Silent Adenomas Research Articles

Clinically silent adrenal adenomas – their relation to the metabolic syndrome and to GNB3 C825T gene polymorphism

Aim of the study was to assess the prevalence of C825T GNB3 gene polymorphism in patients with adrenal incidentaloma (AI) as well as its relation to the metabolic syndrome (MS) and cortisol status. Alltogether 82 subjects (50 patients with AI, mean age 57.9 + 15 years and 32 subjects without AI, mean age 53.8 + 6.9 years) were included in this study. Parameters of glucose and lipid metabolism, serum adiponectin and the single nucleotide polymorphism C825T in GNB3 gene using PCR-RFLP method were examined. To detect subclinical Cushing syndrome an overnight dexamethason test was performed in all patients with AI. Patients with AI had signifcantly higher BMI, HOMA, triacylglycerols (p < 0.05) and significantly lower serum adiponectine (p < 0.05) than controls. There were no significant differences in metabolic parameters between group with and without subclinical Cushing syndrome (SCS). The prevalence of T allele of GNB3 gene in patients with AI was not significantly higher as compared with control group (32% vs. 47%). No significant differences in serum glucose and lipids between carriers of T and C alleles were detected. However carriers of T allele had significantly lower serum adiponectin than those with allele C (p < 0.01). We conclude that patients with AI had significantly higher cardiovascular risk factors that is not related to the presence of SCS. Moreover patients with AI and TC or TT genotype have significantly lower serum adiponectin which may be an early symptom of metabolic syndrome in patients with AI.

Localization of Carboxyl Ester Lipase in Human Pituitary Gland and Pituitary Adenomas

Carboxyl ester lipase (CEL) is an enzyme that hydrolyzes a wide variety of lipid substrates, including ceramides, which are known to show inhibitory regulation of pituitary hormone secretion in experimental models. Because no studies on CEL expression in human pituitary and pituitary adenomas have been reported in the literature, we investigated CEL expression in 10 normal pituitary glands and 86 well-characterized pituitary adenomas [12 FSH/LH cell, 17 α-subunit/null cell, 6 TSH cell, 21 ACTH cell, 11 prolactin (PRL) cell, and 19 GH cell adenomas] using IHC, immunoelectron microscopy, Western blotting, and quantitative RT-PCR. In normal adenohypophysis, CEL was localized in GH, ACTH, and TSH cells. In adenomas, it was mainly found in functioning GH, ACTH, and TSH tumors, whereas its expression was poor in the corresponding silent adenomas and was lacking in FSH/LH cell, null cell, and PRL cell adenomas. Ultrastructurally, CEL was localized in secretory granules close to their membranes. This is the first study demonstrating CEL expression in normal human pituitary glands and in functioning GH, ACTH, and TSH adenomas. Considering that CEL hydrolyzes ceramides, inactivating their inhibitory function on pituitary hormone secretion, our findings suggest a possible role of CEL in the regulation of hormone secretion in both normal and adenomatous pituitary cells.

A clinicopathological and immunohistochemical study of clinically non-functioning pituitary adenomas: A single institutional experience

Non-functioning pituitary adenomas (NFPA) are characterized by the lack of clinical syndrome as compared to functioning adenomas (FA) but not all functioning adenomas have clinical effects. Their exact incidence varies in different series. This study was undertaken to analyze the hormonal profile of NFPA at the immunohistochemical level in the Indian population and to see if any differences exist from the earlier studies. Their biological aggressiveness was also studied by MIB-1 labeling index (MIB-! LI) and Epidermal Growth Factor Receptor (EGFR) expression. These parameters along with their clinical behavior were correlated with radiological features of invasiveness and size. Of the 151 pituitary adenomas diagnosed during a period of one and half years, 77 (51%) were NFPA with a male predominance. There was increase in the incidence of NFPA with increase in age. Immunopositivity for various hormones was observed in 64 (83%) cases, either singly or in various combinations. On the basis of immunohistochemistry, NFPA were classified into three subtypes; gonadotroph adenomas, silent adenomas, and null cell adenomas. Gonadotroph adenomas were the commonest subtype. In general, NFPA showed low MIB-1LI but invasive NFPA had LI on the higher side, however, this difference was not significant. We observed EGFR positivity in two cases only; therefore the tumorigenesis mechanism may be different in NFPA. Although non-functional at the clinical level immunohistochemistry showed reactivity for various hormones. If a battery of immunostains including seven hormones is studied, a significant number of cases are shifted to the functional group.

