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At least 19 recordsLinked to original sources
PubMed1991

[DNA diagnosis in endocrinological disease--pituitary disease].

Endocrine disorders have long been diagnosed by symptoms, before hormones were able to be measured by immunoassays. Recently, as molecular biological methods developed, DNA diagnosis has become available in many diseases including endocrine disorders. We present here DNA diagnosis in connection with anterior pituitary hormones. Our studies on thyrotropin (TSH) producing pituitary adenomas showed that TSH beta-subunit mRNAs of the adenomas were the same as those from normal pituitary tissues. Congenital isolated TSH deficiency is rare disease causing hypothyroidism including cretinism, severe mental and growth retardation. We have studied 3 families with consanguineous marriage and 2 families which were descendants of closed colonies. The molecular pathogenesis were elucidated in the cases of 3 Japanese families with consanguineous marriage. They had a same missense mutation in the 2nd exon of the TSH beta-subunit gene which made a restriction enzyme site, and could be analyzed either by genomic Southern blot analyses or by restriction enzyme digestion after amplification of genomic DNA by PCR. Congenital deficiency of growth hormone, prolactin, and TSH was first described in Snell dwarf mice. The gene encoding the nuclear factor Pit-1/GHF-1, which transactivates promoters of both growth hormone gene and prolactin gene, was shown to be the cause of Snell dwarf mice. A similar human case arose from a family with consanguineous marriage, and the relation with the pit-1/GHF-1 gene is now under study.

DNA↗
PubMed1999

Pituitary disease.

BACKGROUND: Pituitary disease is relatively uncommon, but because failure to recognise and manage it correctly has such severe repercussions, it has an importance out of proportion to its prevalence. OBJECTIVE: Pituitary disease may result in findings due to hormone excess or hormone deficiency. This article revisits the main clinical findings, investigations and treatment options for pituitary disease. DISCUSSION: The clinical presentation of pituitary disease varies from asymptomatic to severe features of endocrine disturbance. Establishing the diagnosis is not easy and requires a strong clinical suspicion supported by radiology and specific biochemical tests. Treatment is directed toward both the underlying pathology and the endocrine disturbances present.

Adult↗
PubMed1992

Adrenocorticotropic hormone and beta-endorphin concentrations in the inferior petrosal sinuses in Cushing's disease and other pituitary diseases.

Aim of the present study was the evaluation of ACTH and beta-endorphin-like-immunoreactivity (beta-ELI) in the inferior petrosal sinuses (IPS's) and in the peripheral blood of patients with Cushing's disease (Group 1), with GH- or PRL-secreting adenomas or nontumoral hyperprolactinemia (Group 2). These patients had undergone selective and bilateral simultaneous IPS sampling for diagnostic purposes or for neurosurgical indications. In the patients of Group 1, ACTH and beta-ELI levels were higher in the IPS ipsilateral than in the contralateral to the adenoma and in the periphery (p < 0.001). In the patients of Group 2 ACTH and beta-ELI levels were higher in the IPS's than in the peripheral blood (p < 0.001) and, in the 9 patients with GH- or PRL-secreting adenomas, they were higher in the IPS ipsilateral than in the contralateral to the adenoma and in the periphery (p < 0.05). A significant correlation exists between ACTH and beta-ELI in the periphery (p < 0.01; r = 0.72), in the IPS ipsilateral (p < 0.05; r = 0.54) and contralateral (p < 0.01; r = 0.66) to the adenoma in Group 1, but not in Group 2. In conclusion, higher beta-ELI levels were detected in the IPS's than in the peripheral blood not only in patients with Cushing's disease but also in those with other pituitary diseases not involving ACTH secretion. The absence of correlation between ACTH and beta-ELI in patients not bearing Cushing's disease suggests that in these conditions corticotrophs release ACTH and beta-endorphin in an independent manner.

Adenoma↗
PubMed1996

Spectrum of pituitary disease in multiple endocrine neoplasia type 1 (MEN 1): clinical, biochemical, and radiological features of pituitary disease in a large MEN 1 kindred.

