Lymphocyte recovery after breast cancer treatment and mindfulness-based stress reduction (MBSR) therapy.

OBJECTIVES: This randomized controlled trial was conducted to examine immune recovery following breast cancer (BC) therapy and evaluate the effect of mindfulness-based stress reduction therapy (MBSR) on immune recovery with emphasis on lymphocyte subsets, T cell activation, and production of T-helper 1 (Th1; interferon [IFN]-γ) and T-helper 2 (Th2; interleukin-4 [IL-4]) cytokines. METHOD: Participants who completed the study consisted of 82 patients diagnosed with Stage 0-III BC, who received lumpectomy and adjuvant radiation ± chemotherapy. Patients were randomized into an MBSR(BC) intervention program or a control (usual care) group. Immune cell measures were assessed at baseline and within 2 weeks after the 6-week intervention. The numbers and percentages of lymphocyte subsets, activated T cells, and Th1 and Th2 cells in peripheral blood samples were determined by immunostaining and flow cytometry. RESULTS: Immune subset recovery after cancer treatment showed positive associations with time since treatment completion. The B and natural killer (NK) cells were more susceptible than T cells in being suppressed by cancer treatment. Women who received MBSR(BC) had T cells more readily activated by the mitogen phytohemagglutinin (PHA) and an increase in the Th1/Th2 ratio. Activation was also higher for the MBSR(BC) group if <12 weeks from the end of treatment and women in MBSR(BC) <12 weeks had higher T cell count for CD4(+). CONCLUSION: MBSR(BC) promotes a more rapid recovery of functional T cells capable of being activated by a mitogen with the Th1 phenotype, whereas substantial recovery of B and NK cells after completion of cancer treatment appears to occur independent of stress-reducing interventions.

Safety and efficacy of anastrozole for the treatment of pubertal gynecomastia: a randomized, double-blind, placebo-controlled trial.

Pubertal gynecomastia is thought to result from transient imbalances between estrogen and androgen concentrations. Anastrozole (ARIMIDEX), a potent and selective aromatase inhibitor, decreases estrogen and increases testosterone concentrations in pubertal boys. The safety and efficacy of anastrozole for the treatment of pubertal gynecomastia were evaluated. In a randomized, double-blind, placebo-controlled study of 80 boys, aged 11-18 yr, with pubertal gynecomastia that had not reduced over a 3-month interval, subjects received either anastrozole (1 mg) or placebo once daily for 6 months. A response was defined as a 50% or greater reduction in the calculated volume of both breasts combined using ultrasonography measurements. A comparison of response rates was performed using logistic regression analysis. Secondary end points included changes in serum hormone concentrations. The percentage of patients with a response was 38.5% for the anastrozole group and 31.4% for the placebo group (odds ratio, 1.513; 95% confidence interval, 0.496-4.844; P = 0.47). At 6 months, the median percent change in the testosterone/estradiol ratio was 166% for the anastrozole group and 39% for the placebo group. Anastrozole treatment was well tolerated. In patients with pubertal gynecomastia, no significant difference in the percentage of patients with a 50% or greater reduction in total breast volume, as calculated from ultrasonography measurements, was demonstrated between the anastrozole and placebo groups.

Fatigue, weight gain, lethargy and amenorrhea in breast cancer patients on chemotherapy: is subclinical hypothyroidism the culprit?

BACKGROUND: The purpose of this study was to prospectively observe the relative contribution of each viable mechanism such as hyperphagia, physical activity, body composition, steroid hormonal and thyroid function, fatigue scores on changes in body weight in breast cancer patients, receiving adjuvant chemotherapy. METHODS: This was a prospective observational research design where 198 consecutive breast cancer patients receiving adjuvant chemotherapy were monitored from start to end and 6 months post-therapy on changes in anthropometics, fatigue, nutritional intake, physical activity, thyroid and steroid hormones. RESULTS: We observed a weight gain over >5 lb in 22.2% of this patient population with a significant and progressive gain of 6.7 lb (P < 0.0001) at 6 months. Ninety four percent of all patients reported fatigue and 56% of patients reported lowered physical activity. A significant reduction in serum free and total estradiol (P < 0.0001) was observed indicative of reduction in ovarian function with 86% amenorrehic at the end of treatment. A significant reduction in mean serum triiodothyronine uptake levels (P < 0.05), in addition to a significant increase in TBG (P < 0.0001) from baseline to end of chemotherapy, was observed. In addition 20-25% of this patient group was already diagnosed with clinical hypothyroidism at diagnosis and treated. Changes in fatigue frequency and serum sex-hormone-binding globulin (SHBG) were variables significantly predictive of weight gain (P < 0.0001). CONCLUSIONS: Cytotoxic agents may influence thyroid function in breast cancer patients contributing to and progressively worsening symptoms such as weight gain, amenorrhea, fatigue and lowered physical activity in this population. The present study indicates the value of screening breast cancer patients for thyroid function at diagnosis or pre-treatment.

Effects of one year of recombinant human growth hormone (GH) therapy on cardiac mass and function in children with classical GH deficiency.

Cardiac mass and function were evaluated in 10 children with classical GH deficiency. Echocardiograms were performed at baseline, 3, 6, and 12 months after initiation of recombinant human (rh) GH therapy (0.3 mg/kg.wk). Before treatment, left ventricular (LV) mass indexed to body surface area (BSA) was low or low normal (<50 g/m(2)) in five children compared with reference control data. Height SD score (-3.2 +/- 0.9 vs. -1.8 +/- 1.3 yr; P < 0.01), growth velocity SD score (-2.7 +/- 1.6 vs. 5.8 +/- 3.1; P < 0.01), LV mass (36 +/- 9 vs. 60 +/- 30 g; P < 0.02), LV mass/BSA (51 +/- 12 vs. 72 +/- 11 g/m(2); P < 0.01), LV mass/height (36 +/- 9 vs. 54 +/- 15 g/m; P < 0.02), and LV mass/m(2.7) (36 +/- 12 vs. 45 +/- 8; P < 0.05) increased significantly with rhGH therapy. Pretreatment LV mass/BSA correlated inversely with fold increase in LV mass/BSA over the year (r = -0.83; P < 0.01). Load-dependent indices of diastolic performance were normal at baseline and did not change with rhGH therapy. Percentage increase of mean velocity of circumferential shortening, an index of systolic function, correlated with fold increase in LV mass/BSA (r = 0.88; P < 0.02) over the year of rhGH administration. LV mass can be lower than predicted for body size in some children with severe GH deficiency but is responsive to rhGH replacement. LV mass/BSA increases into the normal range during the first year of rhGH therapy. The rate of increase of LV mass is greater than the increase in BSA during rhGH treatment, suggesting that GH could also be a trophic factor for the heart.