Ultrastructure of mitochondria in various human pituitary tumor types

The mitochondria, the major powerhouse for cellular functions, are predominantly ovoid or rod‐shaped cytoplasmic organelles enclosed by double outer membrane. The cristae, are formed by the infoldings of the inner membranes. Morphologic variations in size, shape, number of cristae exist, attuned to the function of the resident organ. Specific ultrastructural features characteristic of certain tumor types may occur. Such mitochondrial alterations were recorded by EM in more than 5000 various types of surgically removed pituitary adenomas. Changes are chiefly quantitative: A) size and density of internal structures (large/small; active/functionally suppressed prolactinoma); B) increase in number, i.e. oncocytic change. Generally occurring within the endocrine system owing to functional decline. Most prevalent in gonadotroph adenomas lineage. Specific alterations: A) giant mitochondria: specific marker of acidophil stem cell adenoma. With preservation of the double membranes, progressive enlargement and disappearance of the internal compartment and occurrence of unidentified tubular structures take place; B) Mitochondrial enlargement and homogenization of the entire internal compartment evident only in gonadotroph adenoma. C) Close spatial association of mitochondria and RER. It occurs only in silent adenoma subtype 3. The specific alterations may be used as ultrastructural markers.

Pituitary Hemorrhage : Classification and Related Factors

Clinical features of pituitary hemorrhage vary from asymptomatic to catastrophic. The purpose of this study was to evaluate the factors related to severity of hemorrhage of pituitary adenoma. Pituitary hemorrhage was noted in 32 of 88 patients who underwent operations between January 2000 and December 2007. Clinical status was classified into group I (no hemorrhage symptoms), II (mild to moderate symptoms without neurological deficit), and III (with neurological deficit), and was compared to radiological, pathological, and operative findings. All patients were operated by transsphenoidal approach, and hemorrhage-related symptoms were relieved. Groups I, II, and III comprised 15, 10 and 7 patients, respectively. In group I, hemorrhage volume was under 1 mL in 11 (73.3%), but, it was above 1 mL in 7 (70%) of group II and in all cases of group III. Hemorrhage stage based on MRI findings was chronic or subacute in 11 (73.3%) of group I, acute in 6 (60%) of group II, and acute or hyperacute in 6 (85.7%) of group III. Pathological examination revealed chronic-stage hematomas in 5 (50%) group II patients. Functioning adenomas were found in 5 (33.3%) group I patients but none in group II or III patients. Silent adenomas were found in 4 (26.7%), 8 (80%), and 3 (42.9%) in groups I, II, and III, respectively. Clinical features of pituitary hemorrhage may differ with the radiological and immunohistopathlogical findings. Persistent symptoms are related to the chronic stage of hematoma requiring surgery for symptom relief. Neurological deficits are caused by large amount of acute hemorrhage requiring emergency operation. Silent adenoma is related to the severity of pituitary hemorrhage.

Cushing’s syndrome due to unilateral multiple adrenal adenomas as an extraintestinal manifestation of familial adenomatous polyposis

To the Editor: Familial adenomatous polyposis (FAP) is an autosomal dominantly inherited disorder that results when adenomatous polyposis coli (APC) protein function is lost due to a mutation in the APC gene on chromosome 5q21. The development of colorectal cancer stands out as the most prevalent complication, with an incidence of almost 100% by the age of 35–40 years if left untreated. Moreover, extraintestinal complications for which medical attention is essential are not rare, and estimated life time risk presumably exceeds 30%. Affected individuals can develop thyroid and pancreatic cancer, hepatoblastomas, central nervous system tumors (especially medulloblastomas), and various benign tumors like adrenal adenomas, osteomas, desmoid tumors, and dental abnormalities. We report a case of Cushing’s syndrome due to multiple adrenal adenomas as an extraintestinal manifestation of FAP. A 32-year-old man was referred to the Department of Endocrinology because of ankle edema, facial plethora and spontaneous hematomas. He gained 15 kg during the last 4 years. His medical history was remarkable for a subtotal colectomy with ileorectal anastomosis at age 16, as primary prophylactic treatment for FAP. Five years later, he underwent a proctectomy with an ileal pouch-anal anastomosis. Regular endoscopic follow-up according to current guidelines was performed. On physical examination, there were clear features of hypercortisolism such as a moon face, buffalo hump, enlarged fat pads that fill the supraclavicular fossae, easy bruisability of the skin, huge purple striae at the enlarged lower abdomen, proximal muscle wasting, and hypertension. Endocrine analyses revealed an increased urinary cortisol excretion (4,300 mmol/24 h, reference <270), while plasma adrenocorticotropic hormone concentrations were suppressed, pointing to an adrenal cause of Cushing’s syndrome. Subsequently, computed tomography revealed two tumors (3.5×3.5 and 3.2×3.0 cm) of the left adrenal gland with benign radiological characteristics. Adrenal masses are frequently occurring extraintestinal manifestations of FAP. They are two to four times more common in FAP than in the general population, but the clinical spectrum of these masses in FAP does not seem to be different. This can range from benign clinically silent adenomas to classical Cushing’s or Conn’s syndrome. Adrenocortical carcinomas and pheochromocytomas have also been described. Once a mass in the adrenals is identified, hormonal and (serial) radiological evaluation according the NIH conference guidelines needs to be performed. Patients should be referred to an endocrinologist. This is especially important since recent reports suggest that up to 20% of patients with an incidentally found adrenal mass have some form of subtle hormonal overproduction resulting in an increased risk for metabolic disorders and cardiovascular disease. Our patient was cured after left sided adrenalectomy. Histologic evaluation confirmed the presence of two adenomas, both with monomorphic cellular characteristics. Osteoporosis and two impression fractures of thoracic vertebrae had developed as a consequence of the longstanding hypercortisolemia. Genetic analysis showed a mutation of the APC gene at codon 1353 (c.4057delG, p.Glu1353fsX62), predicted to result in a premature stop codon.

