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Biomedical subjects

V V Ragavan

Publications and source records attributed to V V Ragavan.

6 recordsLinked to original sources
PubMed2005

Hormone replacement therapy and breast density changes.

OBJECTIVES: To compare the incidence of increased breast density and tenderness in postmenopausal women associated with transdermal (Estalis/Combipatch), Novartis, Basel, Switzerland) and oral (Kliogest), Schering AG, Berlin, Germany) hormone replacement therapy (HRT). METHODS: A total of 202 postmenopausal women were randomized to transdermal or oral HRT. Mammograms obtained at study entry and after 1 year of treatment were assessed for percent breast density by means of the digital segmentation and thresholding technique. Breast tenderness was assessed at each study visit. RESULTS: The mean breast density by ANCOVA after adjusting for screening value at study end was significantly lower for women using Estalis (38.4%, standard error 0.9%) compared with Kliogest (46.9%, standard error 1.5%) (p<0.0001). Significantly fewer women using transdermal HRT had an increase in mammographic breast density or breast tenderness compared to oral HRT. Of the women using transdermal HRT, 39.1% had no change in breast density compared to 15.7% for women using oral HRT. Only 4% of women using transdermal HRT had a marked increase in density (>25%) compared to 15.7% of women using oral HRT. Overall, 36.0% of patients in the transdermal group reported breast tenderness at some point during the 1-year study, compared with 57.6% in the oral HRT group (p=0.0002). CONCLUSION: Transdermal HRT use is associated with a significantly lower incidence of increased mammographic breast density and breast tenderness compared with oral HRT.

Administration, Cutaneous↗
PubMed1983

Effect of chronic naltrexone and methadone administration on brain immunoreactive beta-endorphin in the rat.

The effects of chronic treatment with methadone, a long-acting opiate agonist, and naltrexone, a long-acting opiate antagonist on brain immunoreactive beta-endorphin (IR-beta-EP) concentrations were studied in the rat. Male rats were treated for 30 days with either methadone, 2.5 mg/kg/day; naltrexone 2 mg/kg/day, or saline. In a repeat experiment, rats were treated for 36 days with either methadone 2.5 mg/kg/day; naltrexone 4 mg/kg/day, or saline. Brain regions were homogenized in 0.2 N HCl and assayed for IR-beta-EP by RIA. No change in the IR-beta-EP content of the hypothalamus, thalamus, midbrain, or amygdala was measured in either experiment after methadone treatment. Naltrexone, however, significantly lowered brain IR-beta-EP in both experiments. In the first study hypothalamic IR-beta-EP fell from 189 +/- 17 (SEM) to 132 +/- 7.0 ng/g wet weight of tissue after naltrexone treatment (p less than 0.01). In the second experiment naltrexone lowered IR-beta-EP in the hypothalamus from 23.4 +/- 3.6 to 15.5 +/- 1.2 ng/mg protein (p less than 0.005). Similar decreases in the IR-beta-EP content of the thalamus (from 6.74 +/- 0.59 to 4.59 +/- 0.38 ng/mg protein) and amygdala (from 1.31 +/- 0.08 to 0.90 +/- 0.10) were also measured (p less than 0.01). We conclude that occupancy of opiate receptors by an opiate antagonist reduces brain levels of IR-beta-EP and suggests that chronic opiate receptor blockade may result in a compensatory increase in brain beta-EP release.

Animals↗
PubMed1981

Opioid regulation of prolactin secretion: evidence for a specific role of beta-endorphin.

Previous studies have shown that exogenously administered opioids, including beta-endorphin, stimulate prolactin release. The fact that naloxone has been shown to lower baseline and stress-induced serum prolactin in rats suggests that endogenous opioids may participate in prolactin regulation, but does not specify which opioid is involved. In a previous study we showed that intravenously administered anti-beta-endorphin antiserum had no effect on either baseline or stress-induced prolactin release in rats. In the present study we have repeated our earlier experiments, but have given the antiserum into the cerebral ventricles rather than intravenously. Significant lowering of baseline serum prolactin, to 56.6% +/- 10.6% (SEM) that of controls (p less than 0.005), was noted. Also noted was blunting of the stress-induced prolactin rise, to 69.2% +/- 6.7% that of controls (p less than 0.002). These results indicate that beta-endorphin is specifically involved in both the tonic and stress-mediated release of prolactin. Because the magnitude of prolactin lowering with antiserum was at least as great as what we had earlier observed with naloxone, they suggest that beta-endorphin is the major and possibly the sole opioid involved in prolactin regulation. They also indicate that the previous lack of effect of anti-beta-endorphin antiserum on serum prolactin was due to its failure, after intravenous administration, to achieve effective concentration at critical controlling sites within the brain.

Animals↗
PubMedDate not supplied

Vitamin A toxicity and hypercalcemia.

A patient hospitalized with hypercalcemia and a history of chronic vitamin A ingestion was studied in order to investigate the rarely reported association between elevated serum calcium and vitamin A toxicity. The clinical presentation marked by profound weight loss, a psychiatric disturbance, total body alopecia, erosive dermatitis, and liver disease, was compatible with hypervitaminosis A. The diagnosis of vitamin A toxicity was established by elevated total vitamin A levels and the component due to retinyl esters. Other etiologies for hypercalcemia were excluded. In view of these results and the well-known effects of vitamin A on bone metabolism, it is concluded that the most likely etiology of the hypercalcemia in this patient was vitamin A toxicity.

Alopecia↗