An Unusual Case of Recurrent Hyperparathyroidism and Papillary Thyroid Cancer

ObjectiveTo report an unusual occurrence of recurrent hyperparathyroidism due to papillary thyroid carcinoma.MethodsWe describe the clinical history, physical examination findings, laboratory values, imaging findings, and pathologic findings of a woman who developed recurrent hyperparathyroidism 13 years after successful parathyroidectomy.ResultsA 59-year-old woman presented to our clinic with recurrent primary hyperparathyroidism. In 1994, she presented with nephrolithiasis and underwent resection of a right superior parathyroid adenoma that resulted in clinical and biochemical cure. Her clinical course had been followed at periodic intervals, and she had been symptom-free and normocalcemic. In 2007, she again developed nephrolithiasis and was documented to have recurrent hyperparathyroidism. Imaging studies suggested a parathyroid adenoma near the right inferior pole of the thyroid. The patient had reoperative neck exploration. No obvious parathyroid adenoma was found and a right thyroid lobectomy was performed, which resulted in normalization of intraoperative intact parathyroid hormone levels, and the incision was closed. Final pathology demonstrated no parathyroid adenoma, but instead, a 1-cm papillary thyroid carcinoma that stained positive for parathyroid hormone. More than 6 months after surgery, she remains clinically and biochemically cured.ConclusionsRecurrent hyperparathyroidism occurs secondary to multiple causes. This case demonstrates the challenge a surgeon faces in managing recurrent disease and highlights a rare phenomenon of papillary thyroid cancer causing recurrent hyperparathyroidism. (Endocr Pract. 2009;15:349-352)     

Three large, functioning cystic parathyroid adenomas

ObjectiveTo report a very rare case of 3 large, functioning cystic parathyroid adenomas causing primary hyperparathyroidism.MethodsWe present the history, clinical findings, laboratory test results, radiologic findings, endocrine workup results, intraoperative surgical challenges, and surgical pathology report of the study patient. We review the literature and discuss the importance of intraoperative parathyroid hormone (PTH) measurement in such cases.ResultsA 79-year-old woman presented with primary hyperparathyroidism and elevated levels of calcium and PTH. Localization studies confirmed the presence of a large right upper parathyroid adenoma. On exploration, a very large cystic parathyroid gland was identified at that location. Because intraoperative PTH levels remained elevated, further exploration was pursued, which revealed 2 more large cystic glands on the left side that were resected. This resulted in an adequate but slow PTH drop. The right lower gland appeared normal. On follow-up 4 days and 6 weeks after surgery, the calcium and PTH levels had normalized.ConclusionThis case highlights the aspects of intraoperative PTH use and underscores the need to exclude multigland disease even in the setting of a very large parathyroid cyst with concordant localization studies. (Endocr Pract. 2012;18:e14-e16)     

Parathyroid adenoma with coeliac disease: primary or quaternary hyperparathyroidism?

Coeliac disease is a gluten-sensitive enteropathy of varying severity. Osteomalacia and hypocalcaemia can result from malabsorption of vitamin D and calcium, which, in turn, can lead to secondary hyperparathyroidism. If coeliac disease remains untreated for long, tertiary hyperparathyroidism can also develop through autonomy of the parathyroid glands via chronic stimulation. Primary hyperparathyroidism also has been reported in some cases of coeliac disease. We report the case of an adolescent with coeliac disease presenting with severe hypercalcaemia from a parathyroid adenoma. A 14 year-old girl was admitted to our department for delayed puberty and growth retardation. Laboratory examination revealed iron deficiency anaemia, low 25OH vitamin D level (7 ng/ml), high parathyroid hormone level (PTH) (955 pg/ml), and hypercalcaemia (13.4 mg/dl). Endoscopic biopsy was compatible with gluten enteropathy. Endomysium antibody was positive. A gluten-free diet was started. Her calcium returned to normal after excision of the parathyroid adenoma. After four months of the gluten-free diet, she began to mature, and puberty began with development of breasts and axillary-pubic hair growth. It has been suggested that autonomous four-gland hyperplasia or tertiary hyperparathyroidism may progress to adenoma formation, and that this should be termed "quaternary hyperparathyroidism". More studies are required to explain the relationship between coeliac disease and hyperparathyroidism.     