Analysis of mRNA expression for steroidogenic enzymes in the remaining adrenal cortices attached to adrenocortical adenomas.

We have recently demonstrated that the adrenal cortices attached to aldosterone-producing adenoma (APA) contained microscopic subcapsular micronodules suggestive of active aldosterone production. In this study, we used in situ hybridization to investigate the mRNA expression of steroidogenic enzymes in the adrenal cortices attached to cortisol-producing adenoma (CPA) and clinically silent adenoma (non-functioning adenoma; NFA), in addition to APA. Microscopic subcapsular micronodules, which were several hundreds of micrometers in size and spheroid in shape, were observed in the cortices attached to CPA and NFA, as well as APA, at high frequency. Most of the cortical nodules in zona fasciculata to zona reticularis showed a suppressed steroidogenesis in the cortices attached to adenoma, but some expressed intensely all necessary steroidogenic enzyme mRNAs for cortisol synthesis. It is thus necessary to keep in mind, on the occasion of subtotal adrenalectomy, that lesions with the potential to later develop into functional adrenocortical nodules may be present in other parts of the ipsilateral or contralateral adrenal cortices.

Silent Parathyroid Adenoma Mistakenly Interpreted on FDG-PET as Thyroid Cancer Metastasis in a Patient With Elevated Thyroglobulin and Negative I-131 Whole Body Scan and Removed by Radioguided Minimally Invasive Surgery

Detection of recurrent and metastatic thyroid cancer remains a considerable challenge in patients presenting with rising thyroglobulin levels but with negative I-131 whole body scintigraphy. Such is the case in this patient with follicular thyroid cancer in whom subsequent FDG PET scanning showed a solitary hypermetabolic cervical lesion. With definitive management and multidisciplinary approach in mind, radioguided surgical excision came into play through the use of Tc-99m sestamibi, leading to successful removal of the lesion. Histopathology, however, revealed a parathyroid adenoma. This highlights the importance of considering differential diagnoses in apparent cases of recurrence to avoid potential pitfalls.

Relevance of Ki-67 and prognostic factors for recurrence/progression of gonadotropic adenomas after first surgery

Gonadotropin-secreting pituitary adenomas carry a high risk of local recurrence or progression (R/P) of remnant tumor after first surgery. The clinical characteristics and the long-term outcome of these silent adenomas, which show no signs of endocrine hyperfunction, differ from those of other types of pituitary adenomas. However, to date, no study has focused specifically on gonadotropic adenomas. To identify prognostic factors of R/P of remnants, we studied the postoperative outcome of 32 gonadotropic pituitary adenomas, defined on immunohistochemical staining, according to their clinical and radiological characteristics as well as the Ki-67 labeling index (LI). The Ki-67 LI failed to provide independent information for the identification of patients at risk of progression of remnants or recurrence. Multivariate survival analysis (Cox regression) showed that neither invasiveness nor remnant tumors nor hyposomatotropism influenced tumor recurrence. The strongest predicting factors of R/P were the antero-posterior (AP) diameter in the sagittal plane (P = 0.014), and the age of the patient at surgery (P = 0.047), with younger patients being at greater risk. Hazard ratios were 2.11 for each 5 mm increase in AP diameter and 0.57 for every 10 years of age. The two simple clinical criteria revealed by our study, the AP diameter of the tumor and the age of the patient, should be helpful in planning clinical management and radiological monitoring after first surgery of gonadotropic adenomas, while awaiting the identification of other pathological parameters.

