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

Addison's disease is an uncommon endocrine condition manifested by a variety of nonspecific symptoms, such as malaise, anorexia and nausea. Symptoms usually do not occur until most of the adrenal gland has been destroyed. Autoimmune disease has surpassed tuberculosis as the primary cause of Addison's disease. Nevertheless, tuberculosis still accounts for a significant proportion of cases. The rapid adrenocorticotropic hormone (ACTH) stimulation test is useful for identifying adrenal insufficiency. Maintenance therapy consists of hydrocortisone and fludrocortisone.
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PMID:Addison's disease. 200 21

The immunoradiometric assay of the blood serum was performed in 61 patient with cancer and in 57 patients with tuberculosis of the lungs to determine the content of adrenocorticotropic hormone (ACTH), hydrocortisone, triiodothyronine++ (T3), thyroxin (T4), ferritin and carcinoembryonic antigen (CEA). In 200 patients (104 suffered from pulmonary tuberculosis, 9--pulmonary cancer), entropy of the protein fractions of the blood serum was determined. It was established that in differential diagnosis of pulmonary cancer and tuberculosis, the determination of CEA, hydrocortisone and entropy of the protein fractions of the blood serum in the complex with the other methods were of significant importance, the determination of ACTH and ferritin content were less important.
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PMID:[Use of non-traditional methods of examination in the differential diagnosis of cancer and tuberculosis of the lungs]. 255 39

The pituitary glands of 18 patients with untreated Addison's disease were studied by histologic and immunocytochemical methods. Adrenal destruction was caused by tuberculosis (13 cases) or autoimmune adrenalitis (five cases), and the duration of the adrenal insufficiency ranged from one to 16 years. Both diffuse and nodular hyperplasia of corticotropic cells were evident in each case, and the extent of hyperplasia correlated with the duration of disease. In five cases, nodular proliferations with morphologic features between those of hyperplasia and those of adenoma, termed tumorlets, were identified, as were two microadenomas, only one of which was available for study. In all instances, the proliferating corticotrophs stained positively with PAS and were immunoreactive for adrenocorticotropic hormone and beta-endorphin. We conclude that diffuse and nodular corticotroph hyperplasia are common in untreated Addison's disease, although frank adenoma formation seems to be rare. The latter may be related to the short duration of disease or may imply the absence of additional, unknown factors that are required for adenoma growth.
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PMID:The pituitary gland in untreated Addison's disease. A histologic and immunocytologic study of 18 adenohypophyses. 630 13

A 40-year-old man with Addison's disease due to adrenal tuberculosis retained high levels of adrenocorticotropic hormone (ACTH) after conventional hydrocortisone replacement. Plasma ACTH levels were completely suppressed by usual replacement with hydrocortisone (20 mg at 8:00 and 10 mg at 21:00) but rebounded to abnormally high levels the following morning. Administration of 2 mg or 8 mg of dexamethasone suppressed ACTH and cortisol. Magnetic resonance imaging of the brain showed a low-intensity lesion of the pituitary gland. Pituitary hyperplasia or microadenoma with preserved regulation of ACTH was considered to be the cause of the high plasma ACTH levels. The combination of hydrocortisone and dexamethasone reduced plasma ACTH levels.
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PMID:Hyper-adrenocorticotropinemia in a patient with Addison's disease after treatment with corticosteroids. 884 62

Adjuvant arthritis (AA) is an experimental model for rheumatoid arthritis, and is induced most easily in inbred Lewis rats by an intradermal injection of heat-killed Mycobacterium tuberculosis (MT) in incomplete Freund's adjuvant. Susceptivity to the arthritis in Lewis rats is thought to be related to a defect in their responses of the hypothalamo-pituitary-adrenal (HPA) axis to the disease. Because the use of an inbred strain is necessary for our immunological studies, we examined in Lewis rats changes in behavior, the HPA axis, and sympathetic nerve activities during development of the adjuvant arthritis. Following intradermal injections of heat-killed MT in adjuvant, the arthritis began to develop on day 12, reaching its maximum severity on day 21, and remained at the level for over a month. The body temperature rose from day 0 to 5 (the primary phase--before the onset of the arthritis). It then fell to normal temperature, and again rose from day 10 to 21 (the secondary phase--with fully developed arthritis). The behavioral (physical activity, food, and water intake) and hormonal parameters [plasma adrenocorticotropic hormone (ACTH) and corticosterone levels] also changed in two phases, similar to those observed in the temperature responses. No change in plasma vasopressin level was observed. Sympathetic nerve activities, assessed by changes in plasma noradrenalin levels, increased more in the primary than in the secondary phase. The possible causes for the biphasic changes associated with development of arthritis are discussed.
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PMID:Biphasic changes in behavioral, endocrine, and sympathetic systems in adjuvant arthritis in Lewis rats. 884 5