Suppressibility of Parathyroid Hormone in Primary Hyperparathyroidism

ObjectiveTo describe an unusual case of pathologically confirmed primary hyperparathyroidism in a patient presenting with severe hypercalcemia and an undetectable parathyroid hormone (PTH) level.MethodsWe present a detailed case report and outline the serial laboratory findings. In addition, the possible causes of low serum PTH levels in the setting of primary hyperparathyroidism are discussed.ResultsA 16-year-old female patient presented with severe epigastric pain, found to be attributable to acute pancreatitis. At hospital admission, her serum calcium concentration was high (14.0 mg/dL); the patient also had a normal serum phosphorus level of 3.6 mg/dL and an undetectable PTH level (< 0.2 pmol/L). An evaluation for non-PTH-mediated causes of hypercalcemia revealed a partially suppressed thyroid-stimulating hormone concentration and a below normal 1,25-dihydroxyvitamin D level, consistent with her suppressed PTH. One week after the patient was dismissed from the hospital, repeated laboratory studies showed a serum calcium value of 11.1 mg/dL, a serum phosphorus level of 2.8 mg/dL, and an elevated PTH concentration of 11.0 pmol/L, consistent with primary hyperparathyroidism. A repeated 1,25-dihy-droxyvitamin D measurement was elevated. A parathyroid scan showed a parathyroid adenoma in the left lower neck area, and she subsequently underwent successful surgical resection of a pathologically confirmed parathyroid adenoma.ConclusionThis case demonstrates that the serum PTH level can be suppressed in patients with primary hyperparathyroidism. Moreover, it emphasizes the need for careful evaluation of the clinical context in which the PTH measurement is determined. Consideration should be given to repeating measurement of PTH and serum calcium levels when the initial laboratory evaluation of hypercalcemia is unclear because dynamic changes in calcium metabolism may occur in the presence of secondary contributing factors. (Endocr Pract. 2007;13:785-789)     

Unusual Manifestation of Parathyroid Carcinoma in the Setting of Papillary Thyroid Cancer

ObjectiveTo describe a rare manifestation of parathyroid carcinoma in association with papillary thyroid carcinoma.MethodsWe describe the clinical history, findings on physical examination, results of laboratory studies, imaging findings, and histopathologic features of a woman with 2 previously palpable thyroid nodules and mild hypercalcemia.ResultsA 79-year-old woman presented to our endocrinology clinic for reevaluation of 2 thyroid nodules and long-standing hyperparathyroidism. She initially had undergone assessment 6 years previously, at which time an intact parathyroid hormone level was 89 pg/mL (reference range, 10 to 69) and the serum calcium concentration was 10.4 mg/dL (reference range, 8.2 to 10.2) in conjunction with normal alkaline phosphatase, creatinine, and 25-hydroxyvitamin D levels. Subsequently, she was found to have multifocal papillary thyroid cancer in the right thyroid lobe and a 5-cm parathyroid carcinoma in the left side.ConclusionSynchronous parathyroid and thyroid carcinomas are extremely rare. To our knowledge, our current case is the first documented patient with parathyroid carcinoma who had a clinical presentation consistent with longstanding mild adenoma in addition to synchronous papillary thyroid carcinoma. (Endocr Pract. 2010;16:664-668)     

Recombinant Human Parathyroid Hormone Therapy (1-34) In an Adult Patient with a Gain-of-Function Mutation in the Calcium-Sensing Receptor-a Case Report

