The co-existence of parathyroid and thyroid disease. I. Primary hyperparathyroidism and thyroid carcinoma.
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Adenoma↗
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Primary hyperparathyroidism. A personal experience with 242 cases.
Two hundred forty-two patients with primary hyperparathyroidism operated on at Akron City Hospital are reviewed. The importance of the association of peptic ulcer and pancreatitis with primary hyperparathyroidism is stressed. Nineteen percent of the patients had associated peptic ulcer or pancreatitis. The mechanisms involved in the production of these diseases in patients with primary hyperparathyroidism are emphasized. The two deaths occurred in the small but challenging group of patients with acute parathyroid crisis and carcinoma. The decision concerning the extent of parathyroidectomy should be made by the surgeon for each patient, based on the number, location and gross appearance of the identified glands. Removal of a single enlarged gland, if the other three glands are normal, is all that needs to be done in most cases. A recurrence rate of 1 percent and an appreciable decrease in postoperative tetany support this conservative approach. Subtotal parathyroidectomy should be reserved for patients with diffuse hyperplasia.
Adenoma↗
Autografts of normal and hyperplastic human parathyroid: experience in eleven patients with immunoassay monitoring of function in seven.
Parathyroid autografts were implanted in 11 patients at this institution. Four patients had total or subtotal parathyroidectomy and implantation for parathyroid hyperplasia or adenoma, while 7 had one or more parathyroids removed and implanted during total thyroidectomy for carcinoma of the thyroid. Hyperplastic parathyroid was implanted in 4 instances and normal parathyroid in 7. Recurrent hyperparathyroidism occurred in 1 patient with an implanted adenoma who was returned to a normocalcemic state by partial reexcision ("titration") of the implanted tissue. All implants were placed in muscle pockets, a single site being used for patients receiving normal parathyroid tissue, and multiple sites for patients receiving hyperplastic glands. Those patients receiving forearm implants were followed up by serial parathyroid hormone determinations in venous blood drawn from both arms. In all cases, elevated levels were found on the implanted side, as compared to the contralateral control side.
Adenoma↗
Chromogranin A in human neuroendocrine tumors: an immunohistochemical study with region-specific antibodies.
Antibodies to six specific regions of the chromogranin A (CgA) molecule were used to study their immunoreactivity in human neuroendocrine (NE) tumors. Tissue specimens from endocrine pancreatic tumors (n = 14), duodenal carcinoids (n = 2), bronchial carcinoids (n = 5), ileal carcinoids (n = 5) appendix carcinoids (n = 2), medullary thyroid carcinomas (n = 6), parathyroid adenomas (n = 2), and pheochromocytomas (n = 8) were analyzed. The results showed that the NE tumor types expressed varying numbers of CgA fragments. A variation in frequency of the expression of immunoreactive cells was sometimes seen also within the same tumor type. The midportion fragment CgA 176-195 (chromacin) was the only fragment expressed in all tumors. Benign and malignant tumors expressed different patterns, being especially true of insulinomas and pheochromocytomas. These findings suggest that region-specific antibodies to CgA fragments can be used as a diagnostic tool for the characterization of NE tumors.
Adenoma↗
In situ demonstration of parathyroid hormone-related protein mRNA in sclerosing hepatic carcinoma.
A 69-year-old man had a hepatic tumour occupying the left and half of the right lobe, with portal vein thrombus. There were hypercalcaemia and hypophosphataemia with increased nephrogenous cyclic adenosine monophosphate; bone metastases were excluded. Serum parathyroid hormone-related protein (PTHrP) was elevated, but no increase in intact parathyroid hormone (PTH) or vitamin D3 metabolites was found. At autopsy the histological features were typical of sclerosing hepatic carcinoma. By immunohistochemistry PTHrP was detected in cancer cell nests but not in the fibrous stroma. PTHrP transcripts were demonstrated by in situ hybridization using a polymerase chain reaction (PCR)-derived single-stranded DNA probe. Tumour cells expressed AE1 and CA19-9 (markers for cholangioepithelium) and CEA (for bile canaliculi). Electron microscopy revealed microvilli on the apical surface, and secretory granules 100 nm in diameter were observed. These findings indicate that this case is one of cholangiocellular sclerosing hepatic carcinoma. The interaction between cancer and stromal cells may be the cause of PTHrP overexpression.
