scholarly journals Severe hypercalcemia caused by parathyroid hormone in a rectal cancer metastasis: a case report

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Vegard Heimly Brun ◽  
Erik Knutsen ◽  
Helge Stenvold ◽  
Hanne Halvorsen
Keyword(s):  
Parathyroid Hormone ◽  
Bone Metastasis ◽  
Cancer Metastasis ◽  
Hormone Secretion ◽  
Rectal Adenocarcinoma ◽  
Intact Parathyroid Hormone ◽  
First Case ◽  
Severe Hypercalcemia ◽  
Colorectal Origin ◽  
Proper Diagnosis

Abstract Background Hypercalcemia of malignancy is relatively common in several cancers. However, in colorectal cancer, paraneoplastic phenomena that cause hypercalcemia is uncommon. In the few cases that are reported, secretion of parathyroid hormone-related peptide mediates the effect. We describe the first case of severe hypercalcemia mediated by intact parathyroid hormone secretion from a bone metastasis of colorectal origin. This was a diagnostic and therapeutic challenge. Case presentation A 68-year-old male treated for rectal adenocarcinoma 10 years earlier developed a bone metastasis. After initial treatment of the metastasis with surgery and irradiation, he developed a relapse with severe hypercalcemia and corresponding elevated parathyroid hormone levels. The workup showed no signs of parathyroid adenomas, but the metastasis produced intact parathyroid hormone. The hypercalcemia was successfully treated by irradiation and osteoclast inhibitor, and the patient received chemotherapy. Survival was 24 months from the onset of hypercalcemia. Conclusions Proper diagnosis of the uncommon endocrine disturbance allowed targeted therapy and avoidance of neck exploration for wrongly suspecting primary hyperparathyroidism. Intact parathyroid hormone should be measured in cases of malignant hypercalcemia.

scholarly journals Severe Hypercalcemia Associated with Hepatocellular Carcinoma Secreting Intact Parathyroid Hormone: A Case Report

2011 ◽  
Vol 50 (4) ◽  
pp. 329-333 ◽  
Author(s):  
Yoko Abe ◽  
Hiroaki Makiyama ◽  
Yomo Fujita ◽  
Yasuhiro Tachibana ◽  
Go Kamada ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Case Report ◽  
Parathyroid Hormone ◽  
Intact Parathyroid Hormone ◽  
Severe Hypercalcemia

Regulation of acute parathyroid hormone release in normal humans: combined calcium and citrate clamp study

1992 ◽  
Vol 263 (2) ◽  
pp. E195-E198 ◽  
Author(s):  
P. Schwarz ◽  
H. A. Sorensen ◽  
I. Transbol ◽  
P. McNair
Keyword(s):  
Steady State ◽  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Ionized Calcium ◽  
Intact Parathyroid Hormone ◽  
Hormone Release ◽  
Hormone Regulation ◽  
Clamp Technique ◽  
Baseline Concentration ◽  
Parathyroid Hormone Release

The objective of the present study was to elucidate the dynamics of parathyroid hormone regulation, with particular reference to the mechanism controlling the acute parathyroid hormone release. Through utilization of the citrate clamp technique and the calcium clamp technique we were able, in a standardized way, to stimulate and suppress the parathyroid hormone secretion. Precise bedside measurements of blood ionized calcium and measurements of intact parathyroid hormone were performed. Twelve healthy young volunteers participated in two trials 6-12 wk apart, a citrate clamp (delta-blood ionized calcium -0.19 mmol/l) and a calcium plus citrate clamp (delta-blood ionized calcium +0.22 mmol/l and -0.19 mmol/l). During the citrate clamp, preceded by normal calcemia, serum intact parathyroid hormone peaked to a maximum after 5-10 min, four to six times above baseline concentration and then declined to a steady state two to three times above baseline concentration. During the citrate clamp, preceded by hypercalcemia induced by a calcium clamp, serum intact parathyroid hormone also peaked immediately to about five to nine times above its suppressed level, approximately two times above the baseline concentration. Subsequently, serum intact parathyroid hormone declined to a steady state just below the baseline concentration. In conclusion, within the range studied, the mechanism eliciting the acute serum intact parathyroid hormone release from its depot is a fall in blood ionized calcium, not the absolute concentration of ionized calcium.

Severe hypercalcaemia from ectopic intact parathyroid hormone secretion treated with continuous renal replacement therapy in a patient with two malignancies

2021 ◽  
Vol 14 (6) ◽  
pp. e242172
Author(s):  
Nathaniel Hocker ◽  
Maria Story ◽  
Alysa Lerud ◽  
Sarat Kuppachi
Keyword(s):  
Parathyroid Hormone ◽  
Renal Replacement Therapy ◽  
Continuous Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Medical Management ◽  
Hormone Secretion ◽  
Intact Parathyroid Hormone ◽  
Poorly Differentiated Adenocarcinoma ◽  
Poorly Differentiated ◽  
Severe Hypercalcaemia

We present a 61-year-old Caucasian woman with endometroid carcinoma as well as a poorly differentiated adenocarcinoma who developed severe hypercalcaemia in the setting of an elevated intact parathyroid hormone. The patient was hospitalised twice for her condition. During her first hospitalisation, she was diagnosed with an endometroid carcinoma and hypercalcaemia. With medical management, she had a normal calcium level on discharge. She presented 3 weeks later with hypercalcaemia and encephalopathy. This time her hypercalcaemia was refractory to medical management, and required continuous renal replacement therapy (CRRT) to normalise her serum calcium. Lung biopsy revealed a poorly differentiated adenocarcinoma, suspicious for pancreatic primary. Due to her poor prognosis, rapid elevation of calcium with each attempt to discontinue CRRT, and the poor options for treatment of her cancers, she elected to pursue hospice care.

