoporosis was treated with alendronate. He was subsequently found to have asymptomatic hypocalcemia (serum calcium concentration, 8.3 mg/dL), which resolved after alendronate therapy was discontinued. He was then treated with calcium, vitamin D, and calcitonin nasal spray, which did not cause hypocalcemia. Because of his reduced bone density, however, he was subsequently referred for endocrine consultation. Evaluation at that time showed normal levels of serum calcium, phosphorus, creatinine, alkaline phosphatase, 25-hydroxyvitamin D, thyrotropin, and parathyroid hormone as well as 24-hour urine calcium excretion. An endomysial antibody titer was dramatically elevated. Upper endoscopy showed villous atrophy, and small bowel biopsy confirmed the presence of villous blunting and chronic inflammation, consistent with celiac sprue. He was treated with a gluten-free diet and then subsequently treated with orally administered risedronate, which he tolerated well without evidence of hypocalcemia.ConclusionTo the best of our knowledge, this is the first report of orally administered bisphosphonate-induced hypocalcemia, which subsequently led to the diagnosis of previously unrecognized, otherwise asymptomatic celiac sprue. Patients with unexplained hypocalcemia should be screened for celiac sprue, even in the absence of gastrointestinal symptoms. (Endocr Pract. 2007;13:403-407)     

Celiac Disease Manifesting as Isolated Hypocalcemia

ObjectiveTo describe a patient who presented with hypocalcemia and hypocalciuria as the initial manifestations of celiac disease, despite a normal vitamin D status.MethodsWe review the diagnostic evaluation, treatment, and biochemical and bone mineral density responses of a patient with asymptomatic celiac disease, which was initially suggested because of a low serum calcium level that became attributable to isolated malabsorption of calcium.ResultsA 36-year-old woman presented with hypocalcemia in the presence of normal serum 25- hydroxyvitamin D and high serum 1,25-dihydroxyvitamin D levels. She had hypocalciuria and secondary hyperparathyroidism that were refractory to pharmacologic calcium and cholecalciferol supplementation. Fecal calcium excretion indicated malabsorption of calcium, and biopsy of the small intestine demonstrated pathologic changes characteristic of celiac disease. Bone mineral density, determined by dual-energy x-ray absorptiometry, was in the osteopenic range at the femoral neck. The initiation of a gluten-free diet resulted in correction of all biochemical abnormalities and a substantial increase in bone mineral density.ConclusionPrimary intestinal malabsorption of calcium without concomitant vitamin D deficiency is possible in celiac disease because of the preferential involvement of the proximal small intestine early in the disease process. Our patient had hypocalcemia caused by celiac disease and values for serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D that were normal and elevated, respectively. Correction was demonstrated after dietary gluten withdrawal. (Endocr Pract. 2004;10:203-207)     

Research on Intra-Operative Indocyanine Green Angiography of the Parathyroid for Predicting Postoperative Hypoparathyroidism: A Noninferior Randomized Controlled Trial

Objective: A noninferiority randomized controlled trial was undertaken to clarify whether the postoperative measurements of serum calcium and parathyroid hormone and oral supplementation of calcium and calcitriol could be omitted if patients had at least one well-perfused parathyroid gland evaluated by intra-operative indocyanine green (ICG) angiography.Methods: Patients with at least one parathyroid gland well-perfused by ICG angiography (ICG score >2) were randomized to the control group or test group. For the control group, oral calcium and calcitriol were systematically supplemented. For the test group, no oral calcium or calcitriol was supplemented to the patients. Levels of serum calcium and parathyroid hormone of patients on the first and 30th postoperative day were compared between the two groups.Results: Among all 68 selected patients, 56 patients had at least one well-perfused parathyroid gland evaluated by intra-operative ICG angiography. The 56 patients were randomized to the control group or test group. There were no statistically significant differences in the levels of serum calcium and parathyroid hormone between test group and control group on the first or 30th postoperative day.Conclusion: The postoperative measurements of serum calcium and parathyroid hormone and oral supplementation of calcium and calcitriol were evaluated as redundant, if patients had at least one well-perfused parathyroid gland evaluated by intra-operative ICG angiography.Abbreviations: ICG = indocyanine green; NIR = near infrared; POD = postoperative day; PTH = parathyroid hormone; SBR = signal background ratio     