Expression of Proliferation Markers in Human Pituitary Incidentalomas

This study aimed to immunohistochemically assess the proliferation activity of pituitary incidentalomas. A series of 52 incidentalomas studied included 22 gonadotroph cell adenomas, 21 null cell adenomas, and 9 clinically silent adenomas (identified as functioning by immunohistochemistry). We also analyzed the differences in proliferation activity between 43 non-functioning pituitary incidentalomas (not including 9 silent adenomas), and 43 symptomatic non-functioning adenomas (NFAs) that caused visual disturbance. Cell proliferation markers were immunostained using monoclonal Ki-67 (MIB-1) antibody and monoclonal anti-topoisomerase II alpha (Topo-II alpha) antibody. The average of MIB-1 labeling indices in pituitary incidentalomas was 0.61% +/- 0.06%. Overall, both MIB-1 and Topo-II alpha labeling indices of the incidentalomas were significantly lower than those of symptomatic NFAs. There were no significant differences in immunopositivity between the two groups based on gender, age, or subtype. The MIB-1 index of the smallest adenoma group in pituitary incidentalomas was significantly lower than in symptomatic NFAs, while the Topo-II alpha incidentaloma was significantly lower than in symptomatic NFAs. Our findings suggest that small or less invasive pituitary incidentalomas should be observed with follow-up MRI. Large or invasive incidentalomas should be surgically treated if the patients show visual disturbances, hypopituitarism, or pituitary apoplexy during the follow-up period.

Adenomas hipofisários produtores de glicoproteínas: patogênese, diagnóstico e tratamento

The glycoprotein-secreting pituitary adenomas comprise two distinctive clinical and pathological entities, the gonadotroph and the thyrotroph cell pituitary adenomas. Although they can be grouped together for producing hormones and/or subunits that are glycoproteins, these tumors originate from distinctive cell types (gonadotrophes and thyrotrophes) that are only remotely related. Gonadotroph cell adenomas are among the commonest types of pituitary adenomas, corresponding to the majority of the so-called "nonfunctioning" or clinically silent adenomas, while thyrotroph cell adenomas are extremely rare and usually present with hyperthyroidism due to inappropriate TSH secretion. In this article, we review the literature covering epidemiological, pathological, pathogenetic, clinical, diagnostic and therapeutic aspects of gonadotroph and thyrotroph cell adenomas. Greater emphasis was given to the growing field of molecular pathogenesis of pituitary tumors in general, and a special effort was made to contrast molecular alterations found in these tumors with other tumor types. On the practical side, the authors extensive experience for more than two decades in the diagnosis and management of these tumors at the Neuroendocrine Unit (Endocrinology Division, Unifesp) was used to balance the extensive literature on this subject.

Silent Adenoma Subtype 3 of the Pituitary—Immunohistochemical and Ultrastructural Classification: A Review of 29 Cases

The silent adenoma subtype 3 (SAS-3) of undetermined cellular derivation is a seemingly nonfunctioning aggressive pituitary tumor with a high recurrence rate. At the time of diagnosis SAS-3s are macro- or giant adenomas particularly aggressive in young individuals, especially women. They are usually associated with mild hyperprolactinemia and are unremarkable by histology. Immunohistochemistry, demonstrating scattered immunoreactivity mostly for GH, PRL, TSH, and α-subunit, is not diagnostic. Presently, only TEM permits conclusive diagnosis. Ultrastructurally, the large polar adenoma cells contain abundant RER, masses of SER, extensive multipolar Golgi apparatus, and unevenly clustered mitochondria, displaced by RER and SER, which may show close spatial relationship to RER. Cell membranes often form plexiform interdigitations. Nuclear pleomorphism and nuclear inclusions are common. The 100- to 200-nm secretory granules accumulate heavily in cell processes, which is a hallmark of glycoprotein hormone cell differentiation. The endothelial cells may contain tubuloreticular inclusions. Complete surgical removal of the large often invasive tumors is difficult necessitating postoperative treatment. SAS-3 is sensitive to conventional radiation. Some tumors express somatostatin receptors and respond well to somatostatin analogues, offering long-term control in patients with residual tumor. Possible derivation of SAS-3 from rostral thyrotrophs, a cell type presently known in rodents is comtemplated.