Aged↗
Galectin-3 and Ki-67 expression in multiglandular parathyroid lesions.
Hyperplastic and neoplastic parathyroid lesions may present overlapping morphologic features, and several markers have been proposed to distinguish benign from malignant growths. Recently, it was reported that galectin-3 is a useful marker of malignancy in uniglandular parathyroid diseases. To investigate galectin-3 and Ki-67 immunoexpression in parathyroid hyperplastic disease, 63 multiglandular lesions (13 primary, 40 secondary, and 10 tertiary hyperplasia cases) were analyzed and compared with 45 control cases of parathyroid adenomas and 24 carcinomas. Our data showed that hyperplastic lesions responsible for primary nonfamilial or tertiary hyperparathyroidism, as well as parathyroid adenomas, were negative for galectin-3, as opposed to carcinomas. In addition, secondary and familial primary hyperplasia cases were surprisingly positive for galectin-3 in approximately two thirds of cases. All hyperplastic lesions (positive or negative for galectin-3) had a low Ki-67 index. Based on these findings, secondary hyperplasia has a low proliferative potential but an unexplained galectin-3 reactivity, which reduces its diagnostic role in differentiating benign from malignant nodules in the context of multiglandular parathyroid diseases.
Adenocarcinoma↗
Problems in early diagnosis of bladder cancer in a spinal cord injury patient: report of a case of simultaneous production of granulocyte colony stimulating factor and parathyroid hormone-related protein by squamous cell carcinoma of urinary bladder.
BACKGROUND: Typical symptoms and signs of a clinical condition may be absent in spinal cord injury (SCI) patients. CASE PRESENTATION: A male with paraplegia was passing urine through penile sheath for 35 years, when he developed urinary infections. There was no history of haematuria. Intravenous urography showed bilateral hydronephrosis. The significance of abnormal outline of bladder was not appreciated. As there was large residual urine, he was advised intermittent catheterisation. Serum urea: 3.5 mmol/L; creatinine: 77 umol/L. A year later, serum urea: 36.8 mmol/l; creatinine: 632 umol/l; white cell count: 22.2; neutrophils: 18.88. Ultrasound: bilateral hydronephrosis. Bilateral nephrostomy was performed. Subsequently, blood tests showed: Urea: 14.2 mmol/l; Creatinine: 251 umol/l; Adjusted Calcium: 3.28 mmol/l; Parathyroid hormone: < 0.7 pmol/l (1.1 - 6.9); Parathyroid hormone-related protein (PTHrP): 2.3 pmol/l (0.7 - 1.8). Ultrasound scan of urinary bladder showed mixed echogenicity, which was diagnosed as debris. CT of pelvis was interpreted as vesical abscess. Urine cytology: Transitional cells showing mild atypia. Bladder biopsy: Inflamed mucosa lined by normal urothelial cells. A repeat ultrasound scan demonstrated a tumour arising from right lateral wall; biopsy revealed squamous cell carcinoma. In view of persistently high white cell count and high calcium level, immunohistochemistry for G-CSF and PTHrP was performed. Dense staining of tumour cells for G-CSF and faintly positive staining for C-terminal PTHrP were observed. This patient expired about five months later. CONCLUSION: This case demonstrates how delay in diagnosis of bladder cancer could occur in a SCI patient due to absence of characteristic symptoms and signs.
Adult↗
Cholangiocellular carcinoma that produced both granulocyte-colony-stimulating factor and parathyroid hormone-related protein.