Prolactinomas and somatotropinomas are reported to be the pituitary lesions most frequently associated with multiple endocrine neoplasia type 1 (MEN 1). However, few reports have documented the full spectrum of pituitary disease in this condition. We report herein the clinical, biochemical (PRL, alpha-subunit, insulin-like growth factor-I, cortisol, and thyroid function), and radiological (magnetic resonance imaging and computerized tomography scan) characteristics of pituitary disease occurring in a single MEN 1 pedigree containing 165 MEN 1-affected members. Pituitary lesions were detected in 30 (18%) of 165 patients overall. In the subgroup of MEN 1 patients (n = 131) living after recognition of MEN 1 in the kindred, pituitary lesions were detected in 25 (19%). In 76% of patients with pituitary lesions, the diagnosis was made by prospective screening; the remainder sought medical attention for symptomatic pituitary disease. Prolactinomas accounted for 76%, and nonfunctioning adenomas accounted for the remaining 24%. alpha-Subunit elevation was observed in 29% of 41 patients tested, and an aggressive alpha-subunit secreting macroadenoma developed in 1 subject with a previously documented prolactinoma. Progression of pituitary disease occurred in 47% of patients with prolactinoma. There were no cases of Cushing's disease, thyrotropinoma, or somatotropinoma. We conclude that 1) in addition to prolactinomas, nonfunctioning pituitary tumors are common in MEN 1; 2) alpha-subunit hypersecretion is frequent in MEN 1; 3) comprehensive screening may identify many clinically significant but asymptomatic pituitary lesions; and 4) prolactinomas occurring in MEN 1 may behave more aggressively than sporadic prolactinomas.

Adenoma↗
PubMed1982

Evidence for cellular mediated immunity in an animal model of autoimmune pituitary disease.

The anterior pituitary gland can be involved in an inflammatory reaction mediated by lymphocytes that leads to various degrees of dysfunction. In seven rabbits immunized with homologous pituitary tissue in complete Freund's adjuvant, a focal lymphocytic infiltrate, and increased fibrosis was observed in five. These changes were patchy in distribution and limited to the anterior pituitary. No inflammation was observed in five control animals. When incubated with pituitary extract, partially purified lymphocytes from four of the five animals with altered pituitary histology demonstrated a significant (p less than 0.05) stimulation of 3H-thymidine incorporation. Measures of antipituitary antibodies using indirect immunofluorescence were negative in experimental as well as control animals. The present studies characterize the histologic changes and suggest that cellular immunity plays a role in the pathogenesis of experimentally induced autoimmune pituitary disease.

Animals↗
PubMed2004

MJA Practice Essentials--Endocrinology. 9: Pituitary disease in adults.

Pituitary adenomas are found in 10%-25% of unselected autopsy series and are evident in about 10% of asymptomatic individuals by magnetic resonance imaging. Diagnosis of pituitary disorders is often delayed by lack of awareness and the subtlety of symptoms and signs. Hypopituitarism is suspected when peripheral hormone concentrations are low without an elevation in the corresponding pituitary tropic hormone(s). Severe adult-onset growth-hormone deficiency results in reduced muscle mass, increased fat mass and diminished quality of life, which are reversed by growth hormone replacement therapy. While trans-sphenoidal surgery remains first-line treatment for acromegaly, drug treatment has an important role in controlling residual growth-hormone excess and, in some circumstances, as first-line treatment. Dopamine-agonist therapy (cabergoline or bromocriptine) is the treatment of choice for micro- and macroprolactinomas. In patients with suggestive clinical features, elevated 24-hour urine free cortisol level is usually sufficient to diagnose endogenous Cushing's syndrome; careful additional investigation is needed to determine whether the cause is Cushing's disease (pituitary adenoma secreting adrenocorticotropic hormone [ACTH]), ectopic ACTH secretion or adrenal disease. Heightened awareness is needed to detect the sometimes subtle symptoms and signs of pituitary disease

Acromegaly↗
PubMed1983

Histological classification of pituitary disease.

Morphological features of pituitary disease are classified according to increased and decreased hormone production to allow clinical correlation with pathological processes. Increased hormone synthesis and secretion may be due to pituitary adenomas or carcinomas derived from the five hormone-secreting cell types, or to extrapituitary stimuli causing hypertrophy and hyperplasia of those cells. Various tumour-like conditions can mimic functioning adenomas. Rarely, no lesion is detected and intrinsic abnormalities of adenohypophyseal cells are implicated. Hypopituitarism can be selective or generalized. Diffuse hormone deficiency is usually attributable to tissue destruction by tumours, inflammatory or infiltrative conditions or vascular lesions. Congenital abnormalities of pituitary development may result in hypophyseal dysfunction. Hypothalamic abnormalities may cause generalized hypopituitarism or may involve only selective releasing factors and hormones. Feedback inhibition and receptor abnormalities may be implicated in pituitary hypofunction, and selective deficiencies may be the result of genetic abnormalities, immune reactions or toxic damage to one cell type.

Adenoma↗
PubMed1998

Pituitary diseases in pregnancy.

