Predictive factors for prolonged survival in recurrent endometrial carcinoma: Implications for follow-up protocol.

OBJECTIVE: To evaluate the role of follow-up after curative treatment in endometrial carcinoma, we determined predictive factors for prolonged survival after recurrence. METHODS: We retrospectively studied patients with endometrioid endometrial carcinoma who had a follow-up appointment consisting of pelvic examination, vaginal cytology, imaging and CA-125 measurements and who developed recurrence. Possible prognostic factors were evaluated by univariate and multivariate analyses. RESULTS: Fifty-one patients developed recurrence. The median time from initial treatment to recurrence was 12 months (range, 3-119 months). A total of 25 (49%) and 45 (88%) recurrences were detected within 1 and 3 years of initial treatment, respectively. Twenty (39%) patients were symptomatic, while 31 (61%) were asymptomatic. The median survival time of symptomatic patients was longer than that of asymptomatic patients (27 vs. 12 months); however, the difference was not statistically significant (P = 0.42). No recurrences were detected by vaginal cytology. Of asymptomatic patients with low/intermediate risk (stage I/II), patients with recurrence detected by imaging or CA-125 measurements tended to have shorter survival than patients with recurrence detected by physical examination (7 vs. 31+ months, P = 0.057). Multivariate analysis revealed that site of recurrence (vaginal vs. extravaginal, P < 0.01) and time to recurrence (> 1 year vs. ≤ 1 year, P = 0.01) were significant independent predictors of prolonged survival after recurrence. CONCLUSION: In endometrial carcinoma, site of and time to recurrence are significant predictive factors of prolonged survival after recurrence, suggesting that early detection of recurrence by imaging studies and CA-125 measurements cannot improve prognosis. Although intensive follow-up using these methods may provide psychological reassurance to some patients, the use of these methods must be balanced against the wise use of limited health care resources.

Fetal growth restriction associated with measles virus infection during pregnancy.

We report on a 28-week infant with growth restriction starting after 23 weeks' gestation because of measles virus (MV) infection of the mother. Histological findings for the placenta revealed extensive fibrin deposition and necrosis of the villi, and MV antigen was demonstrated in the syncytiotrophoblast by immunostaining. The MV-specific IgM level in the infant was negative, but that of the mother was positive. Therefore, we speculate that growth restriction is not attributed to direct infection with MV, but to placental dysfunction due to a decrease in intravillous blood flow and oxygen supply to the fetus.

Severe perinatal hypophosphatasia due to homozygous deletion of T at nucleotide 1559 in the tissue nonspecific alkaline phosphatase gene.

OBJECTIVES: Hypophosphatasia is an inherited disorder characterized by defective bone mineralization and deficiency of tissue nonspecific alkaline phosphatase (TNSALP) activity. This disorder is caused by various mutations in the TNSALP gene. We report here hypophosphatasia in two siblings, both of them severely affected by the perinatal (lethal) type. METHODS: We diagnosed the first infant by clinical and radiologic manifestations, and laboratory findings. Laboratory findings were characterized by deficiency of serum alkaline phosphatase. Both parents and the second infant were then analyzed by molecular techniques. RESULTS: The radiograph of the first infant showed severe hypomineralization of the skeleton. Molecular analysis of the second infant showed that this condition was caused by a homozygous single T nucleotide deletion at cDNA number 1559 (1559delT). Both parents were heterozygous carriers for this mutation, although they were not consanguineous. CONCLUSION: This mutation has been frequently found in Japanese hypophosphatasia patients, but this is the first observation of a homozygous deletion. This report shows that homozygosity for the 1559delT mutation of the TNSALP gene results in a severe lethal phenotype.