The Optimal Parathyroid Hormone Cut-Off Threshold for Early and Safe Management of Hypocalcemia After Total Thyroidectomy

ObjectiveTo define optimal intact parathyroid hormone (iPTH) cut-off threshold predictive of hypocalcemia after total thyroidectomy for safe and effective postoperative management.MethodsThis prospective single center study was done in 2 phases. In phase I, predictors of symptomatic hypocalcemia were analyzed and the receiver operating characteristic curve was used to define the optimal iPTH cut-off threshold predictive of hypocalcemia. Phase II studied giving prompt prophylactic supplemental calcium and vitamin D to all patients who had iPTH levels below the calculated threshold, while phase I patients were given prompt selective supplementation if they had postoperative hypocalcemia or symptoms.ResultsUnivariate analysis of patients in phase I showed that postoperative iPTH was the only significant variable that can predict symptomatic hypocalcemia. Using receiver operating characteristic curve and Youden index, the confirmed optimal cut-off threshold predictive of hypocalcemia was iPTH 19.95 pg/mL, with area under the curve of 0.903, 100% sensitivity, negative predictive value, and highest Youden index, while iPTH 15 pg/mL and iPTH 10 pg/mL were less optimal. Symptomatic hypocalcemia occurred in 30% of the phase I cohort who received selective supplementation versus 3% of those in the phase II cohort who received prophylactic supplementation. Return to emergency department and need for intravenous calcium were also significantly better in phase II.ConclusioniPTH cut-off for post-thyroidectomy hypocalcemia was 19.95 pg/mL. Low-risk patients were discharged with no supplementation while all high-risk patients received prompt calcium and vitamin D supplementation, which led to effective hypocalcemia management and safe 24-hour discharge.     

Appreciation Of Osteoporosis Among Men With Hyperparathyroidism

ObjectiveTo define the scope of bone disease among men referred for parathyroidectomy and to document bone density screening trends in this high-risk population.MethodsClinical data were analyzed from a prospectively maintained database of 1000 patients undergoing parathyroidectomy for sporadic primary hyperparathyroidism at the Cleveland Clinic between 2000 and 2006. Information collected included demographics, reason for referral, body mass index, intraoperative findings, preoperative and postoperative laboratory values (serum calcium, phosphorus, parathyroid hormone, 25-hydroxyvitamin D, and 24-hour urinary calcium excretion), and preoperative and postoperative dual-energy x-ray absorptiometry (DXA) findings.ResultsOf the 1000 patients, 243 (24%) were men. As with women, bone health-related issues were the most common reason for referral (32%). In 2000, only 12% of men had preoperative DXA scans; this rose to 42% by 2005. The frequency of prereferral DXA screening increased throughout the study, but even by 2006, referring physicians did not screen most of their male patients. In 2000, the prevalence of bone disease (osteoporosis or osteopenia) in men was 8%, but with improved screening, this increased to 26%, approaching the 34% rate in women. Preoperative and postoperative levels of calcium, parathyroid hormone, phosphorus, 24-hour urinary calcium, and 25-hydroxyvita-min D were the same among men with and without bone disease. Analysis of postoperative DXA scans revealed that gains in postparathyroidectomy bone density were significantly greater in men than in women at all anatomic testing sites. In men, lowest T scores improved by a mean ± SEM of + 0.35 ± 0.09 compared with + 0.098 ± 0.035 in women (P = .009). Men were 4 times less likely than women to have continued bone loss after parathyroidectomy.ConclusionsClinical and laboratory parameters cannot identify men with hyperparathyroidism who have bone loss, illustrating the need for routine DXA screening. Despite this, DXA remains underused. Improved screening practices will favorably effect men’s health. (Endocr Pract. 2008;14:820-831)     

