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Biomedical subjects

E Horvath

Publications and source records attributed to E Horvath.

At least 91 records · Page 5Linked to original sources
PubMed1995

Prolactin-producing pituitary tumor: resistance to dopamine agonist therapy. Case report.

A 14-year-old girl presented with a rapidly growing, invasive prolactin-producing pituitary tumor that failed to respond to dopamine agonist medication. Histological, immunocytochemical, and ultrastructural studies of the surgically removed tissue revealed a pleomorphic, chromophobic, or slightly acidophilic pituitary tumor that was immunoreactive for prolactin and that, according to electron microscopy, consisted of atypical lactotrophs showing no evidence of cell shrinkage. In situ hybridization demonstrated large amounts of prolactin messenger ribonucleic acid (mRNA), moderate amounts of estrogen receptor mRNA and dopamine (D2) receptor mRNA, and an absence of growth hormone mRNA in the tumor cells. Because D2 receptor mRNA was present in the tumor, causes other than D2 receptor loss may have been responsible for the resistance of the lactotrophs to dopamine agonist administration.

Adenoma↗
PubMed1995

Asynchronous pituitary adenomas with differing morphology.

Recurrent pituitary tumors can sometimes pose a diagnostic and therapeutic challenge. We report a case of a 43-year-old man who presented twice, 13 years apart, with pituitary adenoma marked by headaches, visual impairment, and no signs of endocrinologic abnormality. At initial presentation computed tomographic scan documented a pituitary mass eroding the sellar floor, with suprasellar and parasellar extension. The patient underwent transsphenoidal surgery and the tumor was classified as a silent corticotroph adenoma, subtype 2. Thirteen years later, clinical symptoms of a destructive pituitary mass reappeared. This time, the adenoma revealed typical ultrastructural features of an oncocytoma; it had a different immunocytochemical profile from the first tumor. Given these striking morphologic differences, we consider the two adenomas to represent asynchronous, de novo formations. We conclude that the recurrence of a resected pituitary tumor may also represent a metachronous development of two distinct pituitary adenomas.

Adenoma↗
PubMed1994

32P-post-labeling detection of DNA adducts in mononuclear cells of workers occupationally exposed to styrene.

32P-Post-labeling was used to analyze for the presence of DNA adducts in 47 workers exposed to styrene in a boat manufacturing facility. Individual airborne exposures measured several times over the course of 1 year ranged from 1 to 235 mg/m3 with a mean value of 65.6 mg/m3. Two adducts were detected in the DNA of mononuclear cells of these workers. The following levels of adducts were detected: adduct 1, range 0.6-102 x 10(-8) (mean 15.8 x 10(-8); adduct 2, range 0.1-70.9 x 10(-8) (mean 14.2 x 10(-8). Significant linear relationships were found between styrene exposure and both DNA adducts (adduct 2, r = 0.330, P = 0.012; adduct 1, r = 0.244, P = 0.049). Co-chromatography experiments identified DNA adduct 1 in the exposed samples as N2-(2-hydroxy-1-phenylethyl)-2'-deoxyguanosine-3',5'-bisphosphate. DNA adduct 2 remains unidentified. No significant linear relationships were observed between the level of DNA adducts and sister chromatid exchanges, possibly because of the poor precision of the 32P-post-labeling assay (the estimated coefficients of variation for adducts 1 and 2 were 2.54 and 1.96, respectively). These results demonstrate that occupational exposure to styrene results in the formation of DNA adducts in human mononuclear cells.

DNA↗
PubMed1994

Effects of spaceflight on morphology of the rat adenohypophysis.

