Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhibition of dermal activity by cortisol in culture was partially reversed by two naturally occurring androgens, testosterone and dihydrotestosterone. ACTH and the androgen precursor dehydroepiandrosterone sulphate showed not such antagonistic effect. These results suggest that increased production of adrenal androgens during ACTH therapy may account for the relative absnece of 'skin-thinning' and 'steroid-bruising' which are common side-effects of corticosteroid therapy.
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PMID:Effects of steriod hormones on human fibroblasts in vitro. II. Antagonism by androgens of cortisol-induced inhibition. 18 91

Adrenomyeloneuropathy (AMN), a clinical variant of child adrenoleukodystrophy (ALD), is an adult-onset progressive disorder which presents spastic paraparesis with peripheral nerve involvement and affects mainly the pyramidal tracts from the brainstem to the spinal cord. We report a case of AMN in which serial MRI showed unusual development of areas of high signal in the right striatum. The patient was in good health until the age of 12, when he began to lose his hair. At age 25 he started to have progressive gait disturbance and erectile impotence. In his first admission to our hospital at age 33, he showed diffuse baldness. He was intelligent but childish. His cranial nerves were normal. Muscle strength was weak (3-4/5) in the lower extremities. Deep tendon reflexes were hyperactive in the lower extremities while normal in the upper extremities. Babinski signs were elicited bilaterally. Pinprick and vibratory sensation was impaired in the lower legs. Proprioceptive sensations were normal. Co-ordination was intact. There were urinary incontinence and impairment of erection with preserved libido and ejaculation. Routine laboratory data including hematological studies, serum chemistry and urinalysis were all normal except for mild hyperlipidemia. Serum cortisol response to ACTH was low and serum levels of very long chain fatty acids were increased. Nerve conduction studies were abnormal and consistent with peripheral polyneuropathy. A biopsy specimen of left sural nerve revealed a mild loss of myelinated fibers with thinning of the myelin. These findings and the clinical features confirmed the diagnosis of AMN. MRI in SE2000/40 scans at age 34 disclosed areas of high signal in the bilateral internal capsules.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Striatal involvement on MRI in adrenomyeloneuropathy]. 165 65

There have been reports of adrenal failure in patients treated with suramin, an agent that has recently been used as therapy for acquired immune deficiency syndrome. We conducted this study to assess the effect of suramin on adrenal function and structure in a primate, the cynomolgus monkey. Five male monkeys were treated with suramin (800 mg/m2, im) once a week, for 5 weeks. Five other animals (controls) received saline. The treated animals had progressive elevations of plasma ACTH (P less than 0.05) and PRA (P less than 0.02) and decreased serum cortisol responses 30 min after the administration of synthetic ACTH (P less than 0.05) compared to controls. There was disruption of the architecture of the adrenal cortex, a diffuse inflammatory cell infiltrate, and thinning of the zona glomerulosa and zona fasciculata in the suramin-treated animals. We conclude that suramin is toxic to adrenal cortical tissue and might be useful in treating conditions with adrenal cortical hyperfunction, such as adrenal cortical carcinoma and Cushing's syndrome.
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PMID:Effects of suramin on the function and structure of the adrenal cortex in the cynomolgus monkey. 303 53

A 45-yr-old man with primary pigmented nodular adrenocortical disease (PPNAD) is described. This patient underwent unilateral adrenalectomy for ACTH-independent Cushing's syndrome (CS) in 1969. Although his daily urinary free cortisol (UFC) excretion rate normalized, and the major clinical manifestations of CS subsided, loss of a circadian cortisol rhythm persisted after surgery. Twenty-seven years later, the patient presented again with short stature, severe osteopenia, skeletal deformities, thinning of the skin, and myopathy.
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PMID:Primary pigmented nodular adrenocortical disease: reevaluation of a patient with carney complex 27 years after unilateral adrenalectomy. 910 Jun 6

The majority of pituitary tumors that cause Cushing's disease are small (<1 cm diameter), and most disease morbidity is due to the effects of elevated, non-suppressible, ACTH levels that these tumors secrete. Tumor-derived ACTH leads to adrenal-derived steroid hypersecretion and results in many disabling and sometimes life-threatening symptoms including abnormal fat deposition, skin thinning, psychological disturbances, hypertension, diabetes, osteoporosis and muscle weakness. Cushing's disease is associated with high morbidity and ultimately mortality. In experienced specialized centers, 70% of corticotroph microadenomas can be successfully resected by transsphenoidal pituitary surgery. However, surgical "cure" rates for larger ACTH-secreting pituitary tumors are achieved in only 30% of cases, and recent reports highlight a significant recurrence rate after longer term follow-up even in smaller tumors. Post-surgical persistence of ACTH hypersecretion may require pituitary-directed radiation, but this treatment may take some time to be effective, and like extensive surgical pituitary tumor resection, ultimately leads to partial- or total hypopituitarism in approximately 80% of cases. Although hypercortisolism may be completely resolved by adrenalectomy, this procedure does not suppress, and may act as a stimulus to pituitary tumor growth, and is associated with other co-morbidity. Although some currently available drug-based treatments for Cushing's disease effectively control hypercortisolism, their drawback has been that they do not impact on pituitary tumor growth. Recent studies have identified the potential utility of peroxisome-proliferator activating receptor-gamma (PPAR-gamma) novel ligands in in vitro, and in vivo Cushing's disease models, and have paved the way for early clinical studies to develop novel therapeutic approaches in Cushing's disease.
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PMID:PPAR-gamma in Cushing's disease. 1641 39