Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypercalcaemia in squamous cancer of head and neck is not uncommon. Atypical symptoms make the diagnosis difficult. Immediate therapeutic intervention is necessary to prevent life-threatening complications. The causes include dietary calcium excess, vitamin-D-intoxication, bone metastasis and primary hyperparathyroidism. The paraneoplastic syndrome of ectopic hyperparathyroidism leading to the hypercalcaemia syndrome is induced by several different hormones. Ectopic production of parathyroid hormone or similar substances, increased synthesis of prostaglandins and vitamin-D-like steroids are proposed. Two typical cases are demonstrated.
HNO 1986 Mar
PMID:[Tumor-associated hypercalcemia syndrome in patients with squamous cell carcinomas of the head and neck. Differential diagnosis of a paraneoplastic syndrome]. 370 Jan 42

Nitric oxide (NO) is a novel gaseous intercellular transmitter thought to play important physiological roles in the regulation of blood flow and hormone secretion in, for example, the pituitary, the thyroid, and the endocrine pancreas. Whether nitric oxide synthase (NOS) is present in the human parathyroid glands has not yet been demonstrated. In the present study, histologically normal, but functionally suppressed human parathyroid glands and parathyroid adenomas from patients with primary hyperparathyroidism were investigated by immunocytochemistry with antibodies against neuronal NOS and by reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemistry. We also used H&E to identify the NOS-immunoreactive cells. Immunocytochemistry demonstrated the presence of neuronal-type NOS in a subpopulation of glandular cells, identified as oxyphilic cells, in both normal parathyroid glands and adenomas. NADPH-diaphorase staining visualized NOS in the endothelium of blood vessels and in glandular cells, corresponding to those containing immunoreactive NOS. In addition, we found NADPIH-diaphorase staining in many chief cells. Our results indicate that both glandular cells and vascular endothelium in human parathyroid glands and adenomas express NOS. There is thus a morphological substrate for locally produced NO that may be involved in the regulation of parathyroid blood flow and hormone secretion.
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PMID:Nitric Oxide Synthase in Human Parathyroid Glands and Parathyroid Adenomas. 1211 33

Brown tumors are focal bone lesions caused by an increased osteoclastic activity and fibroblastic proliferation within a primary or more rarely secondary hyperparathyroidism. They are named after their typical brown hemorrhagic stroma with its also typical giant cell formations. We report the case of a 31-year-old pregnant patient with a rapidly growing tumor of her left maxilla whose first symptoms during pregnancy mimicked chronic sinusitis. After swelling of the cheek, diplopia, and recurrent epistaxis appeared, she was referred to our Department for further diagnostics. After CT scan, biopsy was performed under the presumption of a malignant process with the surprising histological result of a reparative giant cell granuloma. At the same time, hyperthyroidism and nodular goiter were diagnosed and further endocrinological examinations were planned. Not until a parathyroid adenoma was diagnosed after urgent operation of the maxillary process (loose molar teeth and displacement of the left bulbus) could the tumor be interpreted and detected within this context of primary hyperparathyroidism as a brown tumor. The brown tumor should be taken into consideration as a rare differential diagnosis of a bone-destroying process of the facial bones. We discuss the clinical signs, diagnostics, and therapy for this case as well as the relevant literature. The reparative giant cell granuloma represents an important differential diagnosis and cannot be distinguished from a brown tumor by histological examination or radiological findings without complete information about the clinical signs and the endocrinological status of the patient.
HNO 2003 Mar
PMID:[A bone-destroying tumor of the maxilla. Reparative giant cell granuloma or brown tumor?]. 1262 53

Brown tumors are focal bone lesions caused by an increased osteoclastic activity and fibroblastic proliferation within a primary or more rarely secondary hyperparathyroidism. They are named after their typical brown hemorrhagic stroma with its also typical giant cell formations.We report the case of a 31-year-old pregnant patient with a rapidly growing tumor of her left maxilla whose first symptoms during pregnancy mimicked chronic sinusitis.After swelling of the cheek, diplopia, and recurrent epistaxis appeared, she was referred to our Department for further diagnostics.After CT scan, biopsy was performed under the presumption of a malignant process with the surprising histological result of a reparative giant cell granuloma. At the same time, hyperthyroidism and nodular goiter were diagnosed and further endocrinological examinations were planned.Not until a parathyroid adenoma was diagnosed after urgent operation of the maxillary process (loose molar teeth and displacement of the left bulbus) could the tumor be interpreted and detected within this context of primary hyperparathyroidism as a brown tumor.The brown tumor should be taken into consideration as a rare differential diagnosis of a bone-destroying process of the facial bones.We discuss the clinical signs, diagnostics, and therapy for this case as well as the relevant literature. The reparative giant cell granuloma represents an important differential diagnosis and cannot be distinguished from a brown tumor by histological examination or radiological findings without complete information about the clinical signs and the endocrinological status of the patient.
HNO 2003 Mar
PMID:[A bone-destroying tumor of the maxilla. Reparative giant cell granuloma or brown tumor?] 2827 Dec 43