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Calcium Stimulation Test (calcium + stimulation_test)
Selected AbstractsSpurious hypercalcitoninemia in patients with nodular thyroid disease induced by heterophilic antibodiesHEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 1 2010Jung Min Kim MD Abstract Background Serum calcitonin is the most useful tumor marker for the diagnosis and follow-up of medullary thyroid carcinoma (MTC). Spurious hypercalcitoninemia caused by heterophilic antibody interference (HAI) is rarely found in patients without MTC. Methods We studied 2 patients with hypercalcitoninemia and thyroid nodules, but no evidence of MTC on fine-needle aspiration cytology. We performed calcium stimulation tests, measured serum calcitonin with another calcitonin kit, performed dilution tests, and remeasured serum calcitonin after applying heterophilic blocking tubes. Results In a 31-year-old woman with no response to the calcium stimulation test, serum calcitonin was <5 pg/mL using another kit. After we applied heterophilic blocking tubes, the serum calcitonin level decreased to normal range. We concluded that patient had spurious hypercalcitoninemia. In a 63-year-old woman, all tests revealed that the patient had true hypercalcitoninemia. The patient underwent total thyroidectomy that revealed MTC. Conclusions We suggest that patients suspected for spurious hypercalcitoninemia should undergo further investigation due to HAI. © 2009 Wiley Periodicals, Inc. Head Neck, 2010 [source] Clinical features and morphological characterization of 10 patients with noninsulinoma pancreatogenous hypoglycaemia syndrome (NIPHS)CLINICAL ENDOCRINOLOGY, Issue 5 2006Justin G. S. Won Summary Objective, Noninsulinoma pancreatogenous hypoglycaemia syndrome (NIPHS), characterized by postprandial neuroglycopaenia, negative prolonged fasts and negative perioperative localization studies for insulinoma, but positive selective arterial calcium stimulation tests and nesidioblastosis in the gradient-guided resected pancreas, is a rare hypoglycaemic disorder of undetermined aetiology. We analysed the clinical, morphological and immunohistological features to further clarify the aetiology and pathogenesis of this rare disease. Patients, Ten consecutive patients with NIPHS (nine men and one woman, aged 29,78 years) were included in the study. Six of the 10 received a gradient-guided subtotal (70%) or distal (50%) pancreatectomy. In the remaining four patients, diazoxide treatment was initiated and the precise mechanism of its action was assessed by meal tests. Results, All of the patients showed a combination of postprandial neuroglycopaenia, negative prolonged fasts (except one patient) and negative localization studies for insulinoma, but positive calcium stimulation tests and nesidioblastosis in the gradient-guided resected pancreas. Immunohistological studies of the resected pancreatic tissues revealed neither an increased rate of proliferation of ,-cells nor an abnormal synthesis and/or processing of either proinsulin or amylin. Evidence of overexpression of the two pancreatic differentiation factors, PDX-1 and Nkx-6·1, as well as the calcium sensing receptor (CaSR) was absent. Nevertheless, abnormal expression of islet neogenesis-associated protein (INGAP), a human cytokine expressed only in the presence of islet neogenesis, in ducts and/or islets, was identified in three of the five patients studied. All of the six patients who received a surgical operation were relieved of further neuroglycopaenic attacks, but one patient who received a subtotal pancreatectomy developed diabetes. In the remaining four patients who received diazoxide treatment, hypoglycaemic episodes were satisfactorily controlled with an attenuated response of ,-cell peptides to meal stimulation. Conclusions, Our results strengthen the existence of this unique clinical hypoglycaemic syndrome from ,-cell hyperfunction as well as the value of the selective arterial calcium stimulation test in its correct diagnosis and localization. The mechanisms underlying ,-cell hyperfunction and release of insulin to calcium, however, remain poorly characterized. Nevertheless, in a subset of patients with NIPHS, there exists some, as yet undefined, pancreatic humoral/paracrine factor(s) other than proinsulin, amylin, PDX-1, Nkx-6·1 and possibly glucagon-like peptide-1 (GLP-1) that are capable of inducing the INGAP gene and, if activated, will initiate ductal proliferation and islet neogenesis. As for the treatment, we recommend that diazoxide be tried first in each patient and, should it fail, a gradient-guided