ObjectiveTo describe a case of hypocalcemia in a patient with a gain-of-function mutation in the calcium-sensing receptor that was undetected until adulthood and successfully treated with recombinant parathyroid hormone.MethodsThe clinical findings, laboratory data, and a review of the pertinent literature are presented.ResultsA 55-year-old woman was hospitalized and seen by the endocrinology consult service for hypocalcemia that was refractory to repeated doses of intravenous calcium gluconate. She expressed concern about chronic leg muscle cramps and paresthesias of the lips and fingertips. In addition, she had no history of neck surgery, neck irradiation, or any autoimmune disease. She was a well-appearing female with no dysmorphic features or skin changes. Laboratory tests revealed hypocalcemia, hyperphosphatemia, hypomagnesemia, and hypovitamino-sis D. Her parathyroid hormone concentration (PTH) was low at 14.2 pg/mL. Her PTH and calcium concentrations remained low despite repletion of magnesium and treatment with calcitriol and oral calcium replacement. A 24-hour collection for urinary calcium showed inappropriate hypercalciuria. Medical records showed her hypocalcemia to be chronic. Additionally, several family members had also complained of muscle cramps. A congenital cause of her hypoparathyroidism was considered, and genetic testing confirmed heterozygosity for a gain-of-function mutation in the calcium-sensing receptor gene associated with autosomal dominant familial isolated hypoparathyroidism (ADH). Treatment with subcutaneous recombinant human parathyroid hormone teriparatide (rhPTH [1-34]) 20 mcg twice daily for three days normalized her calcium and phosphorus concentrations.ConclusionrhPTH (1-34) is an effective treatment for patients with hypoparathyroidism due to gain-of-function mutations in the calcium-sensing receptor. ADH can be insidious in presentation and the diagnosis can be missed unless there is a high index of suspicion. (Endocr Pract. 2013;19:e24-e28)     

Mediastinal parathyroid carcinoma: a case report

A 72 year-old woman with primary hyperparathyroidism was operated for parathyroid crisis. PTH serum level was 808 pg/mL. During the operation, only two superior parathyroid glands were found. One was normal, and hypertrophy was revealed in the other. After the surgical procedure, PTH serum level was 726.5 pg/mL. Helical computer tomography examination showed a heterogeneous mass in the anterior mediastinum. The tumour was removed via a sternotomy approach. Histopathological examination revealed parathyroid carcinoma. PTH level dropped to 5.74 pg/mL. Cytofluorometric examination revealed diploidy (DI = 1) in both the hypertrophic and the unchanged upper glands, whereas parathyroid cancer was aneuploid. After the initial operation, the woman was discharged from the hospital on the 27th postoperative day. One year after surgical procedures, she is well. She has to take calcium.     

Unusual Case of Calciphylaxis Associated with Primary Hyperparathyroidism Without Coexistent Renal Failure

ObjectiveTo report a case of calciphylaxis in a patient with primary hyperparathyroidism without coexistent renal failure.MethodsThe clinical, laboratory, and radiographic details of this case are reviewed, and the pathogenesis of calciphylaxis and the associated prognosis are discussed.ResultsA 52-year-old woman had progressive fatigue, cachexia, severe osteoporosis, and necrotizing skin lesions. Her serum calcium level was 16 mg/dL, serum phosphorus level was 2.13 mg/dL, and parathyroid hormone level was 2,257 pg/mL (reference range, 15 to 65). On physical examination, gangrenous skin lesions with black crusts were noted on her legs, abdomen, and gluteal region. A mass lesion was detected in the parathyroid region by both ultrasonography and a parathyroid scan. The patient underwent a bilateral neck exploration, and a parathyroid adenoma measuring 3.5 by 1.5 by 1.2 cm was found on pathologic examination. After the operation, biochemical findings normalized, and the skin lesions progressively improved.ConclusionSevere primary hyperparathyroidism may be a factor leading to calciphylaxis, even in the absence of renal failure and a high calcium-phosphate product. This potentially life-threatening condition should not be left untreated if the levels of serum calcium and parathyroid hormone are severely elevated. (Endocr Pract. 2008;14:368-372)     

Calcium,Parathyroid Hormone,and Vitamin D in Patients with Primary Hyperparathyroidism: Normograms Developed from 10000 Cases