Pituitary adenomas are the most common pituitary disorder affecting pregnancy, and prolactinomas are the most common of the hormone-secreting pituitary adenomas. Hyperprolactinemia must be corrected to allow ovulation and fertility. Bromocriptine has been shown to be safe for use during early gestation. There is less than a 2% risk of microprolactinoma enlargement during pregnancy but a greater than 15% risk of symptomatic enlargement of a macroprolactinoma. Treatment options for patients with macroadenomas include stopping bromocriptine when pregnancy is diagnosed and reinstituting with tumor enlargement, continuous bromocriptine throughout pregnancy, and prepregnancy tumor debulking by surgery. The diagnosis of acromegaly may be difficult to make during pregnancy and relies, in part, on the persistence of the normal pulsatile secretion of growth hormone and loss of this secretory characteristic with a tumor. The growth hormone oversecretion may exacerbate tendencies to gestational diabetes, fluid retention, and hypertension. Treatment for acromegaly and other tumors generally may be deferred until after delivery. There are rare reports of enlargement of clinically nonfunctioning and growth hormone secreting tumors during pregnancy, and surveillance is needed. Tumors may need to be differentiated from lymphocytic hypophysitis. Patients with chronic hypopituitarism usually will need treatment with gonadotropins or pulsatile GnRH to become pregnant and may need increased steroid coverage during labor and delivery. Hypopituitarism developing during pregnancy is usually caused by lymphocytic hypophysitis and usually also will require steroid replacement therapy. Hypopituitarism arising postpartum may be caused by either lymphocytic hypophysitis or Sheehan's syndrome, and the latter may present as an acute or chronic syndrome. Borderline diabetes insipidus may manifest during pregnancy because of increased vasopressin degradation caused by markedly increased levels of placental vasopressinase. Treatment with desmopressin usually is satisfactory. Patients presenting with either anterior or posterior pituitary insufficiency in the peripartum period should always be evaluated for function of the other portion of the pituitary.

Acromegaly↗
PubMed2005

Apathy and pituitary disease: it has nothing to do with depression.

Increasingly, patients with pituitary disease are evaluated and treated at cancer centers. In many ways, these patients resemble patients with other malignant brain tumors. Although the majority of pituitary adenomas are benign, the physical, emotional, and cognitive changes that these patients experience on their well-being is malignant. Pituitary disease causes a variety of physical illnesses resulting from the alterations in the hypothalamic-pituitary-end organ axis. In addition, patients with pituitary diseases may experience many emotional problems, including depression, anxiety, behavioral disturbances, and personality changes, above and beyond the many reactions these patients may have to the myriad of adjustments that they must make in their lives. There is a growing understanding that pituitary patients may experience these emotional problems as a result of long-term effects that the pituitary tumor itself, treatment, and/or hormonal changes have on the hypothalamic-pituitary-end organ axis. The authors present a series of cases, in which patients with pituitary disease were diagnosed and treated for depression and showed little response to the treatment for depression. When the diagnosis of apathy syndrome was considered and treatment implemented, the patients' condition improved. A review of the literature on apathy, hypothalamic-pituitary-end organ axis dysfunction, and treatment for apathy syndrome is included.

Adenoma↗
PubMed1982

Polyamine levels in CSF from patients with pituitary tumors or nonneoplastic pituitary disease.

Cerebrospinal fluid polyamine determinations were performed in 21 patients harboring pituitary tumors and six patients with nonneoplastic pituitary disease. Although CSF putrescine levels were significantly elevated in some patients harboring tumors, other patients showed no elevation. Polyamine levels did not correlate with tumor size, as assessed by the presence or absence of suprasellar extension. Data on patients harboring nonneoplastic pituitary disease were variable. Compared with other findings from this laboratory on the use of polyamine levels for the diagnosis and management of other brain tumors, these findings suggest that CSF polyamine levels will not have a significant diagnostic role in the treatment of patients suspected to have pituitary disease.

Acromegaly↗
PubMed1997

[Disorders of gonadal function in hypothalamic-pituitary diseases].

Hypothalmic-pituitary-gonadal hormones are regulated by number of factors including GnRH, LH and FSH, and gonadal hormones. They are regulated also by pituitary prolactin, activin and inhibin. Hypogonadism is divided into primary and secondary hypogonadism. Secondary hypogonadism is caused by various lesions involving either the hypothalmus or the pituitary. In this paper, etiology, diagnosis and treatment of the secondary hypogonadism are described. The most frequent causes of hypothamic hypogonadism are hypothalamic tumors, such as germinoma. As the pituitary hypogonadism, pituitary tumors, and Sheehan's syndrome are most common disorders. Diagnosis of the secondary hypogonadism is made based on the diagnostic criteria established by The Research Group of the Japanese Ministry of Health and Welfare. The criteria includes signs and symptoms in addition to laboratory examinations such as measurement of serum gonadotropin, sex steroid and LH-RH test. First choice of the treatment of hyothalmic hypogondism is continuous pulsatile injection of synthetic LH-RH. In the pituitary hypogonadism, hCG, hMG, estrogen and testosterone or the combination of these are applied depending upon the age and other factors of the patients.

