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Breast neoplasm may develop in ectopically located glandular tissue. This paper presents an interesting and rare case of a 50-year-old female who despite regular mammography screening examination developed an invasive accessory breast cancer. Clinical examination revealed a 2 cm - tumour localized 4 cm below the left inframammary fold. The lesion was immobile, the skin and the atrophic nipple were retracted, the tumour infiltrated the thoracic wall. Oligobiopsy and additional examinations showed an invasive stage IIIB ductal breast cancer (Bloom II, G-2). The receptor status was: ER(+), PGR(+), HER2(-). The increased level of cancer antigen 15.3 was found. The patient was submitted to pre-operative chemotherapy. She also underwent surgery and subsequently post-operative chemotherapy and radiotherapy. On the basis of the presented case, it could be concluded that the accessory mammary glands are out of the image of screening breast examinations. Accessory breast cancer is usually diagnosed by clinical examination and ultrasonography. Preventive resection of accessory breast in women at high risk of developing breast cancer can be considered as the treatment of choice in most patients.

Celosomy is a term used for a group of congenital anomalies characterized by opening of the somatic wall with evisceration. The most common types of celosomy are gastroschisis and omphalocele. They have been associated with maternal age, cigarette smoking, environmental pollution, as well as prenatal exposure to vasoconstrictors and recreational drugs. The aim of this study was to evaluate the effect of prenatal exposure to various selective and non-selective cyclooxygenase-2 (COX-2) inhibitors on the abdominal wall defects in rat. A retrospective statistical analysis was performed on the basis of data collected in our laboratory in the years 1997-2004, during different teratological studies with COX-inhibitors (aspirin, DFU, DuP-697, ibuprofen, paracetamol, piroxicam, propyphenazone, tolmetin). Out of 6744 live born fetuses celosomy was revealed only in four animals exposed to different non-selective COX inhibitors. A single case of gastroschisis was also found in a rat exposed to the selective COX-2 inhibitor. The fetal body weight was significantly lower in COX-exposed group of fetuses when compared with untreated control. It was also significantly decreased in non-malformed fetuses prenatally exposed to COX inhibitors when compared with untreated control. The fetal body weight and length were lower in fetuses born with gastroschisis than with omphalocele. However, when animals with both anomalies were pooled in one group the mean fetal body weight was marginally lower (p = 0.0523) when compared with non-malformed group, while no statistically significant differences were found for fetal length. The pooled statistical analysis done for the concurrent and our own historic data showed that only aspirin statistically increased the risk of abdominal wall defects in rat fetuses. The expected ratio for aspirin is 56.41 per 10,000 offsprings (p < 0.05), which is over 10-times higher than ratio for all non-selective COX inhibitors, including aspirin (6.01/10,000; p < 0.05). No differences were found for selective COX-2 inhibitors. It could be stressed that aspirin, unlike other non-selective and selective COX-2 inhibitors increases the risk of the abdominal wall defects, which are observed more often in growth-retarded fetuses.

Cyclooxygenase (COX) inhibitors are the most commonly ingested drugs. The aim of the study was to evaluate the prenatal skeletal effect of selective (DFU) and nonselective (tolmetin, ibuprofen, piroxicam) COX-2 inhibitors. All the tested compounds were administered intragastrically to pregnant Wistar rats from 7 to 21 gestation day. The initial dose was set at 8.5mg/kg/dose for tolmetin and ibuprofen, 0.3 and 0.2mg/kg/dose for piroxicam and DFU. The middle dose was increased 10-times. The highest dose, except for ibuprofen, was elevated 100-times. The highest dose for ibuprofen was set at 200mg/kg/dose. Tolmetin and ibuprofen were administered three times a day. Piroxicam and DFU were dosed once daily. After routine teratological examinations, extremities of randomly selected 21-day-old fetuses were taken for histological, immunohistochemical and molecular studies. The proximal femoral epiphyses were separated and their ultrastructure evaluated. The expression of genes coding cytokines (IL-1alpha, IL-1beta, IL-6, TNF-alpha, TNF-beta) and proteins (COX-1, COX-2, cathepsin K, collagen types I, II and X; osteocalcin, osteopontin) was evaluated in femoral epiphyses by RNase Protection Assay and/or immunohistochemically. The articulate development was checked histologically and found undisturbed in any of the experimental groups. The epiphysis of the 21-day-old fetuses, presented physiological expression of COX-1 and COX-2, as well as cathepsin K, collagen types I, II and X; osteopontin, osteocalcin and TNF-alpha. Increased developmental skeletal variation was noted in groups exposed to the highest dose of nonselective drugs. Unlike the increased number of skeletal variations observed in fetuses exposed to highest doses of nonselective compounds, both groups of COX inhibitors did not disturb joint formation and morphology of femoral epiphyses when administered even in high maternal toxic doses.