Calcium Carbonate Toxicity: The Updated Milk-Alkali Syndrome; Report of 3 Cases and Review of the Literature

ObjectiveTo describe 3 patients with calcium carbonate-induced hypercalcemia and gain insights into the cause and management of the milk-alkali syndrome.MethodsWe report the clinical and laboratory data in 3 patients who presented with severe hypercalcemia (corrected serum calcium ≥ 14 mg/dL) and review the pertinent literature on milk-alkali syndrome.ResultsThe 3 patients had acute renal insufficiency, relative metabolic alkalosis, and low parathyroid hormone (PTH), PTH-related peptide, and 1,25-dihydroxyvitamin D concentrations. No malignant lesion was found. Treatment included aggressive hydration and varied amounts of furosemide. The 2 patients with the higher serum calcium concentrations received pamidronate intravenously (60 and 30 mg, respectively), which caused severe hypocalcemia. Of the 3 patients, 2 were ingesting acceptable doses of elemental calcium (1 g and 2 g daily, respectively) in the form of calcium carbonate. In addition to our highlighted cases, we review the history, classification, pathophysiologic features, and treatment of milk-alkali syndrome and summarize the cases reported from early 1995 to November 2003.ConclusionMilk-alkali syndrome may be a common cause of unexplained hypercalcemia and can be precipitated by small amounts of orally ingested calcium carbonate in susceptible persons. Treatment with hydration, furosemide, and discontination of the calcium and vitamin D source is adequate. Pamidronate treatment is associated with considerable risk for hypocalcemia, even in cases of initially severe hypercalcemia. (Endocr Pract. 2005;11: 272-280)     

Primary hyperparathyroidism and familial hypocalciuric hypercalcemia: relationships and clinical implications

ObjectiveTo discuss the unusual occurrence of both familial hypocalciuric hypercalcemia (FHH) and primary hyperparathyroidism in the same patient and to explore potential mechanisms of association and issues related to clinical management.MethodsWe discuss the diagnosis, compare the clinical presentations of FHH and primary hyperparathyroidism, review the literature regarding patients who have presented with both disorders, and discuss management considerations. We also describe 2 patients who have both FHH (confirmed by genetic testing for a mutation in the gene encoding the calcium-sensing receptor [CASR]) and primary hyperparathyroidism.ResultsThe occurrence of both FHH and primary hyperparathyroidism in the same patient has been reported in a few cases, including 2 patients described here, one of whom was documented to have a novel CASR mutation. Inthose with clinical sequelae of hyperparathyroidism, parathyroidectomy has led to reduction, but not normalization, of serum calcium levels.ConclusionsThe coexistence of FHH and primary hyperparathyroidism should be considered in patients with hypercalcemia, hypophosphatemia, frankly elevated parathyroid hormone levels, and low urinary calcium excretion. Genetic testing for inactivating CASR gene mutations can confirm the diagnosis of FHH. Although surgical intervention does not resolve hypercalcemia, it may be beneficial by reducing the degree of hypercalcemia, alleviating the symptoms, and preventing potential complications of hyperparathyroidism. (Endocr Pract. 2012;18:412-417)     

Proton Pump Inhibitor-Induced Hypocalcemic Seizure in A Patient with Hypoparathyroidism

