Bartholin gland abscess during pregnancy: Report on 40 patients.

OBJECTIVE(S): To study the clinical and bacterial characteristic of Bartholin gland abscesses during pregnancy and the obstetric and neonatal outcomes. STUDY DESIGN: Retrospective cohort study of all patients with surgical treatment of Bartholin gland abscesses between 2004 and 2015 in our university center. Clinical and bacterial characteristics between pregnant and non-pregnant women were compared. RESULTS: During the period study, 156 patients were included (40 pregnant and 116 non pregnant). The incidence of Bartholin gland abscesses during pregnancy was 0.13%. Eight (20%) abscesses occurred in the first, 18 (45%) in the second, 11 (47.5%) in the third trimester and 3 (7.5%) in the post-partum course. No severe perineal and neonatal infections occurred during pregnancy. One late miscarriage and one preterm delivery were observed. We found more multiparity in the pregnant woman group than in non-pregnant women (62.5% versus 45%, p<0.05). A history of Bartholin gland abscesses were also more frequent in pregnant women (55% versus 30.1%, p<0.05). First line antibiotic therapy was more frequent in non-pregnant women (20% versus 45%, p<0.05). The rate of positive culture did not differ between the two groups (70% versus 55.2%). Among negative pus cultures, no patient in the pregnant woman group had received a first line antibiotic therapy, in contrast with non-pregnant women (0% versus 25%, p<0.05). E. coli was the most common pathogen in the two groups (48.9% of positive cultures and 28.2% of the overall population). The distribution of bacterial taxa was not different between the two groups. CONCLUSION: Bacterial characteristics did not differ from non-pregnant women. Pregnancy could increase the occurrence of Bartholin gland abscesses in patients with previous surgical treatment of abscesses. When appropriate management is applied, maternal and neonatal outcomes are favorable, and severe infections are not to be expected.

Platelets in nonresponders to epinephrine stimulation showed reduced response to ADP.

It has been reported that platelets from some healthy donors did not respond to epinephrine (Epi). To identify the cause for the lack of response, we examined the alpha(2) adrenoceptor in the platelets and their signal transduction pathways. No differences in the genomic (-2076 to 1526 bp) and coding region of alpha(2A) adrenoceptor complementary DNA (cDNA) were found between the responders (R) and nonresponders (NR). No expression of alpha(2B) or alpha(2C) adrenoceptor was detected in platelets. When UK14,304 was used to induce platelet aggregation, similar effect to Epi was observed between R and NR, and any involvement of the alpha(1) and beta adrenoceptor was ruled out. Radioligand binding assay showed similar number of alpha(2) binding sites between the two groups (139+/-25/platelet vs. 145+/-37/platelets). However, platelets from NR showed a weaker response to adenosine diphosphate (ADP, 52.3+/-17.8% vs. 80.5+/-8.7% from R, P<.01). In the presence of P2Y(1) antagonist adenosine 3',5'-diphosphosulfate (A3P5PS), ADP failed to induce platelet aggregation in NR (7.8+/-4.7% vs. 64.7+/-11.2% in R, P<.01). Addition of SQ22,536 to inhibit adenylyl cyclase did not convert NR to R. These observations demonstrate that there is an impaired platelet responsiveness to ADP as well as to Epi in NR, due to a difference in downstream of the signal transduction pathway but independent of adenylyl cyclase inhibition.