To determine the effects of spaceflight on the anterior pituitary gland, the adenohypophyses of rats after a 7-day spaceflight aboard the space shuttle Endeavor (STS-54) were investigated by histology, immunohistochemistry, morphometry, electron microscopy, and in situ hybridization and were compared with synchronous control rats. Morphometry revealed the corticotrophs of space-flown rats to be significantly enlarged, demonstrating 46-48% increases in mean cell, nuclear, and cytoplasmic areas. These corticotrophs also exhibited striking ultrastructural signs of heightened secretory activity. Furthermore, their expression of proopiomelanocortin mRNA, the transcript encoding the precursor protein from which adrenocorticotropic hormone is posttranslationally cleaved, was also significantly enhanced, a finding consistent with their hypersecretory state. Gonadotrophs also exhibited significant increments in mean nuclear, cell, and cytoplasmic areas of 22, 45, and 51%, respectively; however, they were not accompanied by ultrastructural evidence of increased secretory function. There were no morphological changes in somatotrophs, lactotrophs, or thyrotrophs, nor were there any significant changes in the overall frequency of any one adenohypophyseal cell type in comparison with control. The structural integrity of all adenohypophyseal secretory and vascular elements was preserved after spaceflight, as there was neither evidence of necrosis nor other forms of cellular injury in spaceflown specimens. Capillaries were patent, and neither endothelial damage nor thrombosis was noted. These data suggest that spaceflight is accompanied by a selective morphological response in the anterior pituitary, one characterized by hypertrophy of both corticotrophs and gonadotrophs and by enhanced endocrine activity of the former.

Adrenocorticotropic Hormone↗
PubMed1994

In situ hybridization study of estrogen receptor messenger ribonucleic acid in human adenohypophysial cells and pituitary adenomas.

Estrogen receptor (ER) was demonstrated in nontumorous and adenomatous human pituitaries by autoradiography and biochemical assays. In the present study, we investigated ER mRNA by in situ hybridization applied on paraffin section of 9 nontumorous pituitaries obtained at surgery or autopsy and 109 surgically removed adenomas. In nontumorous pituitaries, in situ hybridization combined with immunocytochemistry revealed hybridization signal in GH-, PRL-, ACTH-, TSH-, and LH/FSH-immunoreactive cells, with the highest intensity in PRL-immunoreactive cells. ER mRNA was also localized in Crooke's cells, corticotrophs extending to posterior lobe, cells lining the pars intermedia cavities, and squamous nests of pars tuberalis. The neurohypophysis, endothelium, and connective tissue expressed no ER gene. ER mRNA was present in all adenoma types, including somatotroph, lactotroph, mixed somatotroph-lactotroph, mammosomatotroph, acidophil stem cell, functioning and silent corticotroph, thyrotroph, gonadotroph, null cell adenomas, and oncocytomas. The strongest signal was seen in some lactotroph and mammosomatotroph adenomas. In 9 lactotroph adenomas exposed to bromocriptine (long-acting repeatable injectable form), the hybridization signal was weak or absent, suggesting that suppression of ER gene plays a role in the inhibition of PRL synthesis and tumor growth.

Adenoma↗
PubMed1994

Somatotroph hyperplasia without pituitary adenoma associated with a long standing growth hormone-releasing hormone-producing bronchial carcinoid.

Acromegaly is most often associated with a pituitary somatotroph adenoma. While multiple lines of evidence suggest an intrinsic somatic cell defect in adenoma formation, the role of hypothalamic hormones in pituitary tumorigenesis remains unclear. We describe the functional and morphological features of the pituitary of a patient with a long-standing ectopic GH-releasing hormone (GHRH)-producing tumor and acromegaly. This 28-yr-old woman with a documented 10-yr history of a disseminated bronchial carcinoid was evaluated for clinical features of acromegaly. Elevated serum GH (88 micrograms/L) was not suppressed after glucose ingestion and was paradoxically stimulated by TRH, but did not respond to GHRH or GnRH administration. Serum insulin-like growth factor-1 (730 micrograms/L; normal, < 333 micrograms/L), insulin-like growth factor-binding protein-3 (9.5 mg/L; normal, 2-4.2 mg/L), and GHRH (26.1 micrograms/L; normal, < 20 ng/L) were elevated. Magnetic resonance imaging revealed a diffusely enlarged pituitary gland. Octreotide treatment for 4 months resulted in suboptimal clinical and biochemical responses. Examination of the transsphenoidally resected pituitary by light microscopy revealed diffuse somatotroph hyperplasia, with intact reticulin network and preservation of the acinar architecture. Electron microscopy showed active somatotrophs interspersed with other cell types. In situ hybridization revealed very strong positivity for GH mRNA, whereas fewer cells contained GHRH and somatostatin mRNA signals. Dispersed pituitary cells secreted GH into culture medium. GH release was stimulated by GHRH and GHRH plus TRH, but not by TRH alone; GH was suppressed by octreotide in vitro. We conclude that sustained exposure to ectopic GHRH leads to somatotroph hyperplasia, but, at least in this case, was not sufficient for adenomatous transformation.

