Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute and prolonged alpha 1-24 corticotropin stimulation was performed on a treated chromophobe adenoma patient with partial ACTH deficiency and extreme hyperprolactinemia. Cortisol and aldosterone stimulated normally. However, the basal concentrations of androstenedione (A) and dehydroepiandrosterone (DHA) were low, and that of DHA-sulfate (DHAS) was undetectable. Furthermore, A and DHA did not stimulate normally, and DHAS did not stimulate at all. It has been claimed that adrenal androgen production is increased in hyperprolactinemia. However, the inability of prolactin (Prl) to maintain adrenal androgen (AA) secretion, with and without added ACTH, is demonstrated in this patient.
 ...
PMID:Lack of adrenal androgen stimulation by ACTH in extreme hyperprolactinemia. 22 82

Thyroid hormone and thyrotropin (TSH) levels were evaluated before and after adrenal replacement in eight patients (six men and two women, 35-62 years old) with isolated adrenocorticotropin (ACTH) deficiency. Six patients (cases 1-6) showed TSH excess before treatment. Four patients (cases 1-4), who initially had subnormal thyroid hormone levels, showed resolution of biochemical features of primary hypothyroidism after treatment, although TSH excess has persisted in two patients (cases 1 and 2). Case 1 had an extremely high titer of antimicrosomal antibody (MCHA), and cases 2 and 3 showed histologically and cytologically chronic thyroiditis, despite negative results for MCHA and antithyroglobulin antibody, respectively. Two patients (cases 5 and 6), who had had normal thyroid hormone levels and did not show the significant rise in serum T3 in TSH releasing hormone testing, showed TSH normalization without changes in serum thyroid hormone levels after treatment. The other two patients (cases 7 and 8), who initially had normal TSH and thyroid hormone levels, did not show the significant changes in serum TSH and thyroid hormone levels after treatment. The prevalence of chronic thyroiditis coexistence in isolated ACTH deficiency may be higher than predicted. Therefore, TSH excess before adrenal replacement may be attributed to not only direct enhancement of TSH release due to chronic cortisol deficiency but also to thyroid dysfunction due to chronic thyroiditis. It is possible that hypothyroidism due to chronic thyroiditis can be improved only by adrenal supplementation.
 ...
PMID:Evaluation of thyroid function in patients with isolated adrenocorticotropin deficiency. 133 72

In a 46 year old man, who arrived at our observation suffering for three months from considerable increasing weakness and progressive impairment of libido, we documented a condition of secondary hypocorticism due to an isolated ACTH deficiency associated with a reduced somatotropin reserve, the last improved after treatment with corticosteroids. We found low serum levels of ACTH and cortisol, good response of adrenal glands to corticotropin depot, normalization of the clinical board during glucocorticoid replacement. Stimulating test with CRH (corticotropin releasing hormone) did not cause a response in ACTH, suggesting the presence of primitive damage of the hypophyseal corticotroph cells.
 ...
PMID:[Isolated ACTH deficiency and transient GH deficiency. Presentation of a case]. 133 49

We describe 2 patients presenting with severe chronic hyponatremia in whom clinical and biochemical features strongly suggested the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Both, however, were proven to have a primary pituitary deficiency of corticotropin. Their short synacthen tests were only mildly abnormal but associated with low basal ACTH levels. The diagnosis of ACTH deficiency was made more convincingly by their dramatic response to glucocorticoid replacement therapy. In patients in whom no cause for SIADH can be found, a trial of maintenance cortisol therapy is warranted to exclude this eminently treatable condition.
 ...
PMID:Corticotropin deficiency: a rare cause of hyponatremia mimicking SIADH. 164 96

We found symptomatic hyponatremia in four elderly patients in which serum sodium (Na) levels ranged from 101 to 122 mEq/l. All 4 patients had low levels of plasma adrenocorticotropic hormone (ACTH), serum cortisol, and urinary excretion of 17-OHCS, and poor responses of ACTH to exogenous insulin and antidiuretic hormone (ADH). Other pituitary hormones were all normal. They were therefore diagnosed as having isolated ACTH deficiency. Plasma ADH was relatively high despite hypoosmolality which was associated with the hyponatremia. Water loading test revealed impaired water excretion and poor suppression of plasma ADH. Replacement with 20-30 mg hydrocortisone completely restored the serum Na level and restored the plasma ADH level to the normal range in all 4 patients. Other factors such as decreased glomerular filtration, enhanced urinary Na loss and decreased Na intake were also included. These results indicate that there is marked hyponatremia and that in the presence of hypoosmolality the sustained secretion of ADH is the key factor in causing the impaired water excretion and hyponatremia in isolated ACTH deficiency.
 ...
PMID:Role of antidiuretic hormone in hyponatremia in patients with isolated adrenocorticotropic hormone deficiency. 166 14