ObjectiveTo report a case of proton pump inhibitor-induced hypocalcemic seizure in a patient with hypoparathyroidism.MethodsWe describe the clinical history, physical examination findings, and laboratory values of the patient and briefly review the relevant literature.ResultsA 48-year-old woman with a history of postsurgical hypoparathyroidism who was taking calcium carbonate, 1500 mg 3 times daily, and cholecalciferol, 1200 IU daily, presented with a generalized seizure in the setting of hypocalcemia 12 days after initiating therapy with the proton pump inhibitor lansoprazole. Physical examination revealed a positive Chvostek sign. Electrocardiogram was notable for a prolonged QT_c interval of 576 milliseconds. Laboratory data were notable for the following values: total serum calcium, 5.3 mg/dL; ionized calcium, 2.51 mg/dL; and intact parathyroid hormone, 5.8 pg/mL. The patient’s condition responded to therapy with intravenous calcium gluconate, oral calcium carbonate, and calcitriol. As an outpatient she remained asymptomatic off lansoprazole, treated with calcium carbonate and calcitriol.ConclusionsCaution should be exercised in prescribing proton pump inhibitors to patients with a history of hypoparathyroidism treated with calcium carbonate supplementation because severe hypocalcemia is a potential adverse effect. (Endocr Pract. 2011;17:104-107)     

Falsely Low Parathyroid Hormone Secondary to Biotin Interference: A Case Series

ObjectiveTo present a case series on biotin interference in parathyroid hormone (PTH) level measurement.MethodsWe review the presentation and management of patients at our institution evaluated for unexpectedly low PTH levels while taking biotin supplements in the setting of high or normal serum calcium.ResultsTwo patients presented with surprising low parathyroid levels—one during preoperative evaluation for hyperparathyroidism and another during postoperative follow-up after subtotal parathyroidectomy. The patients were found to be taking 1,500 mcg and 5,000 mcg of biotin per day, respectively. The role of biotin interference was confirmed in one of the patients when she was retested off biotin, and PTH levels responded appropriately. Biotin supplements remain as unbound molecules in the serum, thus interfering with PTH enzyme-linked immunosorbent assay (ELISA) results and falsely depressing the PTH level.ConclusionBiotin supplement use has expanded over the years, ranging from medically endorsed therapies to home remedies. Review of the 2 ELISA systems used at our institution demonstrates that free biotin mimics the biotinylated antibody used in the detection process. Screening for biotin use prior to PTH measurement and automatic biotin levels for clinically aberrant PTH levels provide the clinician with a true PTH level-lowering the disease burden of untreated hyperparathyroidism while avoiding unnecessary work-ups for other processes. (Endocr Pract. 2013;19:451-455)     

Calcium Challenge to Confirm Secondary Hyperparathyroidism Caused by Decreased Calcium Intake

ObjectiveSecondary hyperparathyroidism commonly occurs in the setting of mid-to low-normal serum calcium levels, often in the setting of chronic kidney disease, phosphate loading, vitamin D deficiency, or insufficient calcium intake or absorption. In this article, we report 9 patients who had adequate kidney function (estimated glomerular filtration rate >60 mL/min/1.73 m²) and normal 25-hydroxy vitamin D level (≥30 ng/dL) and whose secondary hyperparathyroidism resolved after starting adequate oral calcium intake.MethodsOur retrospective case series included 8 women and 1 man; the mean age was 69.0 ± 12.2 years (mean ± standard deviation). The initial intact parathyroid hormone (iPTH) level was 80.6 ± 13.4 pg/mL (reference range [ref], 10-65 pg/mL), corrected serum calcium level was 9.2 ± 0.2 mg/dL (ref, 8.5-10.5 mg/dL), serum phosphate level was 3.6 ± 0.4 mg/dL (ref, 2.5-4.9 mg/dL), 25-hydroxy vitamin D level was 42.2 ± 10.5 mg/dL (ref, 20-50 ng/mL), and estimated glomerular filtration rate was 72.6 ± 14.4 mL/min/1.73 m². Patients were treated clinically with oral calcium 600 mg twice a day.ResultsiPTH was retested after a mean duration of 17.6 ± 12.7 days of calcium supplementation; the iPTH level decreased to 51.0 ± 10.6 pg/mL, with all patients achieving iPTH in the normal range with normocalcemia, consistent with hyperparathyroidism being because of insufficient calcium intake or absorption. All patients were normocalcemic after supplementation.ConclusionSecondary hyperparathyroidism can result from insufficient oral calcium intake. Calcium challenge is an efficacious and cost-effective tool for confirming and treating secondary hyperparathyroidism in the setting of normal vitamin D levels and kidney function.     