Adolescent↗
PubMed1999

Comparison of the low dose short synacthen test (1 microg), the conventional dose short synacthen test (250 microg), and the insulin tolerance test for assessment of the hypothalamo-pituitary-adrenal axis in patients with pituitary disease.

There is still uncertainty about what is the most appropriate test for assessment of the integrity of the hypothalamo-pituitary-adrenal (HPA) axis. Many advocate the insulin tolerance test (ITT), but this is unpleasant and resource intensive, and may occasionally give misleading results. The conventional [250 microg tetracosactrin, ACTH-(1-24)] short synacthen test (SST) has been used as a simple alternative to the ITT, but it has produced some falsely reassuring results with potentially serious consequences. A low dose [1 microg tetracosactrin, ACTH-(1-24)] short synacthen test (LDSST) has recently been advocated as a more reliable and safer alternative to ITT. Some studies, however, have failed to demonstrate any difference between SST and LDSST. The purpose of this study was to assess the clinical usefulness of LDSST compared to SST and ITT in patients with pituitary disease. We studied 64 patients with suspected or proven pituitary disease. All patients underwent SST and LDSST. Forty-two patients underwent ITT. There was a high correlation between the ITT and LDSST peak cortisol responses (r = 0.89; P < 0.0001), the ITT and SST 30 min cortisol levels (r = 0.83; P < 0.0001), and the LDSST peak cortisol response and the SST 30 min cortisol level (r = 0.85; P < 0.0001). In the LDSST, all but six patients achieved maximal cortisol response by 30 min. A plasma cortisol cut-off of 600 nmol/L is more helpful than 500 nmol/L for clinical decision-making using either the SST 30 min cortisol level or the LDSST peak cortisol response. The sensitivity of the LDSST was 100% (cortisol response of >600 nmol/L indicates intact HPA axis), with no falsely reassuring results. SST (pass cortisol level, >600 nmol/L) was less sensitive than LDSST, it produced 2 of 64 (3%) falsely reassuring results. Even the ITT (pass cortisol level, >500 nmol/L) failed to identify one patient with clinically evident cortisol deficiency. The results of this study indicate that both SST and LDSST, at a cortisol cut-off of 600 nmol/L, are safe for the purpose of clinical decision-making with regard to steroid replacement therapy in patients with pituitary disease. As the LDSST produced no falsely reassuring decisions, we suggest that this could replace the SST and ITT for initial evaluation of the HPA axis in patients with pituitary disease. We suggest administering 1 microg tetracosactrin, i.v., with sampling at 0, 20, and 30 min.

Adult↗
PubMed2002

Pituitary disease in MEN type 1 (MEN1): data from the France-Belgium MEN1 multicenter study.

To date, data on pituitary adenomas in MEN type 1 (MEN1) still have to be evaluated. We analyzed the data of a large series of 324 MEN1 patients from a French and Belgian multicenter study. Data on pituitary disease were compared with those from 110 non-MEN1 patients with pituitary adenomas, matched for age, year of diagnosis, and follow-up period. Genetic analysis of the MEN1 gene was performed in 197 of the MEN1 patients. In our MEN1 series, pituitary disease occurred in 136 of 324 (42%), less frequently than hyperparathyroidism (95%, P < 0.001) and endocrine enteropancreatic tumors (54%, P < 0.01). Mean age of onset of pituitary tumors was 38.0+/-15.3 yr (range, 12-83 yr). Pituitary disease was associated with hyperparathyroidism in 90% of cases, with enteropancreatic tumors in 47%, with adrenal tumors in 16%, and with thoracic neuroendocrine tumors in 4%. Pituitary disease was the initial lesion of MEN1 in 17% of all MEN1 patients. MEN1 pituitary adenomas were significantly more frequent in women than in men (50% vs. 31%, P < 0.001). Among the 136 pituitary adenomas, there were 85 prolactinomas and 12 GH-secreting, 6 ACTH-secreting, 13 cosecreting, and 20 nonsecreting tumors. Eighty-five percent of MEN1-related pituitary lesions were macroadenomas (vs. 42% in non-MEN1 patients, P < 0.001), including 32% of invasive cases. Among secreting adenomas, hormonal hypersecretion was normalized, after treatment, in only 42% (vs. 90% in non-MEN1 patients, P < 0.001), with a median follow-up of 11.4 yr. No correlation was found between the type of MEN1 germ-line mutation and the presence or absence of pituitary adenoma. Our study, based on a large group of MEN1 patients, shows that pituitary adenomas occur in 42% of the cases and are characterized by a larger size and a more aggressive presentation than without MEN1.

Adenoma↗