Sources/Clones
Biodesign (polyclonal), Biogenesis (Bo, polyclonal), Biogenex (polyclonal), Dako (3B3) and Fitzgerald (polyclonal).
Fixation/Preparation
This antibody is applicable to formalin-fixed, paraffin-embedded tissue, frozen sections and cytologic preparations. Although not always required, enzyme pretreatment before immunodetection may improve results on paraffin-embedded tissue.
Background
The parathormone gene, closely linked to that ofb-globin, is located on the short arm of chromosome 11 in humans (as are the genes for calcitonin and insulin). The initial form in which parathormone is synthesized within the cell is a single-chain polypeptide of 115 amino acid residues, preproparathyroid hormone. This is cleaved within the cell to form a proparathyroid hormone, from which a further six amino acids are split, leaving the 84-amino acid chain of parathormone (Habener et al, 1984). The rate of parathormone secretion is directly responsive to the level of calcium in the serum, and indeed the cytoplasm, of parathyroid cells, as has been shown by studies both in vivo and in vitro. (Brown 1982).
Applications
Surgical pathologists are familiar with the ability of parathyroid proliferations to assume a variety of histological guises increasing the difficulty of categorizing any given lesion as hyperplastic, adenomatous or carcinomatous in nature (Wick et al, 1997). This is usually resolved with the macroscopic appearance of the remaining parathyroid glands as assessed by the surgeon. The role of the surgical pathologist is to identify the lesion as parathyroidal in nature and to assess whether it is normocellular or hypercellular. Although easily accomplished in the majority of instances, rare examples of parathyroid hyperplasia/adenoma showing a follicular/trabecular arrangement may cause concern over the alternative diagnosis of a thyroid adenoma. This becomes more pertinent when the parathyroid lesion protrudes into the thyroid gland or lies within the thyroid capsule. Immunodetection for thyroglobulin and parathyroid hormone (PTH) is especially useful to resolve the problem (Permanetter et al, 1983). Nevertheless, caution should be exercised since parathyroid cells often discharge their hormonal product almost as soon as it is packaged in the cytoplasm, resulting in false-negative PTH immunostaining, although the cells are biologically synthetic (Wick et al, 1997).
PTH antibody is also useful to distinguish cell parathyroid hyperplasia/neoplasms from thyroid and metastatic neoplasms (Wick et al, 1997) although the pathologist is typically aware of the preoperative hypercalcemic status. Occasionally when this information is not supplied by the surgeon, PTH immunohistochemistry is then essential. Even more problematic are situations in which clear cell parathyroid carcinomas are non-secretory, without an abnormality in mineral metabolism (Aldinger et al, 1982). In such situations, metastatic renal cell carcinoma or metastatic clear cell carcinoma of the lung is evident, warranting PTH immunohistochemistry to arrive at the correct diagnosis (Wick et al, 1997). The other instance in which PTH antibodies are useful is in the consideration of parathyroid carcinomas located primarily in the anterior mediastinum (intrathymically). In this situation distinction from primary thymic metastatic carcinomas, non-Hodgkin's lymphoma and germ cell tumors is necessary (Murphy et al, 1986).
Comments
The diagnosis of the majority of parathyroid proliferation may be accomplished with an adequate history, biochemistry profile and histomorphological assessment. However, rare instances in which the tumors have an abnormal location or clear cell morphology or are non-secretory may result in erroneous diagnoses, warranting PTH immunohistochemistry. Normal parathyroid glands are adequate for positive control tissue.
References
•Aldinger KA, Hickey RC, Ibanez ML, Samaan NA 1982 Parathyroid carcinoma: a clinical study of seven cases of functioning and two cases of nonfunctioning parathyroid cancer. Cancer 49: 388-397.
•Brown EM 1982 PTH secretion in vivo and in vitro. Regulation by calcium and other secretagogues. Mineral Electrolyte Metal 8: 130-150.
•Habener JF, Rosenblatt M, Potts JT 1984 Parathyroid hormone; biochemical aspects of biosynthesis, secretion, action and metabolism. Physiology Reviews 64: 985-1053.
•Murphy MN, Glennon PG, Diocee MS et al 1986 Nonsecretory parathyroid carcinoma of the mediastinum. Cancer 58: 2468-2476.
•Permanetter W, Nathrath WBJ, Lohrs U 1983 Immunohistochemical analysis of thyroglobulin and keratin in benign and malignant thyroid tumors. American Journal of Surgical Pathology 7: 535-546.
•Wick MR, Ritter JH, Humphrey PA, Nappi O 1997 Clear cell neoplasms of the endocrine system and thymus. Seminars in Diagnostic Pathology 14: 183-202.
Bibliografia
Manual of diagnostic antibodies for immunohistology / Anthony S.-Y. Leong, Kumarasen Cooper, F. Joel W.-M. Leong.