A 56-year-old man was admitted to our hospital because of consciousness disturbance. Abdominal computed tomography revealed a large low-density tumor in the left lobe of the liver. He presented with marked leukocytosis and hypercalcemia with high levels of serum granulocyte-colony-stimulating factor (G-CSF) and parathyroid hormone-related protein (PTH-rP). A diagnosis of cholangiocellular carcinoma (CCC) of the liver was confirmed by histological examination of an autopsy specimen. The tumor cells showed positivity for both G-CSF and PTH-rP with immunohistochemical staining. These results suggest that the tumor was producing both G-CSF and PTH-rP. This paraneoplastic G-CSF and PTH-rP production caused by CCC is very rare. Such cases must be followed up carefully, since tumors associated with paraneoplastic syndrome progress rapidly, resulting in a poor prognosis.
Bile Duct Neoplasms↗
Mediastinal carcinoid with an incomplete Sipple's syndrome.
A 60-year-old woman with a mediastinal carcinoid of probable thymic origin, widely metastatic, had associated parathyroid hyperplasia, medullary carcinoma of thyroid with amyloid stroma and an adrenal neuroma. This case demonstrated features of an incomplete Sipple's syndrome (MEA II). The relationship of these diverse tumors is consistent with the concept of the APUD system and neurocristopathies.
Carcinoid Tumor↗
Calcitonin gene-related peptide in patients with endocrine tumors.
The plasma level of calcitonin gene-related peptide (CGRP) was measured by RIA in 41 patients with endocrine tumors [22 medullary thyroid carcinomas (MTC), seven parathyroid adenomas, four benign insulinomas, five carcinoids, and three pheochromocytomas]. Of the 22 patients with MTC, all five preoperative patients had elevated CGRP levels. The correlation between CGRP and calcitonin levels was significant (P less than .001) in 22 patients with MTC. Six of 19 patients with endocrine tumors other than MTC showed elevated CGRP levels. Immunohistochemical study showed that tumor tissues from all 22 cases of MTC and seven from other endocrine tumors contained immunoreactive CGRP. CGRP reactivity was found in only small numbers of tumor cells. Thus, although CGRP appeared to be a useful additional marker for MTC, the role of CGRP in the pathophysiology of endocrine tumors was not elucidated.
Adenoma↗
Germline mutations of the RET proto-oncogene in eight Japanese patients with multiple endocrine neoplasia type 2A (MEN2A).
Multiple endocrine neoplasia type 2A (MEN2A) is a dominantly inherited cancer syndrome characterized by medullary thyroid carcinoma, pheochromocytoma, and parathyroid hyperplasia. The gene responsible for MEN2A was localized by linkage analysis to chromosome 10q11.2 in 1987, and recently mutations in RET, a proto-oncogene in the candidate region, were discovered in patients with MEN. The majority of mutations found so far in MEN2A patients have been located in nucleotide sequences encoding cysteine residues in the extracellular domain of RET. To characterize MEN2A germline alterations in the Japanese population, we screened DNA from eight unrelated patients for mutations in exons 10 and 11 of the RET proto-oncogene and found mutations in all eight patients, at codons 618, 620, or 634; each of these sites encodes a cysteine residue in the extracellular domain of RET. The mutations were confirmed in other affected individuals in the respective families by digestion of polymerase chain reaction (PCR) products containing the mutated codons with restriction enzymes (Rs alpha I, CfoI, or AluI) for which cleavage sites had been generated by the specific genetic alteration. These PCR-restriction enzyme systems will be useful for genetic diagnosis in members of families carrying these mutations.
Base Sequence↗
Carcinoid tumour of the thymus. A case report including discussion of the morphological diagnosis and the cell of origin.
This report concerns a 49 year old asymptomatic male who had a mediastinal mass demonstrated on routine radiography. A large encapsulated tumour composed of small regular cells arranged in clumps and acini with fine vascular stroma was removed. The differential diagnosis on routine H&E section included parathyroid tumor, medullary carcinoma arising in ectopic thyroid tissue, epithelial thymoma or carcinoid tumor of the thymus. The presence of compressed thymic tissue around the tumor, and of argentaffin granules together with the electron microscopic appearance characteristic of the "enterochromaffin" or "APUD" group of cells allowed the diagnosis of carcinoid tumor of the thymus to be made. Electron microscopy showed that the cell cytoplasm contained electron dense membrane bound granules, together with bundles of microfilaments. Vesicles of smooth surfaced reticulum were present but rough surfaced reticulum was inconspicuous. No desmosomes were demonstrated. Special stains for amyloid and glycogen were negative.