Hypocalcemia and Parathyroid Function in Metastatic Prostate Cancer

ObjectiveTo report the occurrence of hypocalcemia in a patient with metastatic prostate cancer, discuss its pathogenesis, and review the related medical literature.MethodsAn 82-year-old man with a known history of prostate cancer was found to have a serum calcium level of 5.4 mg/dL during an admission to the hospital for small bowel obstruction. A thorough review of his medical history revealed a temporal relationship between the diagnosis of malignant disease and progressive hypocalcemia. A complete evaluation was performed, including laboratory and imaging studies, to ascertain the cause of the hypocalcemia.ResultsThe patient had no history of hypocalcemia before the diagnosis of, and initiation of antiandrogen therapy for, advanced prostate cancer. Serum magnesium and phosphorus levels were within normal limits. The serum calcium level responded to therapy in the hospital but remained between 5.8 and 7.1 mg/dL. The parathyroid hormone level was normal, and the 25-hydroxyvitamin D value was low. A 24-hour urine collection showed substantially reduced calcium excretion, and a whole-body bone scan revealed widespread metastatic deposits. These findings were compatible with hypocalcemia related to prostate cancer and bone metastatic lesions.ConclusionThis case serves as a reminder that hypocalcemia can be a manifestation of prostate cancer metastatic to bone. In contrast to the occurrence of secondary hyperparathyroidism in this setting, however, this patient had normal levels of parathyroid hormone. Review of similar previous reports and the causes and implications of a possible functional hypoparathyroid state are discussed. (Endocr Pract. 2005;11:254-258)     

Falsely Elevated Plasma Parathyroid Hormone Level Mimicking Tertiary Hyperparathyroidism

ObjectiveTo report a case of misdiagnosed tertiary hyperparathyroidism attributable to heterophile antibody interference in a parathyroid hormone (PTH) assay.MethodsWe present clinical and laboratory data relative to this case and review the pertinent English-language literature.ResultsA 36-year-old woman with a functioning renal allograft, PTH excess (3, 374 pg/mL) refractory to medical therapy, and a history of renal osteodystrophy presented for consideration of a third parathyroidectomy. Remedial parathyroidectomy was performed. The PTH levels did not decline postoperatively, but the patient developed severe hypocalcemia. Reanalysis of the patient’s serum specimens was performed with (1) addition of heterophile blocking agents to the murine-based immunoassay and (2) use of a different, goat antibody-based immunoassay. The true PTH level was found to be 5 pg/mL with use of both methods.ConclusionPrevious administration of muromonab-CD3 (Orthoclone OKT3) for immunosuppression may have resulted in the development of human antimurine heterophile antibodies, causing a falsely elevated PTH result. (Endocr Pract. 2011;17:e8-e11)     

Chemotherapy-Induced Hypocalcemia

ObjectiveTo present a unique case of transient, asymptomatic chemotherapy-induced hypocalcemia not attributable to hypomagnesemia or tumor lysis syndrome and review causes of hypocalcemia related to cancer with and without use of chemotherapy.MethodsWe present a case detailing the clinical and laboratory findings of a patient who had severe hypocalcemia during chemotherapy and discuss causes of hypocalcemia with an extensive literature review of chemotherapeutic agents associated with this biochemical abnormality.ResultsIn a 90-year-old man, hypocalcemia developed during 2 courses of chemotherapy for Hodgkin lymphoma, with partial recovery between courses and normal serum calcium 10 months after completion of treatment. Magnesium, vitamin D, and parathyroid hormone levels were low normal. There was no evidence of tumor lysis syndrome. Of the various agents administered, vinca alkaloids seemed the most likely cause. Serial testing suggested that the underlying mechanism may have been acquired, reversible hypoparathyroidism. No other similar case was found in the published literature.ConclusionThe severe hypocalcemia in our patient could not be attributed to hypomagnesemia or tumor lysis syndrome, and it was clearly associated with the timing of his chemotherapeutic regimen. Possibilities include direct parathyroid hormone suppression or alteration of calcium sensing by the chemotherapeutic drugs. Serum calcium surveillance before and during chemotherapeutic management of cancer patients may reveal more instances and provide insight into the exact mechanism of this lesser known yet striking complication. (Endocr Pract. 2010;16:284-290)     

