A prospective study was made of clinical symptoms, liver function and pregnancy prognosis in women with cholestasis of pregnancy (CP). We used several positive and negative criteria to allow a clinical definition of CP as itching limited to time of pregnancy with or without laboratory evidence of liver dysfunction. The incidence during 1971-74 was 1.5% (100/6798 women) and lower during 1980-82 (52/5441 = 1.0%). One hundred consecutive pregnant women without itching were used as clinical controls. The incidence of CP showed a distinct seasonal variation, culminating in November. Women with CP had often had itching during previous pregnancies and during use of contraceptive pills and described anamnestically itching in mother and sisters. Laboratory data in CP were compared with reference intervals for healthy pregnant women. Serum enzyme levels were significantly increased for serum alkaline phosphatase, 5-nucleotidase, aspartate aminotransferase and alanine aminotransferase in the second and especially in the third trimester. The enzyme distribution was often markedly skewed to the right, i.e. some patients reacted more than others. Most patients with cholestasis only had itching without pronounced abnormalities in laboratory data. This mild form of CP was associated with a good prognosis for both mother and child.

Cytogenetic analysis was performed on short-term cultures of primary ovarian carcinomas from 62 patients. Cytogenetic analysis was successful in 59 cases. Clonal chromosome aberrations were detected in 35 tumors. Only numerical changes or a single structural change were found in five carcinomas: trisomy 12 was the sole anomaly in two tumors, one tumor had the karyotype 50,XX, + 5, + 7, + 12, + 14, a fourth tumor had a balanced t(1;5), and the fifth tumor had an unbalanced t(8;15). The fact that four of these five carcinomas were well differentiated suggests that simple karyotypic changes are generally characteristic of these less aggressive ovarian tumors. The majority of the cytogenetically abnormal tumors (n = 30) had complex karyotypes, with both numerical and structural aberrations and often hypodiploid or near-triploid stemlines. The numerical imbalances (comparison with the nearest euploid number) were mostly losses, in order of decreasing frequency -17, -22, -13, -8, -X, and -14. The structural aberrations were mostly deletions and unbalanced translocations. Recurrent loss of genetic material affected chromosome arms 1p, 3p, 6q, and 11p. The breakpoints of the clonal structural abnormalities clustered to several chromosome bands and segments: 19p13, 11p13-15, 1q21-23, 1p36, 19q13, 3p12-13, and 6q21-23. The most consistent change (16 tumors) was a 19p + marker, and in 12 of the tumors the 19p + markers looked alike.

Cytogenetic analysis of short-term cultures from 11 moderately to poorly differentiated ovarian seropapillary cystadenocarcinomas revealed clonal chromosomal abnormalities in nine tumors. Two bands were involved in structural rearrangements in more than half of the tumors. The band most frequently affected was 19p13; rearrangements giving rise to a 19p+ marker chromosome were found in seven tumors, and in four of them the 19p+ markers appeared to be identical. Structural rearrangements resulting in loss of 11p13-11pter material were found in six tumors.

Cytogenetic analyses were performed on the tumors from both ovaries in 15 patients with bilateral ovarian carcinoma. In 4 of them, omental implants were also examined. Abnormal karyotypes were detected in 11 cases. The baseline karyotypes in the 2 tumorous ovaries were identical in each patient, indicating that bilateral ovarian cancer develops by metastatic spreading. There was no clear-cut evidence of differences in the clonal evolution between the tumors of the 2 ovaries, and hence the side harboring the primary tumor could never be determined. The metastatic nature of the omental implants was proved by the fact that their karyotypes were indistinguishable from those of the ovarian tumor tissue.

No abstract