Adult↗
PubMed1994

Morphological effects of octreotide on growth hormone-producing pituitary adenomas.

The SRIH analog octreotide is a potent GH-inhibiting agent that has been used to effectively treat patients with acromegaly. To investigate the morphological changes induced by octreotide on GH-producing pituitary tumors, we examined 86 adenomas from acromegalic patients who participated in a multicenter study. GH- producing pituitary adenomas removed from 43 patients treated preoperatively with octreotide for 4 months were compared to those obtained from 43 untreated acromegalic patients. Tissue samples were studied by histology, immunohistochemistry, and transmission electron microscopy as well as light microscopic and ultrastructural morphometry. The morphological appearance of some tumors was unaltered by octreotide treatment. Necrotic changes were not apparent in any. Acidophilia and GH immunoreactivity were more pronounced in the octreotide-treated tumors. Perivascular and interstitial fibrosis was more prevalent in the octreotide group (72% vs. 42%). An increase in hormone granularity was obvious in 4 of 15 densely granulated and 2 of 9 sparsely granulated (SG) tumors from treated patients. A decrease in cell size was conspicuous in 4 of 15 densely granulated and 2 of 10 SG adenomas. There was a slight downward trend in the cell and cytoplasmic size in all treated tumors and a slight upward trend in secretory granule size in treated SG adenomas. Only 2 of 9 SG adenomas in the octreotide group, however, demonstrated a statistically significant reduction in cell and cytoplasmic size. There was no statistically significant change in the size of nuclei, secretory granules, or lysosomes between the 2 groups. Decreased cell size and increased granularity were not linked, however. We conclude that there are no striking morphological alterations in GH pituitary adenomas that can be consistently associated with octreotide treatment.

Adenoma↗
PubMed1994

Pituitary adenomas in childhood and adolescence.

A clinicopathological study of 56 pediatric patients with non-ACTH-secreting pituitary adenomas removed by a transsphenoidal neurosurgical approach was undertaken to better define the clinical presentation, to assess demographic factors, to determine the immunohistochemical staining characteristics of the tumors, and to evaluate the outcome of transsphenoidal surgical treatment and other adjuvant therapies. A separate analysis of prolactinoma patients was performed. All tumors were confirmed histologically and immunophenotyped for pituitary hormones. Forty-one patients had tumors that stained for PRL alone, eight patients had tumors that stained for PRL and GH, six patients had plurihormonal adenomas, and one patient had a tumor that stained for glycoprotein hormones. No tumors contained GH alone. Macroadenomas exceeded microadenomas (1.4:1). There were no male patients with microadenomas of any type. Females outnumbered males (3.3:1). Patients presented most frequently with headache, menstrual dysfunction (in females), galactorrhea, and hypopituitarism. All but one of the patients with hypopituitarism at presentation had macroadenomas. Tumor staining characteristics did not always correlate well with clinical status, especially with regard to GH-containing tumors. Pediatric pituitary tumors did not appear to be more invasive or more aggressive than adult pituitary tumors, contrary to some previous reports. The patients with microadenomas had a 70% operative cure rate and a 65% long term cure rate; the recurrence rate for microadenoma patients was 25%. Macroadenoma patients had a 33% operative cure rate, a 55% long term cure rate, and a recurrence rate of 33%. Thus, microadenoma and macroadenoma patients had similar long term cure rates, but macroadenoma patients required more aggressive adjuvant therapy (second surgery, radiation, or bromocriptine) and had higher rates of hypopituitarism (52% of macroadenoma patients vs. 0% of microadenoma patients required long term hormone replacement).

Adenoma↗
PubMed1994

Large clear cell adenoma of the parathyroid in a patient with MEN-1 syndrome. Ultrastructural study of the tumour exhibiting unusual RER formations.

A 48 year old man presented with hyperparathyroidism and acromegaly. Although pancreatic tumour was not demonstrated, the diagnosis of MEN-1 syndrome was made. The parathyroid adenoma was removed surgically and investigated by histology and transmission electron microscopy and was diagnosed as large clear cell adenoma with extensive deposition of glycogen. Much of the endoplasmic reticulum was present in two special forms: annulate lamellae and the rare rail-like configurations both of which showed continuity with the conventional RER as well as with each other. No obvious correlation was apparent between presence of special RER formations and growth rate or endocrine activity of tumour; they may be regarded as signs of cellular dedifferentiation.