Genitourinary tuberculosis (TB) rarely involves the adrenal gland. A 67-year-old man presented with progressively hyperpigmented skin and an enlarged mass over both testes. Early morning plasma cortisol concentration was low and adrenocorticotropic hormone (ACTH) concentration was high. A rapid ACTH stimulation test revealed the absence of plasma cortisol response and confirmed a diagnosis of primary adrenocortical insufficiency. An abdomen computed tomography (CT) scan disclosed enlargement of the right adrenal gland and punctuate calcification over the left one. This is compatible with tuberculous adrenalitis. Currettage biopsy of the prostate demonstrated chronic granulomatous inflammation with Langerhan's giant cells, but without TB bacilli. Anti-TB treatment, in addition to glucocorticoid and mineralocorticoid replacement, was administered. The testicular mass decreased progressively though the results of a subsequent ACTH stimulation test, six months later, disclosed no significant change. A follow-up CT scan, one and a half years later, showed a decrease in the size of the right adrenal mass.
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PMID:Genitourinary tuberculosis complicated with adrenal involvement and primary adrenocortical insufficiency: a case report. 955 50

The emergence of a severe infection in albino rats during cortisone administration is reported. Evidence is present that the causative agent of the disease was Corynebacterium pseudotuberculosis murium, a microbial species not demonstrably a part of the usual bacterial flora of the host. It has been possible to reproduce the disease in rats by a relatively large infecting inoculum of this strain of Corynebacterium, but the susceptibility of normal rats to infection has been found to be low. The disease occurred in 41 of 50 rats given cortisone and in 28 of 30 instances in which isolation of the etiologic agent was attempted, this strain of Corynebacterium was recovered. The disease was characterized by widespread necrotizing lesions, with multiple coalescent lesions occurring in the lungs, and similar, though smaller lesions of the pericardium, pleurae, liver, and kidneys. In its gross appearance the pulmonary disease was similar to that of a disseminated, far advanced tuberculous process. The histologic appearance of the lesions, however, was sufficiently distinctive so that they could be readily differentiated from the lesions characteristically produced by Mycobacterium tuberculosis. Moreover, the host-parasite relationship established by the experimental infection with avian tubercle bacilli, was not markedly altered by the factors which led to the emergence of the pseudotuberculosis. In contrast to the high frequency of pseudotuberculosis in rats given cortisone, no instance of this disease has been encountered in a similar group of animals given large quantities of corticotropin.
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PMID:The emergence of pseudotuberculosis in rats given cortisone. 1493 8

Although opioid peptides such as methionine (met)-enkephalin have been previously shown to enhance or suppress immune responses, few studies in animal models have addressed the immunomodulatory activity of their metabolic derivatives. Hairless (IAF/HA-HO) guinea pigs immunized with Freund's complete adjuvant containing Mycobacterium tuberculosis and repeatedly skin tested with purified protein derivative of tuberculin (PPD) display high levels of stable delayed-type hypersensitivity (DTH) to PPD. Met-enkephalin (YGGFM) and two of its metabolites (YGG, YG) enhanced and accelerated PPD-elicited DTH inflammatory reactions when injected together with elicitor in these animals. At 24 h, 5 x 10(-3) pmol met-enkephalin significantly enhanced DTH responses by 30% over PPD alone, while 5 x 10(-5) pmol of YGG and 5 x 10(-9) pmol of YG significantly enhanced these responses by 62 and 32%, respectively. At much higher doses (5 x 10(3) pmol), met-enkephalin and its metabolites significantly suppressed DTH reactions by 25-32%. Tyrosine and glycine had no effect on PPD-elicited DTH. All DTH reactions (control, enhanced, suppressed) displayed typical perivascular mononuclear cell infiltrates. We conclude that the immunoactivity of met-enkephalin resides in its first two amino acids and suggest that cleavage of enkephalin molecules to YG occurs in serum and/or on the cell surface.
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PMID:Modulation of delayed-type hypersensitivity responses in hairless guinea pigs by peptides derived from enkephalin. 1506 5