Pituitary disease: presentation, diagnosis, and management

The diagnosis of pituitary disease is generally uncomplicated. This is despite the high prevalence of occult pituitary adenomas in the general population, the widespread use of high definition imaging techniques,...

Adenomas corticotropos silentes: Presentación de dos casos que debutaron con apoplejía hipofísaria

Among the group of pituitary adenomas surgically treated, about 25-30% are not associated with clinical or analytical findings of hormonal hypersecretion. The development of immunohistochemical techniques has allowed the demonstration of a subgroup of adenomas that show immunoreactivity against several hormones among the group of, apparently, non-functioning adenomas. This subgroup has been called silent adenomas. Silent adenomas positive for ACTH show a singular clinical picture and different from those adenomas producing Cushing's disease, as they present more frequently as macroadenomas, with more frequent pituitary apoplexy, invasion of cavernous or sphenoidal sinus and recurrences. We present two new cases of silent corticotroph adenomas in two female patients that presented with pituitary apoplexy, one of them after giving birth after a normal full-term pregnancy. Both of them presented with macroadenomas that invaded the sphenoidal and cavernous sinus. Although both tumors were immunoreactive for ACTH, none of the patients presented clinical or analytical findings compatible with Cushing's disease.

Are the silent corticotroph adenomas a new category of ACTH-producing tumours?

A minority of corticotroph adenomas are not related to Cushing's disease so that they have been defined “silent corticotropinomas“. Silent ACTH adenomas present with symptoms of mass effect, they are often haemorrhagic and show more aggressive behaviour than the conventional pituitary adenomas. Likely deriving for the POMC cells of the pars intermedia, silent corticotroph adenomas have been considered a separate entity within the spectrum of ACTH-producing adenohypophysial tumours. We studied 20 patients with non-functioning ACTH adenoma operated over the period January 1992– April 2003 at the Bellaria Hospital, Bologna, Italy. All had normal free urinary 24 hr cortisol level. Nine were female. Their age ranged from 34 to 77 years (mean, 52 years). Despite normal urinary cortisol, serum ACTH was markedly elevated in two patients (42 and 89.6 pmol/L, respectively; normal, 2–11) and slightly increased in 3. Radiologically, all lesions were macroadenoma and 12 were invasive. Cystic component was present in 5. Pathological examination revealed 8 adenomas type I, 3 of which were Crooke's cell adenomas, and 12 lesions of type II. One tumour was atypical in that it showed mitoses, MIB-1 labelling index higher that 3% and p53 nuclear over-expression. Pseudopapillary architecture due to poor cell-to-cell cohesion predominated in the majority of lesions. After a follow-up ranging from 12 to 136 months (mean, 54 months), three patients experience local recurrence but none died of disease. Silent corticotroph adenomas were compared with Cushing's related adenomas, particularly with the 13 macroadenomas operated in the same period. In these latter lesions, symptoms of mass effect were less common than in the silent tumours. Percentage of invasion was similar in the two groups whereas cystic change was more common in silent corticotropinomas. Persistence/recurrence rate was as high as noted in the silent adenoma groups. Pseudopapillary pattern was also a common finding on Cushing-related macroadenomas. Finally, we studied 5 silent corticotroph carcinomas. Patient's age ranged from 26 to 58 years. They had normal serum and free urinary cortisol as well as normal serum ACTH. All tumours were invasive macroadenoma. Histologically, 3 primary tumours were indistinguishable from conventional silent ACTH adenomas and 2 had features of atypical adenoma. All patients experienced local recurrence and, after a follow-up ranging form 2 to 23 years, all had metastases, 3 outside the central nervous system. Four patients died of disseminated disease and 1 of myocardial infarction. No patient developed Cushing's disease. Many of their clinicopathological features were similar to those of previously reported Cushing's disease related carcinomas. Our results suggested that some clinical and pathological features of silent corticotroph adenomas and carcinomas overlap with those of Cushing-related lesions. Therefore, silent adenomas are more likely part of the continuum of ACTH-producing tumours than a separate entity.