Acromegaly↗
PubMed1994

[Imaging of complications of liver transplantation in children].

The authors report their experience of imaging of 286 liver transplantations (LT) in children. Hepatic artery thrombosis is the most serious complication (9%), with a maximum risk during the first two weeks. Its clinical presentation is very variable and its diagnosis is based on Doppler ultrasonography. Emergency surgical disobstruction prevented the development of biliary or ischaemic complications in one half of cases. Portal thrombosis (4.5%) is due, in the majority of cases, to hypoplasia of the recipient's portal vein. Patency of intrahepatic portal branches with inversion of flow can delay the ultrasonographic diagnosis. Biliary complications are frequent (20%) and occur after a very variable interval. Their diagnosis is ultrasonographic, but sometimes delayed compared to the histological signs. Transhepatic cholangiography visualises the lesions and allows external drainage or even percutaneous dilatation. In 1 out of 4 cases, the aetiology was hepatic artery thrombosis. The imaging protocol after LT consists of ultrasonography with daily Doppler (or even twice-daily) in the patient's bed for the first two weeks and then as required. Computed tomography is useful to demonstrate parenchymal ischaemia and intraperitoneal abscess in multi-operated children. Angiography and cholangiography confirm the ultrasonographic signs. Interventional Radiology plays an increasingly important role.

Aortography↗
PubMed1994

Recurrent plurihormonal bimorphous pituitary adenoma producing growth hormone, thyrotropin, and prolactin.

A 48-year-old man with visual disturbances and subtle features of acromegaly had elevated serum thyrotropin (thyroid-stimulating hormone) levels but was clinically euthyroid and initially had normal blood growth hormone (GH) levels. A computed tomographic scan documented a large pituitary tumor; he underwent incomplete transsphenoidal adenomectomy. Postoperative octreotide treatment failed to shrink the tumor. Rising GH levels necessitated repeated transsphenoidal and, subsequently, frontotemporal resection. By histology, the tumor was a chromophobic adenoma. In the first specimen, immunocytochemistry localized GH, beta-thyrotropin, and alpha-subunit of glycoprotein hormones in adenoma cells. The second specimen also contained prolactin, whereas the third contained only GH and beta-thyrotropin. By electron microscopy, the tumor was bimorphous, composed of elongated thyrotrophs and densely granulated somatotrophs. In tissue culture, the first specimen released GH, thyrotropin, and alpha-subunit and smaller quantities of prolactin; the second specimen released only GH and alpha-subunit; and the third released GH, thyrotropin, alpha-subunit, and prolactin. Incubation with somatorelin (GH-releasing hormone) variably stimulated release of all four hormones in the first and third specimens; protirelin (thyrotropin-releasing hormone) had no effect. Somatostatin consistently inhibited release of all four hormones; inhibition by bromocriptine mesylate was variable. The mild degree of clinical and biochemical acromegaly is unusual for a large macroadenoma, and the reasons for the absence of hyperthyroidism are unclear. These discrepancies may be attributed to retarded hormone release and/or synthesis due to suppression by somatostatin in vivo.

Adenoma↗
PubMed1993

Growth hormone (GH) and prolactin (PRL) gene expression and immunoreactivity in GH- and PRL-producing human pituitary adenomas.

Growth hormone(GH)-producing pituitary adenomas are morphologically heterogeneous and frequently contain not only GH immunoreactivity but also variable numbers of prolactin (PRL) immunopositive cells. Paraffin sections of 59 surgically removed GH- and/or PRL-producing adenomas classified by histology, immunocytochemistry (ICC) and electron microscopy were studied using in situ hybridization (ISH) for GH and PRL mRNA and combined with ICC for the coded hormones. Somatotroph adenomas (10 densely and 10 sparsely granulated tumours) and mammosomatotroph adenomas (10 cases) contained both GH mRNA and GH immunoreactivity. In 4 densely and 4 sparsely granulated somatotroph adenomas and 4 mammosomatotroph adenomas, only GH mRNA and its product were found. In 28 cases (6 densely and 6 sparsely granulated somatotroph adenomas, 10 mixed somatotroph-lactotroph adenomas and 6 mammosomatotroph adenomas) both GH and PRL mRNA were present, although no PRL immunoreactivity was not in 2 densely granulated somatotroph adenomas. In these cases, ISH for PRL mRNA combined with GH immunostaining revealed the presence of variable numbers of mammosomatotrophs. In 9 acidophil stem cell adenomas only PRL mRNA and its product were found; one tumour expressed both GH and PRL mRNA and their products. Nine lactotroph adenomas contained only PRL mRNA and PRL immunoreactivity. The results show that GH and/or PRL mRNA content could not be correlated with ICC for coded proteins and ultrastructural features. The mammosomatotrophs were more numerous using ISH when compared with ICC. Somatotroph, mammosomatotroph and mixed adenomas are closely related and they can be considered to represent one basic tumour type originating in a cell committed to GH production. This may undergo clonal differentiation towards a mammosomatotroph and further to the lactotroph line. The results also indicate that lactotroph adenomas arise in a cell committed to PRL production. Acidophil stem cell adenomas seem to be more closely related to lactotroph cells than somatotroph.

