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At least 19 recordsLinked to original sources
PubMed1985

Treatment of true precocious puberty with a potent luteinizing hormone-releasing factor agonist: effect on growth, sexual maturation, pelvic sonography, and the hypothalamic-pituitary-gonadal axis.

We used the LHRH agonist D-Trp6-Pro6-N-ethylamide LHRH (LHRH-A) to treat 19 children (12 girls and 7 boys) with true precocious puberty. Fourteen patients had idiopathic true precocious puberty, 4 had a hamartoma of the tuber cinereum, and 1 had a hypothalamic astrocytoma. Basal gonadotropin secretion and responses to native LHRH decreased within 1 week of initiation LHRH-A therapy, and sex steroid secretion decreased within 2 weeks to or within the prepubertal range. Ultrasonographic evaluation of the uterus indicated a postmenarchal size and shape in all 11 girls studied before treatment, which reverted to prepubertal size and configuration in 5 girls during LHRH-A therapy. The enlarged ovaries decreased in size and the multiple ovarian follicular cysts regressed. Sexual characteristics ceased advancing or reverted toward the prepubertal state in all patients receiving therapy for 6-36 months. All 5 girls with menarche before therapy had no further menses. Three girls had hot flashes after LHRH-A-induced reduction of the plasma estradiol concentration. Height velocity, SDs above the mean height velocity for age, and SDs above the mean height for age decreased during LHRH-A therapy; the velocity of skeletal maturation decreased after 12 months of LHRH-A therapy and was sustained during continued therapy over 18-36 months. In 4 patients, a subnormal growth rate (less than 4.5 cm/yr) occurred during LHRH-A therapy. Six patients had cutaneous reactions of LHRH-A, but no demonstrable circulating antibodies to LHRH-A. In 2 patients in whom LHRH-A therapy was discontinued because of skin reactions, precocious sexual maturation resumed at the previous rate for the ensuing 6-12 months; subsequently, they were desensitized to LHRH-A, and during a second course of therapy, their secondary sexual development and sex steroid levels again quickly decreased. LHRH-A proved an effective and safe treatment for true precocious puberty in boys as well as girls with central precocious puberty whether of the idiopathic type or secondary to a hamartoma of the tuber cinereum or a hypothalamic neoplasm.

Age Determination by Skeleton↗
PubMed1989

Radiation-induced osteosarcoma of the sphenoid bone.

The case of a patient who developed osteosarcoma in the sphenoid bone 15 years after radiation therapy for a craniopharyngioma is reported. Radiation-induced osteosarcoma of the sphenoid bone has not been reported previously. Reported cases of radiation-induced osteosarcomas are reviewed.

Bone Neoplasms↗
PubMed1988

The effect of hypothalamic paraventricular nuclear lesions placed at 108-110 days gestational age on plasma ACTH concentrations in the fetal sheep.

Lesions that completely destroyed the paraventricular nucleus of the hypothalamus were placed in fetal sheep (n = 4) at 108-110 days of gestational age. These fetuses were then subjected to hypotension (50% of initial mean fetal arterial blood pressure), hypoxaemia (a decrease in fetal PaO2 greater than or equal to 5 torr) and bolus injection of corticotropin releasing factor (CRF-1.0 micrograms iv) in random order on successive days. The lesioned fetuses produced significantly less ACTH after hypotension (+10 min: 35.7 +/- 26.9 vs. 358.0 +/- 99.7 and +30 min: 28.2 +/- 12.2 vs. 238.0 +/- 73.0 pg.ml-1) (P less than 0.05), hypoxaemia (+40 min: 23.5 +/- 9.3 vs. 198.3 +/- 75.8 and +60 min: 32.3 +/- 18.8 vs. 295.3 +/- 99.9 pg.ml-1) (P less than 0.05) and intravenous administration of 1 microgram CRF (+15 min: 32.0 +/- 16.8 vs. 145.7 +/- 25.0 and +60 min: 33.0 +/- 23.3 vs. 161.3 +/- 43.1 pg.ml-1) (P less than 0.05). Our experiments suggest an important role for the fetal paraventricular nucleus in control of ACTH secretion. They also indicate that impairment of paraventricular nucleus function at this stage of fetal life may have a detrimental effect on the ability of the anterior pituitary to secrete ACTH in response to exogenous CRF.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Ocular reticulum cell sarcoma. Clinicopathologic correlation of a case with multifocal lesions.

A 56-year-old man presented with recalcitrant uveitis with anterior chamber and vitreous cells. He developed small scattered lesions in the macular areas of both eyes, which disappeared in the right eye and evolved to multifocal, discrete, punched-out lesions resembling birdshot retinochoroidopathy in the left eye. Ocular reticulum cell sarcoma (RCS) was suspected but was not confirmed by diagnostic vitrectomy. The patient died 3 years later and was found to have RCS with central nervous system and ocular involvement. The occurrence of tumor cells under the retinal pigment was the apparent cause of the multifocal lesions that disappeared in the right eye and that led to discrete punched-out lesions with no scarring in the left eye.

Diagnosis, Differential↗
PubMed1984

Acquired nystagmus in early childhood: a presenting sign of intracranial tumor.

This study is a multicenter, retrospective report of 10 infants in whom acquired nystagmus was the initial sign of chiasmal/ parachiasmal glioma. Nine patients presented before the age of 10 months. The nystagmus, primarily described as pendular and asymmetric, was difficult to differentiate from and therefore most often diagnosed as spasmus nutans . On average in the ten patients, the intracranial glioma was not recognized for 8.6 months after the onset of nystagmus. In the five diagnosed as spasmus nutans , the mean delay in recognizing the tumor was 14.5 months. Three associated clinical findings were present or developed in these patients to distinguish this entity from spasmus nutans : optic atrophy in all ten patients, poor feeding due to diencephalic syndrome in 5 of 10, and increased intracranial pressure with hydrocephalus in 3 of 10. The acquired nystagmus in these infants was evidence of a life-threatening chiasmal/ parachiasmal glioma.

Astrocytoma↗