ACTH silent adenoma shrinking under cabergoline

The authors present a case report that proposes the use of cabergoline treatment in silent ACTH adenoma, an unusual member of the heterogeneous group of the so-called clinically non-functioning pituitary adenomas. Following the clinical and radiological improvement of a recurrent silent ACTH adenoma in a 77-year-old patient treated with cabergoline (0.5 mg every 2 days for 2 years), in vitro studies of the original tumor were performed. The original tumor from the patient was studied by in situ hybridization and dopamine D2 receptor autoradiography. It was compared with four macroprolactinomas and two macroadenomas from patients with Cushing's disease. The D2 receptor mRNA signal of the reported case was intense and of the same order of magnitude as that observed in control prolactinomas. Dopamine D2 receptor autoradiography was twice that of control corticotroph adenomas and was close to that observed in prolactinomas. This is the first description of an in vivo shrinkage of an ACTH silent adenoma under cabergoline. We demonstrate in vitro, the presence of D2 receptors in the primitive tumor in concentrations similar to those found in control prolactinomas. These results suggest that therapeutic trials with cabergoline might be undertaken in recurring cases of ACTH silent tumors and more generally, non-functioning pituitary adenomas.

Localization of insulin-like growth factor-II mRNA in human pituitary adenomas.

Insulin-like growth factors (IGFs) have been reported to promote cell proliferation in many tumours, but their contribution to pituitary adenoma development and growth has not been characterized. We report the presence of insulin-like growth factor II (IGF-II) mRNA in pituitary adenomas using in situ hybridization (ISH). The intensity of IGF-II hybridization signal was correlated with adenoma type, and the presence of Ki-67. Among the 109 adenomas examined, 55 (50.4%) were positive for IGF-II mRNA. All acidophil stem cell, functioning corticotrophic and plurihormonal adenomas contained the message; a high incidence of signal was found among sparsely (7/8) and densely (4/6) granulated growth hormone (GH) cell adenomas, mixed GH cell-prolactin (PRL) cell adenomas (6/7), thyrotrophic (4/6) and null-cell (6/7) adenomas. Less frequently, IGF-II mRNA was localized in mammosomatotrophic, silent subtype 3, gonadotrophic, and oncocytic adenomas, whereas all sparsely granulated PRL cell adenomas and silent corticotrophic adenomas of subtypes 1 and 2 were negative. The MIB-I labelling index was significantly higher in adenomas with a moderate to intense IGF-II signal than in adenomas with weak or no signal. The results suggest that IGF-II, when highly expressed, may have a role in pituitary adenoma proliferation.

Late complications in remission from Cushing disease. Recurrence of tumor with reinfarction or transformation into a silent adenoma

Late complications in remission from Cushing disease. Recurrence of tumor with reinfarction or transformation into a silent adenoma

Incidence, Pathology, and Recurrence of Pituitary Adenomas: Study of 647 Unselected Surgical Cases.

The incidence of various types of unselected pituitary adenomas based on correlation of pathologic and clinical data was assessed. We investigated 647 cases of unselected pituitary adenomas, which were surgically removed between 1980 and 1993. All cases were examined by immunohistochemistry and electron microscopy. The mean age of patients was 44.0 years with 40.0 years for women (55.2%) and 49.1 years for men (44.8%). Age distribution indicated a remarkable sex difference: 52.4% of women and 26.8% of men were between 21 and 40 years at the time of surgery. Based on immunohistochemistry and electron microscopy, prolactin (PRL) cell adenomas represented 263% of tumors, growth hormone (GH) cell adenomas 12.5%, adrenocorticotrophic hormone (ACTH) cell adenomas 12.4%, oncocytomas 12,4%, and gonadotroph cell adenomas 9.4%. Seventy-three percent of the prolactinomas occurred in women and 73.8% of the oncocytomas were found in men. The incidence of pediatrics pituitary adenomas was 4.6%. All 647 cases were followed up; the mean follow-up period was 96.6 months. In 40 patients (6.2%), the adenoma recurred. Recurrence was common in functioning ACTH cell adenomas (8 cases: 9.5%) followed by silent adenomas (7 cases: 25.9%). Recurrence was noted after 2-96 months (average 28.7 months) following surgery. The shortest remission period was found in a patient with oncocytoma followed by a patient with prolactinoma.

Hemorrhage from Spontaneous Rupture of a Parathyroid Adenoma (A Case Report)

A case of extracapsular hemorrhage from spontaneous rupture of a parathyroid adenoma is reported. In the case presented here, adenoma was revealed by a sudden onset of a huge ecchymosis and hematoma of the entire anterior neck and right chest, causing recurrent nerve paresis. These cases of hemorrhage from rupture of silent parathyroid adenoma mimicking a dissecting thoracic aortic aneurysm are discussed.