subtotal or distal pancreatectomy be attempted. [source] Spurious hypercalcitoninemia in patients with nodular thyroid disease induced by heterophilic antibodiesHEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 1 2010Jung Min Kim MD Abstract Background Serum calcitonin is the most useful tumor marker for the diagnosis and follow-up of medullary thyroid carcinoma (MTC). Spurious hypercalcitoninemia caused by heterophilic antibody interference (HAI) is rarely found in patients without MTC. Methods We studied 2 patients with hypercalcitoninemia and thyroid nodules, but no evidence of MTC on fine-needle aspiration cytology. We performed calcium stimulation tests, measured serum calcitonin with another calcitonin kit, performed dilution tests, and remeasured serum calcitonin after applying heterophilic blocking tubes. Results In a 31-year-old woman with no response to the calcium stimulation test, serum calcitonin was <5 pg/mL using another kit. After we applied heterophilic blocking tubes, the serum calcitonin level decreased to normal range. We concluded that patient had spurious hypercalcitoninemia. In a 63-year-old woman, all tests revealed that the patient had true hypercalcitoninemia. The patient underwent total thyroidectomy that revealed MTC. Conclusions We suggest that patients suspected for spurious hypercalcitoninemia should undergo further investigation due to HAI. © 2009 Wiley Periodicals, Inc. Head Neck, 2010 [source] Clinical features and morphological characterization of 10 patients with noninsulinoma pancreatogenous hypoglycaemia syndrome (NIPHS)CLINICAL ENDOCRINOLOGY, Issue 5 2006Justin G. S. Won Summary Objective, Noninsulinoma pancreatogenous hypoglycaemia syndrome (NIPHS), characterized by postprandial neuroglycopaenia, negative prolonged fasts and negative perioperative localization studies for insulinoma, but positive selective arterial calcium stimulation tests and nesidioblastosis in the gradient-guided resected pancreas, is a rare hypoglycaemic disorder of undetermined aetiology. We analysed the clinical, morphological and immunohistological features to further clarify the aetiology and pathogenesis of this rare disease. Patients, Ten consecutive patients with NIPHS (nine men and one woman, aged 29,78 years) were included in the study. Six of the 10 received a gradient-guided subtotal (70%) or distal (50%) pancreatectomy. In the remaining four patients, diazoxide treatment was initiated and the precise mechanism of its action was assessed by meal tests. Results, All of the patients showed a combination of postprandial neuroglycopaenia, negative prolonged fasts (except one patient) and negative localization studies for insulinoma, but positive calcium stimulation tests and nesidioblastosis in the gradient-guided resected pancreas. Immunohistological studies of the resected pancreatic tissues revealed neither an increased rate of proliferation of ,-cells nor an abnormal synthesis and/or processing of either proinsulin or amylin. Evidence of overexpression of the two pancreatic differentiation factors, PDX-1 and Nkx-6·1, as well as the calcium sensing receptor (CaSR) was absent. Nevertheless, abnormal expression of islet neogenesis-associated protein (INGAP), a human cytokine expressed only in the presence of islet neogenesis, in ducts and/or islets, was identified in three of the five patients studied. All of the six patients who received a surgical operation were relieved of further neuroglycopaenic attacks, but one patient who received a subtotal pancreatectomy developed diabetes. In the remaining four patients who received diazoxide treatment, hypoglycaemic episodes were satisfactorily controlled with an attenuated response of ,-cell peptides to meal stimulation. Conclusions, Our results strengthen the existence of this unique clinical hypoglycaemic syndrome from ,-cell hyperfunction as well as the value of the selective arterial calcium stimulation test in its correct diagnosis and localization. The mechanisms underlying ,-cell hyperfunction and release of insulin to calcium, however, remain poorly characterized. Nevertheless, in a subset of patients with NIPHS, there exists some, as yet undefined, pancreatic humoral/paracrine factor(s) other than proinsulin, amylin, PDX-1, Nkx-6·1 and possibly glucagon-like peptide-1 (GLP-1) that are capable of inducing the INGAP gene and, if activated, will initiate ductal proliferation and islet neogenesis. As for the treatment, we recommend that diazoxide be tried first in each patient and, should it fail, a gradient-guided subtotal or distal pancreatectomy be attempted. [source] |