APUD Cells↗
HRPT2 gene alterations in ossifying fibroma of the jaws.
Ossifying fibroma (OF) is a benign neoplasm related to bone characterized by a progressive enlargement of the affected jaw. Recently, the candidate tumor suppressor gene HRPT2 was identified and alterations in this gene were related with the Hyperparathyroidism-jaw tumor syndrome that is characterized by parathyroid adenoma or carcinoma, fibro-osseous lesions (mainly OF) of the jaws, and renal lesions. The purpose of the present study was to evaluate the HRPT2 gene in OF. Tumour and blood samples were obtained from 3 patients with OF and one with juvenile ossifying fibroma (JOF). The results demonstrated three novel mutations in two out of three genotyped OF's. Interestingly, one of these patients showed a germ-line mutation after blood analysis. RT-PCR amplification was performed to analyze HRPT2 mRNA expression and only wild-type HRPT2 transcript was found in all tumours. Investigation of the parafibromin protein by immunohistochemistry showed a similar pattern of immunolocalization with strong nuclear and cytoplasmic staining in all cases. In conclusion, the present study shows for the first time mutations of HRPT2 gene in OF and suggests that OF may arise due to haploinsufficiency of the HRPT2 gene.
Adolescent↗
Brown tumor of the orbit associated with primary hyperparathyroidism.
A 70-year-old woman had swelling of her left superior orbital ridge. A tumor was surgically removed, and histologic examination disclosed a tumor containing giant cells. Subsequent tests showed primary hyperparathyroidism caused by a carcinoma of the parathyroid. This rare instance of brown tumor of the orbit led us to review the differential diagnoses of giant-cell lesions of the orbit and to examine published case reports. Laboratory determinations of serum calcium, phosphorus, and alkaline phosphatase levels for all patients with lytic orbital bone lesions can establish whether they have hyperparathyroidism, a diagnosis making orbital surgery unnecessary.
Aged↗
Immunohistochemical assessment of parafibromin in mouse and human tissues.
Parafibromin is a protein encoded by the HRPT2 oncosuppressor gene, whose mutation causes the hyperparathyroidism-jaw tumour syndrome, characterized by the occurrence of parathyroid adenoma or carcinoma, fibro-osseous jaw tumours, and renal neoplastic and non-neoplastic abnormalities. Non-morphological techniques, such as Northern and Western blotting and reverse transcriptase-PCR, indicate that parafibromin is ubiquitously expressed, but extensive immunohistochemical studies have not been performed. To increase our knowledge of the distribution and patterns of expression of parafibromin, we examined its expression and location in many different mouse and human organs by immunohistochemistry. There were no substantial differences in parafibromin expression between mouse and human. We found widespread expression of parafibromin, except in connective tissue, smooth muscle, endothelium and some other types of epithelia (colonic, urinary, tubaric, uterine, thyroid). Heterogeneity of positivity intensity and subcellular location (nuclear, nucleocytoplasmic, cytoplasmic) was found between tissues and cell types, suggesting differential functional involvement of parafibromin. Moreover, higher parafibromin expression was found in cell types, such as hepatocytes, cells of the base of gastric glands, renal cortex tubules and the pars intermedia of the hypophysis, which are characterized by different proliferative capacity, thus indicating that the cellular function of parafibromin may not be reduced only to its anti-proliferative effect.
Adult↗
A genotypic and histopathological study of a large Dutch kindred with hyperparathyroidism-jaw tumor syndrome.