ObjectiveTo better define the typical and atypical biochemical profiles of patients with surgically proven primary hyperparathyroidism.MethodsIn this single-center, prospectively conducted study of consecutive patients with surgically proven primary hyperparathyroidism over a 7-year period, we analyzed serum calcium, parathyroid hormone, and 25-hydroxyvitamin D concentrations.ResultsA total of 10 000 patients were included, and more than 210 000 calcium, parathyroid hormone, and 25-hydroxyvitamin D values were evaluated. Both calcium and parathyroid hormone levels demonstrated a Gaussian distribution with the average calcium concentration being 10.9 ± 0.6 mg/dL and the average parathyroid hormone concentration being 105.8 ± 48 pg/mL. The average highest calcium and parathyroid hormone concentrations were 11.4 ± 0.7 mg/dL and 115.3 ± 50 pg/mL, respectively. At least 1 calcium value of 11.0 mg/dL was seen in 87% of patients, but only 21% had 1 or more calcium value above 11.5 mg/dL. Only 7% had a single serum calcium level reaching 12.0 mg/dL. Normocalcemic hyperparathyroidism was seen in just under 3% of patients who had identical findings at surgery. An average parathyroid hormone concentration less than 65 pg/mL was seen in 16%, with 10% of patients who had no high parathyroid hormone values. The average 25-hydroxyvitamin D concentration was 22.4 ± 9 ng/mL, with levels decreasing as calcium levels increased (P < .001); 36% had 25-hydroxyvitamin D levels below 20 ng/mL.ConclusionsPatients with PHPT present with a number of distinct biochemical profiles, but as a group, they present with a near-normal Gaussian distribution of both calcium and parathyroid hormone levels. Either serum calcium or parathyroid hormone remained normal in 13% of patients, yet the findings at surgery are similar to those of patients with elevated calcium or parathyroid hormone. Low 25-hydroxyvitamin D is an expected finding in patients with PHPT, decreasing as serum calcium levels increase. (Endocr Pract. 2011;17:384-394)     

Hypocalcaemic Primary Hyperparathyroidism

A patient with many symptoms and signs of primary hyperparathyroidism had hypocalcaemia when first seen. Bone section histology showed osteomalacia and osteitis fibrosa, and the hyperparathyroidism at this stage was considered to be secondary to osteomalacia with postgastrectomy steatorrhoea. On treatment with vitamin D (with disappearance of her bone pains and weakness) she developed hypercalcaemia. She regained her health after removal of a 6-g. parathyroid adenoma. Normal histology was shown in another parathyroid gland.We believe that the initial hypocalcaemia was due to vitamin-D deficiency, which produced ineffective hyperparathyroidism until it was corrected. A review of the few reports of patients with autonomous hyperparathyroidism with steatorrhoea and osteomalacia does not support the argument that these patients had “tertiary” disease. It suggests that most of them, like our patient, had primary hyperparathyroidism.     

Severe Primary Hyperparathyroidism Masked by Asymptomatic Celiac Disease

ObjectiveTo present a case that illustrates the importanceof considering asymptomatic celiac disease (CD) asa possible underlying cause in some cases of normocal-cemicprimary hyperparathyroidism.MethodsWe describe the clinical presentation, man-agement,and outcome of a case of severe primary hyper-parathyroidism manifesting with normocalcemia, likely attributable to the presence of asymptomatic CD.ResultsA 24-year-old woman presented with a 5- year history of generalized weakness, which had progressed until use of a wheelchair became necessary. She also had sustained low-trauma fragility fractures of the right tibia and left femur. She had no symptoms suggestive of CD. Physical examination revealed severe proximal myopathy. Laboratory data (and reference ranges) were as follows: serum calcium, 2.34 mmol/L (2.1 to 2.6); phosphorus, 0.91 mmol/L (0.90 to 1.50); alkaline phosphatase, 421 U/L (40 to 135); albumin, 37 g/L (35 to 45); parathyroid hormone, 874 ng/L (15 to 65); urine calcium, 3.76 mmol/d (2.5 to 8); and 25-hydroxyvitamin D, < 13 nmol/L (22 to 116). She was treated with increasing doses of calcitriol, ergocalciferol, and calcium carbonate, but the serum calcium concentration did not increase substantially (reaching a maximum of 2.70 mmol/L on suprapharmacologic doses of these agents). Malabsorption was considered as an explanation for this apparent resistance to these medications. The result of antibody screening for CD was highly positive, and a distal duodenal biopsy confirmed the diagnosis of CD. A technetium Tc 99m sestamibi scan revealed uptake in the neck that was consistent with a single parathyroid adenoma, which was surgically removed. Treatment with a gluten-free diet, calcium carbonate, and ergocalciferol yielded remarkable clinical, biochemical, and radiologic improvementConclusionAsymptomatic CD may be the underlyingcause for some cases of normocalcemic primaryhyperparathyroidism, and it should be considered in thissetting. (Endocr Pract. 2008;14:347-350)     