Improvement of Sleep Disturbance and Neurocognitive Function after Parathyroidectomy in Patients with Primary Hyperparathyroidism

ObjectiveTo investigate the frequency of the nontraditional symptoms of sleep disturbance and impaired cognitive functioning in patients with primary hyperparathyroidism (PHPT) and to assess changes in such patients after parathyroidectomy.MethodsIn this study, we used formal neurocognitive assessment of patients undergoing parathyroidectomy for PHPT. The Brief Sleep Disturbance Inventory assessed sleep disturbance, and Stroop tests evaluated for cognitive impairment. Study patients underwent preoperative and postoperative neurocognitive testing.ResultsFifty-five patients underwent neurocognitive evaluation; the 43 women and 12 men had a mean age of 63 years. Sleep disturbance was assessed in all 55 patients, whereas evaluation for cognitive impairment was performed in 47. Sleep disturbance was identified preoperatively in 24 (44%) of the 55 patients. This disorder affected 17 (31%) of 55 patients postoperatively (P < 0.01). Impaired executive functioning was found at baseline in 6 (13%) of 47 patients and decreased to 1 (2%) of 47 postoperatively (P < 0.01), whereas impaired cognitive processing speed was detected in 12 (26%) of 47 patients at baseline and decreased to 3 (6%) of 47 after parathyroidectomy (P < 0.01). Eight patients did not meet the National Institutes of Health consensus statement criteria for parathyroidectomy; 4 of these patients had preoperative impairment of sleep or cognitive functioning, 3 of whom showed improvement postoperatively.ConclusionSleep disturbance and neurocognitive impairment occur in patients with PHPT, and these disorders improve after parathyroidectomy. Further objective evaluation of nontraditional symptoms in patients diagnosed as having PHPT is warranted. (Endocr Pract. 2007;13:338-344)     

Symptoms In Patients With Primary Hyperparathyroidism: Muscle Weakness Or Sleepiness

ObjectiveTo evaluate the effects of parathyroidectomy on the nonspecific symptoms associated with primary hyperparathyroidism, with an emphasis on distinguishing sleepiness from muscle weakness.MethodsWe conducted a prospective cohort study of consecutive patients presenting for parathyroidectomy for the treatment of primary hyperparathyroidism. Twenty-three patients underwent assessment preopera tively and postoperatively. The Functional Outcomes of Sleep Questionnaire (FOSQ), the Epworth Sleepiness Scale (ESS), and a questionnaire of disease-specific symptoms were administered preoperatively, 2 weeks postoperatively, and 4 to 6 months postoperatively. The FOSQ assesses how sleepiness alters daytime performance, and the ESS reflects the degree of daytime sleepiness.ResultsAll 23 patients achieved normocalcemia postoperatively. Although no significant changes were found in the overall scores for the FOSQ and ESS after parathyroidectomy, there was a significant decline in the overall mean incidence of disease-specific symptoms postoperatively (P<0.0001 after 2 weeks and P= 0.0020 after 4 to 6 months). The five disease-specific symptoms that significantly decreased in frequency postoperatively were (1) muscle weakness, (2) polydipsia, (3)dry skin and itching, (4) memory loss, and (5) anxiety.ConclusionIn this study, patients with primary hyperparathyroidism did not demonstrate daytime sleepiness or difficulty performing everyday activities because of sleepiness at baseline or after successful parathyroidectomy. The overall mean percentage for incidence of disease-specific symptoms, however, significantly declined postoperatively, especially in reference to muscle weakness. (Endocr Pract. 2004;10:404-408)     

