Cystosarcoma phyllodes is a very rare tumor which maybe difficult to diagnose clinically. The epidemiology and pathobiology are different from those of breast carcinoma. Risk factors, multicentricity, bilaterality, as associated with breast carcinoma, are not observed in patients with cystosarcoma phyllodes. Although the term "sarcoma" indicates a malignant tumor, only 10%-30% of cystosarcomas are histologically diagnosed as malignant; clinical diagnosis of malignancy does not exceed 10%. Axillary node involvement is rare, but hematogenous spread of cystosarcoma occurs into lung, pleura, bone, and liver. Clinically, cystosarcoma is a large (usually 3-5 cm in diameter) painless tumor with sudden growth acceleration especially during pregnancy. Cystosarcoma is usually circumscribed, containing firm and soft areas. The differential diagnosis has to include fibroadenoma, fibrocystic disease, mastitis, abscess, and medullary carcinoma. Neither clinical, mammographic or sonographic signs exist to predict a benign or malignant tumor. Therapy of cystosarcoma is not uniformly agreed upon. Radical, modified-radical, and simple mastectomy and tumorectomy are typical treatments; therapeutic results are the same for each treatment modality. For histologically diagnosed malignant cystosarcoma, the relative 5-year survival rate is about 80%. Clinically, malignant metastatic cystosarcoma is incurable; radiotherapy, endocrine treatment, and polychemotherapy are all ineffective. Because of the specific tumor pathobiology of cystosarcoma and its rarity, evaluation of treatment modalities and comparison of survival rates are difficult.

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In 12 nonpregnant women, total iodine, protein-bound iodine, inorganic iodine, and thyroxine values were measured in serum before and 15, 30, 45 or 60 minutes after a two-minute vaginal disinfection with povidone-iodine (Betadine). Only 15 minutes after application, serum iodine levels were raised and remained significantly elevated 30, 45 and 60 minutes after disinfection. Serum concentrations of total iodine and inorganic iodine were increased up to fivefold to 15-fold, respectively; during the relative short period of observation, thyroxine levels were not altered. An overload of iodine can suppress thyroid hormonogenesis, and the fetal and neonatal thyroid glands are especially sensitive. In pregnant women, vaginitis should not be treated with povidone-iodine because of the possible development of iodine-induced goiter and hypothyroidism in the fetus and newborn. The risk is especially high when povidone-iodine is used repeatedly.

Since impurities consisting of neurohypophysical hormones in prolactin powder may be responsible for the vascular and renal effects attributed to prolactin, rat (NIH-RP-1), ovine (NIH-P-S-10, S-12), and bovine (NIH-P-B4) prolactin preparations were examined for their content of ADH and oxytocin by rat antidiuresis, milk-ejection, and blood pressure assays. Activities were identified as due to ADH or oxytocin by incubation of prolactin solutions with antisera against ADH, oxytocin, and prolactin, or with pregnancy plasma. The ADH content of rat, ovine (P-S-10, P-S-12) and bovine prolactin was found to be 104.5 +/- 7.1 (means +/- SE), 2.5 +/- 0.2, 1.6 +/- 0.1, and 1.6 +/- 0.5 mU/mg powder, respectively; the corresponding values for oxytocin content were 155.3 +/- 3.5, 1.2 +/- 0.1, 0.5 +/- 0.1, and 1.2 +/- 0.01 mU/mg powder, respectively. Because antidiuretic, milk-ejection, and blood pressure activities of the various prolactins were eliminated after incubation with antisera against ADH and oxytocin, or with pregnancy plasma, but not with prolactin antisera, it is concluded that the reported vascular and renal prolactin effects are attributable to ADH contamination of the prolactin preparation rather than to the prolactin molecule itself. These findings have implications for renal and vascular prolactin research.