A case of normocalcemic primary hyperparathyroidism with osteomalacia

A 59 year-old patient had lumbago and pain in hip joints, knees, and ribs of long duration. Severe hypophosphatemia and high serum ionized calcium were found in spite of normal level of total serum calcium. The serum parathyroid hormone and alkaline phosphatase levels were elevated, and diffuse demineralization of the bones and renal stones were found by x-ray examination. Parathyroid adenoma was diagnosed from the subtraction image of the 99mTc O-4 and 201Tl-Cl2 scintigrams. Osteomalacia was demonstrated by bone biopsy at the right iliac crest. A right lower parathyroid adenoma of 2.0 X 1.8 cm, weighing 4.0 g was removed. The long standing phosphate depletion and hypophosphatemia, due to hyperparathyroidism causing renal damage with nephrocalcinosis and reduced synthesis of active vitamin D, and milk tolerance due to gastroduodenostomy were probably responsible for producing the clinical picture of normocalcemic hyperparathyroidism complicated with osteomalacia.     

Primary Hyperparathyroidism: Comparing Between Solid and Cystic Adenomas and the Efficacy of Ultrasound and Single-Photon Emission Computed Tomography in their Diagnosis

Objective: Primary hyperparathyroidism (PHPT) is a disorder that results from abnormal functioning of the parathyroid glands. The purpose of this study was to compare cystic and solid adenomas by analyzing different variables associated with PHPT and parathyroid adenomas (age, calcium, phosphorus, and parathyroid hormone &lsqb;PTH] levels, adenoma volume) while comparing the efficacy of ultrasound and single-photon emission computed tomography in differentiating between both types of adenoma.Methods: From 152 patients diagnosed with PHPT between January 2013 and 2014, only 109 patients who had positive ultrasonographic findings for single parathyroid adenoma were included in the study.Results: A total of 26 patients had cystic adenomas and 83 patients had solid adenomas. Sestamibi (MIBI) was negative in 50% of the cystic adenoma group and 27.7% of the solid adenoma group, with an overall technetium-MIBI efficacy of 67%. Age, phosphorus level, and adenoma volume were significantly higher in patients with cystic adenomas (P = .001, P = .02, and P = .02, respectively), whereas calcium and PTH levels were significantly higher in patients with solid adenomas (P = .02, P = .038, respectively). MIBI had a significant correlation with PTH levels (P = .031) and adenoma volume (P = .05) only in patients with solid adenomas. No significant correlation was found between sex and type of parathyroid adenoma.Conclusion: The current study is the first to compare age, PTH levels, and adenoma volume between cystic and solid adenoma patients, providing more information for the poorly understood pathology of cystic adenomas. Our findings showed that age and calcium and PTH levels are significantly higher in patients with solid adenomas, whereas adenoma volume and phosphorus levels are significantly higher in patients with cystic adenomas.Abbreviations: BMD = bone mineral density GFR = glomerular filtration rate iPTH = intact parathyroid hormone MIBI = sestamibi PHPT = primary hyperparathyroidism PTH = parathyroid hormone SPECT = single-photon emission computed tomography Tc = technetium US = ultrasound     

Ultrasound-guided fine needle aspiration cytology of parathyroid lesions. A review of 72 cases

OBJECTIVE: To elucidate the specific cytomorphologic patterns and diagnostic pitfalls in fine needle aspiration cytology (FNAC) of parathyroid lesions. STUDY DESIGN: Seventy-two cases of surgically excised and pathologically verified hyperparathyroidism (20 cases of parathyroid hyperplasia, 51 of parathyroid adenoma and one of parathyroid carcinoma) received preoperative, ultrasound-guided FNAC examination for enlarged parathyroid glands. The smears were reviewed and analyzed. RESULTS: Parathyroid lesions were diagnosed cytologically in 60 cases (83.3%). The presence of colloidlike substance, macrophages or follicular structures in smears led to six cases (8.3%) being misinterpreted as thyroid lesions. The cellularity of the smears was insufficient for interpretation in six cases (8.3%); however, two of these cases were diagnosed by determination of parathyroid hormone (PTH) levels in the fluid. Parathyroid hyperplasia had more tightly cohesive cell clusters with monomorphism, while parathyroid adenoma had more dispersed or loosely cohesive cells with pleomorphism and anisokaryosis. High PTH concentration in an aspirate was noted in all four cases of cystic lesions.     

