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)

The chronic stage of vasospasm occurring several days after subarachnoid hemorrhage (SAH) is characterized by the development of histopathologic changes in cerebral arteries causing cerebral ischemia. Numerous experimental data indicate the involvement of immune mechanisms in the angiopathy caused by SAH. Endogenous opioids play also an important role in the ischemic lesions of the brain. Corticotropin releasing hormone (CRH) induces the release of beta-endorphin (beta-END) from hypothalamic neurons and also from mononuclear white blood cells. The function of CRH and beta-END in vasospasm following SAH and the interrelationship between neuroendocrine and immune changes requires further elucidation. In the present study we investigated the influence of CRH injected into cerebral cisterna magna (CM) of rats on beta-END-like level in cerebrospinal fluid (CSF) in acute and chronic phase of cerebral vasospasm following artificial SAH. Acutely CRH induced a significant rise of beta-END-like in CSF both in SAH and sham SAH rats. However, in rats subjected to SAH, a single injection of CRH caused a prolonged rise of 5-END in CSF, which was also seen 2 days after SAH, during the chronic phase of vasospasm. The obtained results indicate that CRH increases neuroendocrine changes induced by SAH, probably by an activation of immune cells involved in the patomechanism of chronic vasospasm.
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PMID:Corticotropin releasing hormone (CRH) increases beta-endorphin (beta-end like) concentration in cerebrospinal fluid of rats with vasospasm following subarachnoid hemorrhage. 1057 71

Cushing's syndrome is accompanied by many different skin symptoms. A case of a 43-year-old female patient with unrecognized adrenocorticotropic hormone (ACTH)-dependent Cushing syndrome is reported. Besides numerous skin lesions, the patient presented with a rapidly progressive leg ulcer due to venous thrombosis. The initial skin symptoms appeared on her lower leg one month prior to admission. The patient was treated with oral prednisone, however, rapid progression of the skin lesion was observed. On admission the patient presented with a large, very painful ulceration, partially covered with a crust, on the right lower leg with several satellite smaller ulcerations. The other leg showed no changes. Moreover, the patient had pronounced hirsutism and skin darkening on the face, and Muehrcke's lines were observed on all her nails. Microscopic findings of skin biopsy were uncharacteristic, with some signs of angiopathy and vasculitis. Based on the elevated serum levels of ACTH and cortisol, and the result of dexamethasone suppression test, ACTH-dependent Cushing syndrome was diagnosed. Sonography of leg veins revealed a recanalized thrombus of the right popliteal vein with reflux. The patient was transferred to surgical department where both suprarenal glands were removed. Upon suprarenal gland removal, significant improvement of the patient's general condition and rapid healing of the leg ulcer were observed. Briefly, this patient is presented to point out that a leg ulcer caused by venous insufficency may mimic fulminant purpura or some other type of vasculitis in patients with Cushing syndrome.
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PMID:Cutaneous manifestations in a patient with a long-term history of untreated ACTH-dependent Cushing's syndrome. 1660 99