Biodesign (polyclonal), Biogenesis (Bo, polyclonal), Biogenex (polyclonal), Dako (3B3) and Fitzgerald (polyclonal).
Fixation/Preparation
This antibody is applicable to formalin-fixed, paraffin-embedded tissue, frozen sections and cytologic preparations. Although not always required, enzyme pretreatment before immunodetection may improve results on paraffin-embedded tissue.
Background
The parathormone gene, closely linked to that ofb-globin, is located on the short arm of chromosome 11 in humans (as are the genes for calcitonin and insulin). The initial form in which parathormone is synthesized within the cell is a single-chain polypeptide of 115 amino acid residues, preproparathyroid hormone. This is cleaved within the cell to form a proparathyroid hormone, from which a further six amino acids are split, leaving the 84-amino acid chain of parathormone (Habener et al, 1984). The rate of parathormone secretion is directly responsive to the level of calcium in the serum, and indeed the cytoplasm, of parathyroid cells, as has been shown by studies both in vivo and in vitro. (Brown 1982).
Applications
Surgical pathologists are familiar with the ability of parathyroid proliferations to assume a variety of histological guises increasing the difficulty of categorizing any given lesion as hyperplastic, adenomatous or carcinomatous in nature (Wick et al, 1997). This is usually resolved with the macroscopic appearance of the remaining parathyroid glands as assessed by the surgeon. The role of the surgical pathologist is to identify the lesion as parathyroidal in nature and to assess whether it is normocellular or hypercellular. Although easily accomplished in the majority of instances, rare examples of parathyroid hyperplasia/adenoma showing a follicular/trabecular arrangement may cause concern over the alternative diagnosis of a thyroid adenoma. This becomes more pertinent when the parathyroid lesion protrudes into the thyroid gland or lies within the thyroid capsule. Immunodetection for thyroglobulin and parathyroid hormone (PTH) is especially useful to resolve the problem (Permanetter et al, 1983). Nevertheless, caution should be exercised since parathyroid cells often discharge their hormonal product almost as soon as it is packaged in the cytoplasm, resulting in false-negative PTH immunostaining, although the cells are biologically synthetic (Wick et al, 1997).
PTH antibody is also useful to distinguish cell parathyroid hyperplasia/neoplasms from thyroid and metastatic neoplasms (Wick et al, 1997) although the pathologist is typically aware of the preoperative hypercalcemic status. Occasionally when this information is not supplied by the surgeon, PTH immunohistochemistry is then essential. Even more problematic are situations in which clear cell parathyroid carcinomas are non-secretory, without an abnormality in mineral metabolism (Aldinger et al, 1982). In such situations, metastatic renal cell carcinoma or metastatic clear cell carcinoma of the lung is evident, warranting PTH immunohistochemistry to arrive at the correct diagnosis (Wick et al, 1997). The other instance in which PTH antibodies are useful is in the consideration of parathyroid carcinomas located primarily in the anterior mediastinum (intrathymically). In this situation distinction from primary thymic metastatic carcinomas, non-Hodgkin's lymphoma and germ cell tumors is necessary (Murphy et al, 1986).
Comments
The diagnosis of the majority of parathyroid proliferation may be accomplished with an adequate history, biochemistry profile and histomorphological assessment. However, rare instances in which the tumors have an abnormal location or clear cell morphology or are non-secretory may result in erroneous diagnoses, warranting PTH immunohistochemistry. Normal parathyroid glands are adequate for positive control tissue.
References
•Aldinger KA, Hickey RC, Ibanez ML, Samaan NA 1982 Parathyroid carcinoma: a clinical study of seven cases of functioning and two cases of nonfunctioning parathyroid cancer. Cancer 49: 388-397.
•Brown EM 1982 PTH secretion in vivo and in vitro. Regulation by calcium and other secretagogues. Mineral Electrolyte Metal 8: 130-150.
•Habener JF, Rosenblatt M, Potts JT 1984 Parathyroid hormone; biochemical aspects of biosynthesis, secretion, action and metabolism. Physiology Reviews 64: 985-1053.
•Murphy MN, Glennon PG, Diocee MS et al 1986 Nonsecretory parathyroid carcinoma of the mediastinum. Cancer 58: 2468-2476.
•Permanetter W, Nathrath WBJ, Lohrs U 1983 Immunohistochemical analysis of thyroglobulin and keratin in benign and malignant thyroid tumors. American Journal of Surgical Pathology 7: 535-546.
•Wick MR, Ritter JH, Humphrey PA, Nappi O 1997 Clear cell neoplasms of the endocrine system and thymus. Seminars in Diagnostic Pathology 14: 183-202.
Bibliografia
Manual of diagnostic antibodies for immunohistology / Anthony S.-Y. Leong, Kumarasen Cooper, F. Joel W.-M. Leong.