Synchronous Parathyroid Carcinoma,Parathyroid Adenoma,and Papillary Thyroid Carcinoma in a Patient with Severe and Long-Standing Hyperparathyroidism

ObjectiveTo describe a patient presenting with the rare constellation of synchronous parathyroid carcinoma, parathyroid adenoma, and papillary thyroid carcinoma.MethodsWe summarize the clinical presentation, diagnostic work-up, surgical management, and pathologic features of our patient and review the pertinent literature.ResultsThe patient was a 59-year-old man who presented with severe clinical manifestations of long-standing primary hyperparathyroidism, a serum calcium concentration of 14.4 mg/dL, and a parathyroid hormone level of 2,023 pg/mL. He was found to have a 3.4-cm parathyroid carcinoma on the left side and a 3.2-cm papillary carcinoma in the right thyroid lobe. In addition, a 917-mg parathyroid adenoma was found on the right side.ConclusionSynchronous parathyroid and thyroid carcinomas are extremely rare. To our knowledge, our patient is the first documented case with a parathyroid adenoma in addition to synchronous parathyroid and thyroid carcinomas. The presence of concurrent parathyroid carcinoma and parathyroid adenoma can cause diagnostic confusion and should be considered in patients presenting with severe hyperparathyroidism. Any concomitant thyroid nodules must be investigated to rule out thyroid carcinoma. (Endocr Pract. 2009;15:463-468)     

Prolonged Vitamin D Intoxication in a Patient with Hypoparathyroidism

Pitfalls in the management of hypoparathyroidism are illustrated by the case of a patient who developed hypervitaminosis D while receiving doses of calciferol and of calcium in amounts commonly recommended for treatment. Either the patient was very slow to obtain maximum vitamin D effect or else her sensitivity to vitamin D increased, because she did not become hypercalcemic until two years after treatment was started. The dose of vitamin D was halved to 50,000 units per day and the dose of calcium was lowered to 0.26 g. daily. She failed to remain under medical supervision for the next four years and presented with hypercalcemia and evidence of renal impairment. After vitamin D was discontinued she remained hypercalcemic for nine months.These findings are discussed in the light of current knowledge concerning the actions of parathyroid hormone and vitamin D. The influence of adrenocortical hormones on calcium metabolism is considered. The need to follow up hypoparathyroid patients closely, and to check the level of calcium in the serum, is emphasized.     

Evaluation of the parathyroid function in six patients with hypophosphatemic osteomalacia,including a case of tertiary hyperparathyroidism developing during combined oral phosphate and vitamin D therapy

AIM: To describe a case of tertiary hyperparathyroidism after long-term phosphate and vitamin D therapy and the retrospective evaluation of parathyroid function in 6 patients with hypophosphatemic osteomalaica. METHODS: We evaluated the parathyroid function by measuring iPTH before and during treatment and divided the patients into normal and elevated serum iPTH groups. RESULTS: In the normal serum iPTH group, the 4 patients were all males, whereas the 2 patients in the elevated serum iPTH group were females. Clinical characteristics and biochemical results showed no differences between the two groups. One of the women with an elevated iPTH level (224 pg/ml) had a normal serum calcium level and no evidence of increasing parathyroid uptake by (99m)Tc-MIBI scan 52 months after treatment. The other woman also had an elevated iPTH level (483 pg/ml) and a normal serum calcium level 56 months after treatment. However, in this latter case both her iPTH (1,447 pg/ml) and serum calcium (11.3 mg/dl) levels were elevated 113 months after treatment, when a (99m)Tc-MIBI scan showed increased uptake in all four parathyroid glands during early and delayed phases of the scan. Parathyroidectomy was performed after the diagnosis of tertiary hyperparathyroidism was made, and the histological findings showed adenomatous hyperplasia. CONCLUSIONS: Our findings indicate that even with vitamin D therapy, long-term phosphate therapy may lead to the development of secondary or tertiary hyperparathyroidism in hypophosphatemic osteomalacia and, therefore, suggest that it is important to carefully monitor the parathyroid function during therapy in those with hypophosphatemic osteomalacia.     