A 62-year-old man was admitted because of nausea and vomiting. Severe hyponatremia with renal sodium loss was found. Endocrinological studies revealed that the patient had isolated adrenocorticotropin (ACTH) deficiency and secondary adrenocortical insufficiency. Furthermore, an inappropriate secretion of antidiuretic hormone (ADH) in relation to the low plasma osmolality was observed at an early stage of hyponatremia. Hydrocortisone therapy effectively corrected his hyponatremia. Following the correction of hyponatremia, the value of free water clearance increased and the level of the plasma ADH decreased. Thus, the present case indicates that ACTH deficiency can cause the syndrome of inappropriate secretion of ADH.
 ...
PMID:Inappropriate secretion of antidiuretic hormone in isolated adrenocorticotropin deficiency. 185 May 79

A 44-yr-old man with hypocortisolism was shown to have an undetectable basal plasma ACTH level and absent or subnormal ACTH and beta-lipotropin responses to provocative testing with insulin, vasopressin, and CRH. Endocrine function after glucocorticoid replacement was otherwise normal, thus establishing the diagnosis of isolated ACTH deficiency. This patient's serum was tested immunohistochemically for the presence of an antipituitary antibody by indirect immunofluorescence of rat pituitary tissue. Positive immunostaining was observed in stellate-shaped cells in the anterior and intermediate lobes. Immunopositive cells were shown by immunoelectron microscopy to have ultrastructural characteristics of corticotrophs. Immunoreactivity was concentrated in secretory granules 120-170 nm in diameter. In a double immunolabeling procedure, staining by the patient's serum was shown to colocalize with rabbit antiserum to ACTH, but not with antisera to PRL, GH, beta TSH, or beta LH. Immunoabsorption of the patient's serum with ACTH-(1-24), ACTH-(1-39), gamma MSH, corticotropin-like intermediate lobe peptide, beta-endorphin, or beta-lipotropin failed to diminish immunolabeling in the pituitary. We conclude that the antipituitary antibody in this patient's serum shows immunohistochemical specificity for a rat corticotroph antigen located in secretory granules that is neither ACTH nor any of the proopiomelanocortin (POMC)-derived peptides tested. The autoantigen could be a cell-specific granular factor involved in the posttranslational processing of POMC or secretion of ACTH. We postulate that an autoimmune process may account for this patient's disease, and that his antipituitary antibody could play a pathogenic role by either inhibiting a POMC-processing enzyme or initiating an antibody-dependent cell-mediated cytotoxicity reaction, resulting in the selective destruction of corticotrophs.
 ...
PMID:Isolated adrenocorticotropin deficiency associated with an autoantibody to a corticotroph antigen that is not adrenocorticotropin or other proopiomelanocortin-derived peptides. 215 84

A 42-year-old man suffered a head injury in a road traffic accident and subsequently developed anosmia and isolated adrenocorticotropic hormone (ACTH) deficiency. There was no other evidence of pituitary dysfunction. No previous case of isolated ACTH deficiency following head injury has been reported.
 ...
PMID:Anosmia and isolated ACTH deficiency following a road traffic accident. Case report. 216 80

In order to elucidate whether pituitary peptides other than ACTH which are derived from the proopiomelanocortin (POMC) are involved for aldosterone secretion in primary aldosteronism, we administered ovine corticotropin releasing factor (CRF), beta-endorphin and naloxone to seven patients with aldosterone producing adenoma. One hundred micrograms of CRF produced an augmented aldosterone response in patients with aldosteronism, while 500 micrograms of beta-endorphin infusion failed to cause any significant changes in neither normal subjects nor patients. An opioid antagonist, naloxone (10 mg, iv) produced no noticeable change in plasma aldosterone in normal subjects, while it caused a slight increase in patients with primary aldosteronism. Plasma cortisol increased to a similar degree in response to CRF and naloxone in normal subjects and patients. In three patients with isolated ACTH deficiency, neither aldosterone nor cortisol responded to these stimuli. The present results indicate that POMC-derived pituitary peptides other than ACTH are unlikely to participate in the aldosterone secretion in normal subjects or in patients with primary aldosteronism.
 ...
PMID:Pituitary peptides other than ACTH may not be aldosterone secretagogue in primary aldosteronism. 217 3

A 34-year man was admitted to the hospital with symptoms of hypoglycemia. The endocrine investigations indicated adrenocortical insufficiency secondary to isolated ACTH deficiency: low ACTH and cortisol plasma levels, significant increase of cortisol following prolonged stimulation with depot tetracosactrin, normal secretory reserve of other anterior pituitary hormones. The absence of ACTH-response after corticotropin releasing hormone and insulin tolerance tests suggested a primary impairment of corticotropin cells.
 ...
PMID:[Isolated ACTH deficiency: description of a clinical case]. 217 82


1 2 3 4 5 6 7 8 9 Next >>