Transient Thyrotoxicosis Following Minimally Invasive Radio-Guided Parathyroidectomy

ObjectiveWe report a case of thyrotoxicosis following minimally invasive parathyroidectomy.MethodsCase report with literature review.ResultsA 70-year-old woman with primary hyperparathyroidism developed thyrotoxicosis 2 weeks following minimally invasive radio-guided parathyroidectomy. A diagnosis of postparathyroidectomy transient thyrotoxicosis (PTT) was made after excluding other causes of thyrotoxicosis. The patient reverted back to a euthyroid state in 4 weeks with conservative management.ConclusionPTT should be considered in the differential diagnosis in patients developing features of thyrotoxicosis following parathyroidectomy. (Endocr Pract. 2014;20:e1-e3)     

Incidence,Risk Factors,and Clinical Implications of Delayed Hypoparathyroidism on Postoperative Day two Following Total Thyroidectomy for Papillary Thyroid Carcinoma

Objective: This study aimed to investigate the incidence rates, risk factors, and clinical implications of delayed hypoparathyroidism on postoperative day 2 (POD-2) after total thyroidectomy in patients with papillary thyroid carcinoma.Methods: This study included 410 patients with normal serum intact parathyroid hormone (iPTH) and calcium levels on postoperative day 1 (POD-1) who were classified into 2 groups according to the presence or absence of delayed hypoparathyroidism on POD-2.Results: Of the 410 patients, 98 experienced delayed hypoparathyroidism on POD-2 (23.9%). The significant risk factors for delayed hypoparathyroidism on POD-2 included female gender, age older than 45 years, central lymph node dissection, increased number of excised lymph nodes, and low POD-1 versus preoperative iPTH ratios. Additionally, delayed hypoparathyroidism on POD-2 was found to be a significant risk factor for hypocalcemia on POD-2 and permanent hypoparathyroidism.Conclusion: Prophylactic calcium supplementation and long-term surveillance for permanent hypoparathyroidism should be considered in patients with risk factors for delayed hypoparathyroidism on POD-2.Abbreviations: CI = confidence interval; iPTH = intact parathyroid hormone; OR = odds ratio; POD-1 = postoperative day 1; POD-2 = postoperative day 2; PTC = papillary thyroid carcinoma; ROC = receiver operating characteristic     

Serum Monocyte Chemokine Protein-1 Levels Before and After Parathyroidectomy in Patients with Primary Hyperparathyroidism

ObjectiveTo investigate the effects of parathyroidectomy on serum monocyte chemokine protein-1 (MCP- 1) levels in patients with primary hyperparathyroidism (PHPT).MethodsForty-three PHPT patients, age 56 ± 12 years, underwent minimally invasive parathyroidectomy. Serum samples were collected at 0 and 15 to 20 minutes after parathyroid adenoma removal. Serum samples were stored at -70°C until time of assay.ResultsIn 40 PHPT patients with a single adenoma, MCP-1 levels decreased from 342 ± 103 to 250 ± 77 pg/ mL (P < .001) 15 to 20 minutes after parathyroid adenoma removal. MCP-1 levels were positively correlated with intact parathyroid hormone (PTH) levels (R = 0.47; P < .01). In 3 PHPT patients with double parathyroid adenoma, MCP-1 levels did not decrease after removal of the first adenoma but decreased 15 to 20 minutes after second adenoma removal.ConclusionOur results provide evidence that the decrease in serum intact PTH due to minimally invasive parathyroidectomy results in an immediate decrease in serum MCP-1 levels. (Endocr Pract. 2014;20:1165-1169)