Adenoma↗
PubMed1993

Congenital gigantism due to growth hormone-releasing hormone excess and pituitary hyperplasia with adenomatous transformation.

The cause of gigantism in most patients is a GH-secreting pituitary tumor. In this report, a case of congenital gigantism due to probable central hypersection of GH-releasing hormone (GHRH) is described. Normal at birth (4.4 kg; 53 cm), our 7-yr-old male patient grew progressively thereafter to attain a height of 182 cm and a weight of 99.4 kg at the time of our evaluation. The markedly increased baseline plasma levels of GH (730 micrograms/L) did not suppress during a standard 3-h oral glucose tolerance test, but did increase 54% after iv infusion of GHRH. Baseline plasma levels of insulin-like growth factor-I, PRL, and immunoreactive GHRH were also markedly increased. Computed imaging of the head showed a large, partially cystic sellar and suprasellar mass. Extensive imaging studies did not localize a potential source of GHRH. Preoperative treatment with octreotide and bromocriptine for 4 months resulted in a 25% reduction of suprasellar tissue mass. The pituitary tissue removed at transsphenoidal and transfrontal operations showed massive somatotroph, lactotroph, and mammosomatotroph hyperplasia. Areas of GH- and PRL-secreting cell adenomatous transformation were also evident. No histological or immunohistochemical evidence of a pituitary source of GHRH was found. The peripheral plasma immunoreactive GHRH concentration remained unaffected by pharmacological and surgical interventions. We suspect that a congenital hypothalamic regulatory defect may be responsible for the GHRH excess in this case.

Adenoma↗
PubMed1993

Pituitary specific transcription factor messenger ribonucleic expression in adenomatous and nontumorous human pituitary tissues.

BACKGROUND: The pituitary-specific transcription factor, Pit-1/GHF-1 (Pit-1) is a member of the POU family of homeobox genes. This transacting factor has a role in the development and expression of selected anterior pituitary cells including prolactin, growth hormone (GH), and thyrotropin, cell types in rodent pituitary. The expression of Pit-1 mRNA in human pituitaries has not been previously analyzed and the role of specific secretagogues in the regulation of Pit-1 transcripts in human pituitary adenomas has not been examined. Analysis of Pit-1 expression in normal and neoplastic human pituitaries may provide insight into the specificity of this transcription factor for pituitary cell types and the role of Pit-1 in human pituitary function. EXPERIMENTAL DESIGN: In situ and Northern hybridization analyses were used to study the expression of Pit-1 mRNA in surgically removed human pituitary adenomas and nontumorous pituitaries obtained within 6 hours postmortem. A cultured GH surgically removed adenoma was used to analyze the regulation of GH and Pit-1 in vitro. RESULTS: In situ hybridization localized Pit-1 mRNA in all pituitary adenomas, although the mRNA levels in GH and prolactin adenomas were significantly higher than those in ACTH, null cell and gonadotroph tumors. Northern hybridization analysis revealed a 2.4 and a 1.2 kb mRNA transcript for Pit-1. Although GH mRNA transcript was markedly changed by dexamethasone and phorbol 12-myristate 13-acetate in vitro, Pit-1 mRNA transcripts were not changed significantly by these secretagogues. CONCLUSIONS: Pit-1 mRNA transcripts are expressed mainly in prolactin and GH pituitary adenomas, but are also found in other adenomas and in the nontumorous adult human pituitary. Pit-1 mRNA transcript levels are not readily modulated in cultured GH adenoma cells by various secretagogues in vitro compared with the marked modulation of GH mRNA transcripts by these same secretagogues.