Background: Cyclooxygenase (COX) inhibitors are one of the most often ingested drugs during pregnancy. Unlike general toxicity data, their prenatal toxic effects were not extensively studied before. The aim of the experiment was to evaluate the developmental toxicity of the non-selective (piroxicam) and selective (DFU; 5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulphonyl) phenyl-2(5H)-furanon) COX-2 inhibitors., Methods: Drugs were separately, orally once daily dosed to pregnant rats from day 8 to 21 (GD1=plug day). Doses were set at 0.3, 3.0 and 30.0mg/kg for piroxicam and 0.2, 2.0 and 20.0mg/kg for DFU. Fetuses were delivered on GD 21 and routinely examined. Comprehensive clinical and developmental measurements were done. The pooled statistical analysis for ventricular septal (VSD) and midline (MD) defects was performed for rat fetuses exposed to piroxicam, selective and non-selective COX-2 inhibitor based on present and historic data., Results: Maternal toxicity, intrauterine growth retardation, and increase of external and skeletal variations were found in rats treated with the highest dose of piroxicam. Decrease of fetal length was the only signs of the DFU developmental toxicity observed in pups exposed to the highest compound dose. Lack of teratogenicity was found in piroxicam and DFU-exposed groups. Prenatal exposure to non-selective COX inhibitors increases the risk of VSD and MD when compared to historic control but not with selective COX-2 inhibitors., Conclusion: Both selective and non-selective COX-2 inhibitors were toxic for rats fetuses when administered in the highest dose. Unlike DFU, piroxicam was also highly toxic to the dams. Prenatal exposure to selective COX-2 inhibitors does not increase the risk of ventricular septal and midline defects in rat when compared to non-selective drugs and historic control.

The aim of the study was to evaluate the toxicity of non-selective (tolmetin, ibuprofen and piroxicam) and selective (DFU) cyclooxygenase-2 inhibitors on pregnant and non-pregnant rats. The drugs were administered orally once (DFU, piroxicam) or three times (tolmetin, ibuprofen) a day from days 8 through 21 of gestation experiment in three doses. The initial dose was similar to the human antiinflammatory one and set as 8.5 mg/kg (tolmetin, ibuprofen), 0.3 mg/kg (piroxicam) and 0.2 mg/kg (DFU). The middle dose was increased 10 times and the highest one 100 times the initial dose. The highest dose for ibuprofen was set at 200mg/kg due to high mortality. On gestation/experimental day 21 animals were sacrificed, blood was collected and abdominal organs were taken for pathological examination. Activity of alanine and asparate aminotransferases and levels of total protein and urea were determined. Stomach, small and large intestines, and liver were grossly and histologically examined. Dose-dependent mortality, signs of gastrointestinal toxicity, and significant changes of biochemical parameters were found in groups exposed to non-selective COX inhibitors in both pregnant and non-pregnant rats. Mild regressive structural hepatic changes were observed. Significant decrease of protein level in non-pregnant rats treated with high DFU dose, and occasionally observed gastrointestinal changes were the only changes noted in groups exposed to the selective COX-2 inhibitor. Tolerability of non-selective COX inhibitors was lower in both pregnant and non-pregnant groups when compared with DFU. Insignificant mortality and histological changes were noted between pregnant and non-pregnant groups.