Thallium-Technetium Subtraction Scintigraphy of Enlarged Parathyroid Glands after Calcitonin Stimulation of Parathyroid Hormone Secretion

1992 ◽  
Vol 33 (4) ◽  
pp. 319-322 ◽  
Author(s):  
A. Bergenfelz ◽  
J. Tennvall ◽  
B. Ahrén
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Plasma Levels ◽  
Hormone Secretion ◽  
Serum Levels ◽  
Parathyroid Glands ◽  
Preoperative Localization ◽  
Intact Parathyroid Hormone ◽  
Stimulation Of ◽  
Subtraction Scintigraphy

To improve the sensitivity of thallium-technetium subtraction scintigraphy for preoperative localization procedure of enlarged parathyroid glands in primary hyperparathyroidism, we administered calcitonin intramuscularly 4 hours before the scintigraphy in 14 consecutive patients. Injection of calcitonin reduced plasma levels of ionized calcium from 1.47 ± 0.10 mmol/l to 1.41 ± 0.09 mmol/l (p < 0.01). Concomitantly, serum levels of intact parathyroid hormone increased from 6.4 ± 2.5 pmol/l to 7.9 ± 2.6 pmol/l (p < 0.001). The scintigram after calcitonin injection visualized 11 adenomas (sensitivity 78%) compared to only 9 (sensitivity 64%) in conventional scintigrams. In addition, 5 of the adenomas were more distinctly imaged in the scintigram after calcitonin injection, whereas in only one patient was the conventional scintigram better. Thus, the calcitonin injection improved the scintigram in 7 cases and was inferior in only one case (p = 0.031). We conclude that stimulation of parathyroid hormone secretion with calcitonin results in a better preoperative localization of enlarged parathyroid glands in primary hyperparathyroidism.

PARATHYROID HORMONE SECRETION IN DISORDERS OF CALCIUM METABOLISM STUDIED BY MEANS OF EDTA

1974 ◽  
Vol 75 (2) ◽  
pp. 286-296 ◽  
Author(s):  
J. H. Lockefeer ◽  
W. H. L. Hackeng ◽  
J. C. Birkenhäger
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Calcium Metabolism ◽  
Hormone Secretion ◽  
Parathyroid Tissue ◽  
Small Mass ◽  
Idiopathic Hypercalciuria ◽  
List Type ◽  
Immunoreactive Parathyroid Hormone ◽  
Pth Level

ABSTRACT In 22 of 28 cases of primary hyperparathyroidism (PHP) the rise in the serum immunoreactive parathyroid hormone (IRPTH or PTH) level observed in response to lowering of the serum calcium by EDTA, exceeded that obtained in 8 control subjects. In 5 of these 22 patients who were studied again after parathyroidectomy the supranormal response was abolished. Fifteen of these 22 hyper-responsive PHP patients had basal IRPTH levels not exceeding the highest level in the controls and that of other groups of patients investigated (idiopathic hypercalciuria, non-parathyroid hypercalcaemia, operated PHP). Fourteen of the 22 hyper-reactive patients with PHP did not show hypocalcaemia during the infusion of EDTA. The extent of the release of PTH elicited by EDTA in cases of PHP does not as yet allow a prediction of the amount of pathological parathyroid tissue present, although all the PHP patients showing a normal release of PTH had a relatively small mass of parathyroid tissue (up to about 1 g) subsequently removed. In 9 cases of nephrolithiasis (8 of whom had idiopathic hypercalciuria) and in 7 cases of non-parathyroid hypercalcaemia, a normal PTH release was found.

scholarly journals Eosinophilic inflammation promotes CCL6-dependent metastatic tumor growth

2021 ◽  
Vol 7 (22) ◽  
pp. eabb5943
Author(s):  
Fei Li ◽  
Xufei Du ◽  
Fen Lan ◽  
Na Li ◽  
Chao Zhang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Bone Metastasis ◽  
Tumor Cell ◽  
Cancer Metastasis ◽  
Inflammatory Diseases ◽  
Metastatic Tumor ◽  
Eosinophil Infiltration ◽  
Tumor Cell Migration ◽  
Promote Tumor Cell ◽  
Chemokine Ligand

Compelling evidence suggests that inflammatory components contribute to cancer development. However, eosinophils, involved in several inflammatory diseases, were not fully explored in cancer metastasis. We show that airway inflammatory eosinophilia and colonic inflammation with eosinophil infiltration are both associated with increased metastasis in mice. Eosinophilia is responsible for increased bone metastasis in eosinophil-enriched Cd3δ-Il-5 transgenic (Il-5 Tg) mice. We also observe increased eosinophils in the malignant pleural effusion of cancer patients with pleural metastasis. Mechanistically, eosinophils promote tumor cell migration and metastasis formation through secreting C-C motif chemokine ligand 6 (CCL6). Genetic knockout of Ccl6 in Il-5 Tg mice remarkably attenuates bone metastasis. Moreover, inhibition of C-C chemokine receptor 1 (CCR1, the receptor of CCL6) in tumor cells reduces tumor cell migration and metastasis. Thus, our study identifies a CCL6-dependent prometastatic activity of eosinophils, which can be inhibited by targeting CCR1 and represent an approach to preventing metastatic disease.

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