A rare association of hyperparathyroidism and Turner's syndrome--a case report

We present the clinical, laboratory, radiological and pathological findings in the case and review the literature. Our patient, a 37-year-old woman of short stature, was referred because of musculoskeletal pain. After primary evaluation, she underwent treatment with calcium and vitamin D supplement with the diagnosis of osteomalacia in Turner's syndrome. The rise of serum calcium during medical therapy, which was an unusual finding, attracted the clinician's attention to another underlying disorder. Further evaluation revealed primary hyperparathyroidism due to an adenoma of the parathyroid gland. Even though this is a rare diagnosis, its presence should be considered in any patient with Turner's syndrome presenting with severe osteoporosis and a rise in serum calcium during treatment.     

Relationship of parathyroid adenoma volume and biochemical function

We retrospectively studied data of 24 patients with surgically proven hyperparathyroidism to determine whether biochemical function correlated with the calculated volume of parathyroid adenoma. Carboxyl-terminal parathyroid hormone (C-PTH), amino-terminal parathyroid hormone (N-PTH), nephrogenous cyclic AMP (N-CAMP), and other markers of calcium metabolism were measured with standard techniques. Tumors were divided into small (less than 1.0 cm3) or large (greater than or equal to 1.0 cm3) sizes. N-PTH and C-PTH measurements were increased in 10% and 30% of patients with small tumors and in 71 and 78% of patients with large tumors. Serum calcium, N-CAMP, C-PTH and N-PTH tended to be greater with large tumors, but only C-PTH was significant. We concluded that the size of parathyroid adenoma influenced biochemical measurements of its activity and that the measurements of PTH in patients with small tumors are not as sensitive as those in patients with large tumors.     

Asymptomatic Primary Hyperparathyroidism Exists in North India: Retrospective Data from 2 Tertiary Care Centers

Objective: Primary hyperparathyroidism (PHPT) has evolved into an asymptomatic disease in the west. In contrast, classic symptoms of PHPT have been reported to be common in the east. Here we describe clinical and biochemical profiles of patients diagnosed with PHPT between 2009 and 2012.Methods: This was a retrospective study conducted at 2 tertiary care centers in north India. All patients who underwent evaluation and surgery for primary hyperparathyroidism (PHPT) from January 2009 to December 2012 were included.Results: A total of 50 patients were studied between 2009 and 2012. Among them 31 (62%) were symptomatic and 19 (38%) were asymptomatic. The mean age (SD) was 48.3 (15.8) years, and the female to male ratio was 1.9:1. None of the patients had brown tumors or bone deformities. The asymptomatic group had significantly lower median adenoma weight (0.57 vs. 3.4 g, P<.05), a higher mean age (57.3 vs. 42.8 years, P<.05), and a lower median intact parathyroid hormone (iPTH) level (254.5 vs. 295 pg/mL, P<.05) compared to the symptomatic group. Adenoma weight was positively correlated with baseline serum calcium, iPTH, and alkaline phosphatase (ALP) levels.Conclusion: The asymptomatic form of PHPT was found in a significant percentage of north Indian patients in this study. Asymptomatic PHPT patients were older in age and had lower parathyroid adenoma weights and iPTH levels compared to symptomatic PHPT patients. Positive correlations were found between parathyroid adenoma weight and serum calcium, iPTH, and ALP levels.Abbreviations: ALP = alkaline phosphatase iPTH = intact parathyroid hormone MIBI = 2-methoxyisobutylisonitrile 25(OH)D = 25-hydroxyvitamin D3 PHPT = primary hyperparathyroidism PTH = parathyroid hormone