Familial primary hyperparathyroidism is the main feature of 2 familial endocrine neoplasia syndromes: multiple endocrine neoplasia type 1 (MEN 1) and hyperparathyroidism-jaw tumor syndrome (HPT-JT). The latter is a recently described syndrome that has been associated with ossifying fibroma of the jaw and various types of renal lesions, including benign cysts, Wilms' tumor, and hamartomas. To further illustrate the natural history of this syndrome, we describe a large, previously unreported Dutch kindred in which 13 affected members presented with either parathyroid adenoma or carcinoma; in 5 affected individuals, cystic kidney disease was found. Additionally, pancreatic adenocarcinoma, renal cortical adenoma, papillary renal cell carcinoma, testicular mixed germ cell tumor with major seminoma component, and Hürthle cell thyroid adenoma were also identified. Linkage analysis of the family using MEN1-linked microsatellite markers and mutation analysis excluded the involvement of the MEN1 gene. Using markers from the HPT-JT region in 1q2531, cosegregation with the disease was found, with a maximum logarithm of odds score of 2.41 obtained for 6 markers using the most conservative calculation. Meiotic telomeric recombination between D1S413 and D1S477 was identified in 3 affected individuals, and when combined with previous reports, delineated the HPT-JT region to 14 centimorgan. Combined comparative genomic hybridization and loss of heterozygosity data revealed complex genetic abnormalities in the tumors, suggesting different possible genetic mechanisms for the disease. In conclusion, we report a family with hyperparathyroidism linked to chromosome 1q, and exhibiting several types of renal and endocrine tumors that have not been previously described.
Chromosome Mapping↗
Doppler color imaging. Scrotum, breast, thyroid, and extremities.
DCI, when coupled with small-parts gray-scale imaging, has demonstrated great utility in the evaluation of superficial body abnormalities. This technique has rapidly become a primary method of evaluation of suspected testicular torsion, and its results are competitive with those of standard nuclear medicine examinations. DCI evaluation of male impotence, coupled with intracavernous injection of vasoactive substances, is now a leading, noninvasive technique for diagnosis of both arteriogenic and venogenic causes. DCI may provide invaluable information in the evaluation of palpable masses, particularly in the diagnosis of vascular abnormalities such as false aneurysm and arteriovenous fistula. Further studies are needed to corroborate the utility of DCI in the evaluation of focal thyroid and parathyroid abnormalities, breast carcinoma, nodal cancer, and the orbit. Because this technique is applicable to superficial, high-frequency examinations, DCI is rapidly becoming an accepted and frequently necessary part of any small-parts ultrasound study.
Color↗
Systemic investigation of keratoepithelin deposits in TGFBI/BIGH3-related corneal dystrophy.
PURPOSE: To investigate the location and tissue-specificity of the pathologic keratoepithelin (KE) deposition in a patient with a keratoepithelinopathy (KEP), TGFBI/BIGH3-related corneal dystrophy. METHODS: An autopsy was performed in a patient with lattice type I corneal dystrophy (LCDI) after authorization was obtained from the family. Mutation screening in TGFBI/BIGH3 was done on the patient several years ago. Eighteen different tissues or organs, including brain, heart, lung, kidney, liver, lymph nodes, spleen, aorta, esophagus, bone marrow, urinary bladder (including a papillary urothelial carcinoma), samples of a metastatic squamous cell carcinoma, adrenal gland, parathyroid gland, muscle, prostate, and cornea were investigated, and sections from the tissues were labeled with KE2 rabbit TGFBI/BIGH3 antiserum. RESULTS: The patient, diagnosed with LCDI and Alzheimer's disease, died at 79 years of age from a complicated chronic obstructive lung disease. Mutation analysis showed the classical Arg124Cys mutation in exon 4 of TGFBI/BIGH3, associated with LCDI. Except for the cornea, immunostaining with KE2 antisera did not reveal any deposits in any of the 17 other organs analyzed. CONCLUSIONS: Pathologic deposits caused by KE accumulation were only observed in the cornea and in no other tissue or organ in this patient. These results suggest a cornea-specific mechanism in the aggregation of KE. Further studies need to be done to investigate whether the degradation of mutated KE generates cornea-specific fragments that aggregate or whether the clearing of normal fragments is different in affected corneas, which then leads to aggregation.
Aged↗