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D Satgé

Publications and source records attributed to D Satgé.

23 records · Page 2Linked to original sources
PubMedDate not supplied

Antenatal exposure to atenolol and retroperitoneal fibromatosis.

We present a case of retroperitoneal fibromatosis in a fetus whose mother took atenolol during pregnancy. A 25-year-old obese woman was treated for hypertension with 100 mg atenolol daily from the second month until the end of pregnancy. At 29 weeks, echography disclosed a retroperitoneal mass and at 37 weeks, a boy was delivered. A biopsy of the tumor showed a fibromatosis with medullary compression, treated by antimitotics until 3 months of age. At the age of 4, the mass had disappeared but severe scoliosis was present. This in utero exposure to atenolol drew our attention because the retroperitoneal localization of the tumor is similar to that of fibroses reported in adults after exposure to atenolol and for other reasons: transplacental carcinogenesis has been demonstrated in humans, at least for diethylstilboestrol, atenolol crosses the placental barrier, the drug was taken during nearly the whole pregnancy, and retroperitoneal fibromatosis is exceptional as a neonatal tumour.

Adult↗
PubMedDate not supplied

An ovarian dysgerminoma in Down syndrome. Hypothesis about the association.

An 11-year-old girl with Down syndrome (DS) was operated for a stage I right ovary dysgerminoma. She is in good health 33 years later. Some data in the literature suggest that ovarian cancers could be slightly overrepresented in DS. Despite the rarity of ovarian dysgerminoma, our case is the fifth reported in DS. This case is the second one associated with a family history suggesting the possibility of a familial predisposition to cancer. A hypothesis explaining the development of dysgerminoma in DS is proposed.

Child↗
PubMedDate not supplied

A fetus with Down syndrome and intratubular germ cell neoplasia.

A 22-week-old fetus with trisomy 21 demonstrated intratubular germ cell neoplasia. This is the second report of in situ testicular neoplasia in a fetus with trisomy 21, suggesting that the mechanism responsible for the possible excess of testicular germ cell tumors that occur in Down syndrome is operative in early fetal life. Because no examples of neonatal testicular germ cell tumor in trisomy 21 have been reported, we suggest that this in situ neoplasm may disappear during gestation, such as the trisomy 21-associated transient myeloproliferative syndrome does shortly after birth. This disappearance may be due to a controlled regression phenomenon.

Adult↗