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

This two-site immunoradiometric assay for human parathyrin-related protein 1-86 (PTHRP1-86) in plasma uses a mouse monoclonal antibody to PTHRP1-34 coupled to cellulose particles for immunoextraction of N-terminal immunoreactivity, and a rabbit antiserum to PTHRP37-67 that is indirectly labeled with 125I-labeled PTHRP37-67 for quantifying the bound analyte. The detection limit of the assay is 0.23 pmol/L, corresponding to 0.4 pg (0.04 fmol) per tube, for a sample volume of 200 microL. Recovery of PTHRP1-86 added to serum is essentially quantitative, and within- and between-batch precision is 4.4% and 11.1%, respectively. PTH1-84, PTHRP18-34, PTHRP9-34, PTHRP1-34, and PTHRP37-67 do not cross-react in the assay at concentrations up to 2 nmol/L. Plasma concentrations of PTHRP1-86 were below or close to the detection limit of the assay in normal subjects and in patients with primary hyperparathyroidism, hypoparathyroidism, chronic renal failure, and normocalcemic malignancy. In 37 hypercalcemic patients with various malignancies, we found detectable PTHRP1-86 concentrations in 35 (95%, mean 7.4 pmol/L, range 0.46-24.7). The data support the proposed humoral role of PTHRP in cancer-associated hypercalcemia and suggest that the assay has clinical utility in the differential diagnosis of hypercalcemia.
 ...
PMID:Development and validation of an immunoradiometric assay of parathyrin-related protein in unextracted plasma. 203 20

Primary hyperparathyroidism (PHPT) is characterized by the autonomous production of parathyroid hormone (PTH), in which there is hypercalcemia or normal-high serum calcium levels, in the presence of elevated or inappropriately normal serum PTH concentrations. Exceptionally, in symptomatic patients, a diagnosis can be established on the basis of clinical data. PHPT must always be evaluated in patients with clinical histories of nephrolithiasis, nephrocalcinosis, osseous pain, subperiosteal resorption, and pathologic fractures, as well as in those with osteoporosis-osteopenia on dual-energy X-ray absorptiometry (DEXA), a personal history of neck irradiation, or a family history of multiple endocrine neoplasia syndrome (types 1 or 2). Diagnosis of PHPT is biochemical. Asymptomatic hypercalcemia (total serum calcium corrected by albumin), without guiding signs or symptoms, is the most frequent manifestation of the disease. For the differential diagnosis, PTH(1-84) must be measured, as well as phosphate, chloride, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and calcium-to-creatinine clearance. Suppressed or inappropriately low PTH1-84 guides the diagnose toward tumoral hypercalcemia and less frequently to granulomatous disease (sarcoidosis, tuberculosis, etc.), inadequate intake of 1alpha-hydroxyvitamin D or calcitriol, vitamin D or A intoxication, lithium intake, endocrinopathies (hyperthyroidism, Addison's disease, etc.) or treatment with thiazides, among other possibilities. Diagnosis of PHPT is confirmed by demonstrating persistent hypercalcemia (or normal-high serum calcium levels) in the presence of inappropriately normal or elevated serum PTH(1-84) concentrations, unless the urinary calcium-to-creatinine clearance ratio is lower than 0.01. In these cases, in the absence of thiazide intake or severe vitamin D deficiency, diagnosis should focus on benign familial hypercalcemic hypocalciuria. Parathyroid gland imaging is useful for localization of PHPT, but not for diagnosis of this entity.
 ...
PMID:[Diagnostic evaluation and differential diagnosis of primary hyperparathyroidism]. 1962 56