Inflammatory and granulomatous diseases of the pituitary are rare causes of sellar masses. Lymphocytic hypophysitis is the most relevant of these disorders, and it is characterised by autoimmune pathogenesis with focal or diffuse inflammatory infiltration and varying degrees of pituitary gland destruction. Endocrine symptoms may include partial or total hypopituitarism, with adrenocorticotropic hormone (ACTH) deficiency being the earliest and most frequent alteration. Pituitary abscess is a rare but potentially life-threatening disease and, in 30-50% of patients, anterior pituitary hormone deficiencies or central diabetes insipidus (DI) at onset may be observed: the earliest manifestation being growth hormone deficiency (GHD), followed by follicle-stimulating hormone (FSH)/luteinising hormone (LH), thyroid-stimulating hormone (TSH) and ACTH deficiencies. Fungal infections of the pituitary are also very rare and include aspergillosis and coccidioidomycosis. Concerning pituitary involvement in systemic diseases, in sarcoidosis endocrine complications are rare, but the hypothalamus and pituitary are the glands most commonly affected. DI is reported in approximately 25-33 % of all neurosarcoidosis cases and is the most frequently observed endocrine disorder. Hyperprolactinaemia and anterior pituitary deficiencies may also occur. Rarely, partial or global anterior pituitary dysfunction may be present also in Wegener's granulomatosis, either at onset or in the course of the disease, resulting in deficiency of one or more of the pituitary axes. Other forms of granulomatous pituitary lesions include idiopathic giant cell granulomatous hypophysitis, Takayasu's disease, Cogan's syndrome and Crohn's disease. The hypotalamic-pituitary system is involved mainly in children with Langerhans' cells histiocytosis who develop DI, which is the most common endocrine manifestation. Anterior pituitary dysfunction is found more rarely and is almost invariably associated with DI. Pituitary involvement may also be observed in another form of systemic hystiocitosis, that is, Erdheim-Chester disease. Tuberculosis is a rare cause of hypophysitis, which may present with features of anterior pituitary dysfunction, such as hypopituitarism with hyperprolactinaemia. In conclusion, in patients with a sellar mass and unusual clinical presentation (DI, neurological symptoms), aggressiveness and onset and in the presence of systemic diseases, inflammatory and granulomatous pituitary lesions should be carefully considered in differential diagnosis.
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PMID:Pituitary tumours: inflammatory and granulomatous expansive lesions of the pituitary. 1994 28

Tuberculosis, a lung disease caused by Mycobacterium tuberculosis (Mtb), is one of the ten leading causes of death worldwide affecting mainly developing countries. Mtb can persist and survive inside infected cells through modulation of host antibacterial attack, i.e., by avoiding the maturation of phagosome containing mycobacteria to more acidic endosomal compartment. In addition, bacterial phosphatases play a central role in the interplay between host cells and Mtb. In this study, we characterized the Rv2577 of Mtb as a potential alkaline phosphatase/phosphodiesterase enzyme. By an in vitro kinetic assay, we demonstrated that purified Rv2577 expressed in Mycobacterium smegmatis displays both enzyme activities, as evidenced by using the artificial substrates p-NPP and bis-(p-NPP). In addition, a three-dimensional model of Rv2577 allowed us to define the catalytic amino acid residues of the active site, which were confirmed by site-directed mutagenesis and enzyme activity analysis, being characteristic of a member of the metallophosphatase superfamily. Finally, a mutation introduced in Rv2577 reduced the replication of Mtb in mouse organs and impaired the arrest of phagosomes containing mycobacteria in early endosomes; which indicates Rv2577 plays a role in Mtb virulence.
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PMID:Rv2577 of Mycobacterium tuberculosis Is a Virulence Factor With Dual Phosphatase and Phosphodiesterase Functions. 3319 64


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