Adenoma↗
PubMed1992

Ultrastructural diagnosis of human pituitary adenomas.

Electron microscopy, which has been instrumental in the characterization of normal pituitary cell types, has also played a crucial role in the morphologic classification of pituitary adenomas arising in the presently known 5 cell types, and in the recognition of 3 adenoma types with yet undisclosed cell derivation. This review deals with the application of electron microscopy for study of pituitary adenomas in order to provide specific pathological diagnosis and aid the clinician in selecting appropriate postoperative treatment. In addition to the ultrastructural appearance and diagnostic features of 15 adenoma types, the morphology of hyperplastic proliferations and that of known normal counterparts of various adenoma types are also discussed. Specific morphologic diagnosis of pituitary lesions is important not only for adequate postoperative management of patient, but is also a prerequisite for study of the natural history and biological behaviour of various adenoma types.

Adenoma↗
PubMed1992

Ultrastructure of the neurohypophysis.

This review summarizes our current knowledge of the ultrastructure of the human neurohypophysis and includes comments on its anatomy, physiology, and embryology. The neurohypophysis represents a unique tissue having neural and endocrine characteristics and possessing ultrastructural features distinct from those of conventional endocrine organs such as the anterior pituitary, thyroid, pancreatic islets, etc. In contrast to these glands, the neurohypophysis is composed of the processes of mature neurons. As such, it is not capable of synthesizing hormones but only of their storage and release. Neurosecretion is one of the most exciting areas of neuroendocrinology and, although spectacular progress has been achieved in elucidating the process, a number of aspects are incompletely understood. Recent evidence indicates that the magnocellular nuclei of the hypothalamus, the anatomic origin and functional basis of the neurohypophysis, produce not only vasopressin and oxytocin, the so-called "neurohypophyseal hormones," but a number of other biologically active peptides as well. The physiologic function of these substances is largely unknown but they may be of profound importance in endocrine homeostasis. Based on these novel findings, the role of the neurohypophysis in endocrine regulation has to be re-evaluated.

Exons↗
PubMed1992

Hyperthyroidism due to inappropriate secretion of thyrotropin in 10 patients.

PURPOSE: The syndrome of inappropriate thyroid-stimulating hormone (TSH) secretion, characterized by elevated serum free thyroxine and triiodothyronine levels in association with measurable serum TSH concentrations, remains an uncommon cause of hyperthyroidism that is being recognized with increasing frequency. The hyperthyroidism may be due to either neoplastic pituitary TSH secretion or selective pituitary resistance to thyroid hormone. In an effort to better understand this rare cause of hyperthyroidism, we undertook a retrospective analysis of our institution's experience with this condition. PATIENTS: We reviewed our cumulative experience (10 patients) with hyperthyroidism due to the syndrome of inappropriate secretion of TSH. RESULTS: Six patients were diagnosed with TSH-secreting pituitary adenomas and four were found to have selective pituitary resistance to thyroid hormone. One patient with tumor had a TSH-secreting pituitary adenoma in the setting of multiple endocrine neoplasia syndrome. In all patients with tumor, hyperthyroidism was successfully treated with transsphenoidal adenomectomy with or without pituitary radiotherapy. All four patients with pituitary resistance had thyroid ablation or resection prior to their correct diagnosis. Therefore, therapy for this group of patients involved thyroid hormone replacement and efforts to suppress TSH hypersecretion. All 10 patients have done well clinically, with follow-up ranging from 2 weeks to 13 years. CONCLUSIONS: Adequate treatment exists for the two primary causes of TSH hypersecretion. TSH-secreting pituitary adenomas are treated with surgery and, if necessary, adjuvant pituitary radiotherapy. The results are generally good if the tumor is diagnosed and treated at an early stage. Primary therapy for hyperthyroidism due to selective pituitary resistance to thyroid hormone is aimed at suppression of pituitary TSH hypersecretion. The evaluation of any patient with hyperthyroidism must be thorough and, in some cases, should include measurement of TSH to determine the presence of inappropriate secretion. Eliminating this diagnosis will help avoid improper and potentially harmful treatment of hyperthyroid patients.

Adenoma↗