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At least 397 records · Page 22Linked to original sources
PubMed1987

McCune-Albright syndrome with gigantism and hyperprolactinemia.

We describe the case of a 38-year-old man with typical Mc Cune-Albright syndrome and the unusual combination of both growth-hormone and prolactin hypersecretion. The patient was extremely tall, which is unusual in Mc Cune-Albright syndrome, suggesting that he did not have precocious fusion of the epiphysis, a common finding in this syndrome. Unfortunately the patient refused any treatment for his disease. A similar case has been previously described only in a 14-year-old boy.

Adult↗
PubMed1988

Effects of cyproterone acetate, LHRH agonist and ovarian surgery in McCune-Albright syndrome with precocious puberty and galactorrhea.

We have studied the endocrinological pattern in a girl with McCune-Albright syndrome. The young patient showed: normal prepubertal serum levels of gonadotropins, fluctuating estrogen concentrations, which sometimes were similar to the levels in adult women of fertile age, hyperprolactinemia with galactorrhea, ovarian cysts. The effects of treatment with antiandrogen drug, cyproterone acetate, and of a LHRH agonist, buserelin (less than D-Ser[TBU(8)6-des-gly NH2.10 greater than LHRH ethylamide), were studied. Cyproterone acetate with or without buserelin did not fully suppress estradiol concentrations. On the other hand, surgical resection of these cysts resulted in both clinical and endocrinological remission. It is likely that in this case of McCune-Albright syndrome precocious puberty was a result of ovarian estrogen secretion, while pubertal activation of the hypothalamus-pituitary axis was absent. Hyperprolactinemia, which appeared after the beginning of the combined therapy with buserelin and cyproterone acetate, was probably due to the elevated estrogen levels.

Buserelin↗
PubMed1975

Familial polyostotic fibrous dysplasia.

A case of polyostotic fibrous dysplasia of the craniofacial type is presented, together with substantial evidence that this condition had a genetic basis in this patient. A review of the literature indicates that there is absolutely no previous evidence of a genetic basis to this condition. The possibility that the propositus suffered from polyostotic fibrous dysplasia of the Jaffe or the Albright type was excluded.

Child↗
PubMed1984

Albright's syndrome with reactivation of fibrous dysplasia secondary to pituitary adenoma and further complicated by osteogenic sarcoma. Report of a case.

To our knowledge, this is the only reported case of Albright's syndrome with reactivation of the fibrous dysplasia in adulthood, a marked elevation of growth hormone secondary to a pituitary adenoma, and development of osteosarcoma within the reactivated fibrous dysplasia. In addition, this patient also had hyperthyroidism with normal TSH levels, indicating the presence of two separate endocrinopathies. Reactivation of the fibrous dysplasia after years of arrested growth in this patient is good evidence that fibrous dysplasia does not "burn out" after adolescence but that growth ceases only when growth hormone declines to adult levels.

Adenoma↗
PubMed1985

Surgical palliation of respiratory insufficiency secondary to massive exuberant polyostotic fibrous dysplasia of the ribs.

A middle-aged man with long-standing polyostotic fibrous dysplasia had severe progressive restrictive lung disease with hypoxemia and pulmonary hypertension with heart failure because of exuberant intrathoracic, extraosseous proliferation of dysplastic tissue. Subtotal resection of this benign tissue mass ameliorated the respiratory insufficiency and led to sustained improvement in exercise tolerance, increase in pulmonary reserve, and decrease in signs of heart failure and pulmonary hypertension.

Fibrous Dysplasia of Bone↗
PubMed1982

Evidence for the presence of follicle-stimulating hormone receptor antibody in human serum.

A male patient presented with polyostotic fibrous dysplasia, elevated serum gonadotropin levels, primary gonadal failure, and an immunoglobulin M (IgM) monoclonal gammopathy. When the patient's serum was added to radioiodinated human follicle-stimulating hormone (125I-hFSH)-bovine testis membrane-receptor complex solubilized by detergent, followed by the addition of antihuman immunoglobulin G ((anti-hIgG), the preformed complex was precipitated. No such precipitation was seen when normal human or rabbit serum, serum from a patient with polyostotic fibrous dysplasia, or serum from other patients with polyclonal gammopathies were utilized. The patient's serum did not precipitate free 125I-hFSH. Detergent-solubilized testis receptor not complexed to hFSH, as well as highly purified radioiodinated receptor were also precipitated when this serum was added followed by anti-hIgG. Our results indicate that serum from the patient contained antibodies to FSH testis receptor. It is possible that antibodies to gonadal receptors may exist in other patients, although it is not yet possible to assume a causal relationship between the presence of receptor antibodies and gonadal failure.

Autoantibodies↗
PubMed1975

Cushing syndrome, sexual precocity, and polyostotic fibrous dysplasia (Albright syndrome) in infancy.

The sexual precocity of polyostotic fibrous dysplasia is occasionally accompanied by other endocrine disorders, but in only two previous instances has Cushing syndrome been reported. The history of a 6-month-old girl is presented, in whom this syndrome was complicated by congenital Cushings syndrome. Although endocrinopathies of polyostotic fibrous dysplasia have usually been ascribed to a central (hypothalamic) origin, the findings in this patient suggest autonomous hyperfunction of the peripheral endocrine glands, with the Cushing syndrome caused by hyperplastic nodules in the adrenal glands and the precocity by luteinized follicular cysts of the ovary.

Adrenal Glands↗
PubMed1975

Growth hormone excess and sexual precocity in polyostotic fibrous dysplasia (McCune-Albright syndrome): evidence for abnormal hypothalamic function.

A 5-5/12-year-old boy with gigantism and precocious puberty associated with the McCune-Albright syndrome is presented. Serum concentrations of growth hormone were extremely elevated (128-163 ng/ml) and were not suppressed by hyperglycemia or chlorpromazine. Serum LH (7.4 +/- 1.0 SD mIU/ml) and FSH (5.3 +/- 0.3 SD mIU/ml) concentrations were in the range observed in midpuberty. The secretion pattern of LH was episodic. The administration of estradiol suppressed the secretion of FSH and had an apparent positive feedback effect on release of LH. These findings are compatible with abnormal hypothalamic function as the mechanism for the endocrinopathies associated with the McCune-Albright syndrome.

Blood Glucose↗