Intrahepatic cholestasis of pregnancy is seldom associated with significant vitamin K deficiency. We report a case of a 16-year-old primigravid patient at 24 weeks and 3 days of gestation who presented with pruritus, hematuria, and preterm labor. Laboratory work-up showed severe coagulopathy with Prothrombin Time (PT) of 117.8 seconds, International Normalized Ratio (INR) of 10.34, and elevated transaminases suggestive of intrahepatic cholestasis of pregnancy. Her serum vitamin K level was undetectable (<0.1 nMol/L). Initial therapy consisted of intramuscular replacement of vitamin K and administration of fresh frozen plasma. Her hematuria and preterm labor resolved and she was discharged. She presented in active labor and delivered at 27 weeks and 1 day. Her bile acids (93 μ/L) and INR (2.32) had worsened. She delivered a male infant, 1150 grams with Apgar scores 7 and 9. The newborn received 0.5 mg of intramuscular vitamin K shortly after delivery but went on to develop bilateral grade III intraventricular hemorrhages by day 5. Intrahepatic cholestasis in pregnancy and nutrition issues were identified as the main risk factors for the severe coagulopathy of this patient. This case underlines the importance of evaluation of possible severe coagulopathy in patients with intrahepatic cholestasis of pregnancy in order to avoid serious maternal or fetal adverse outcomes.

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Background: Cases with sepsis after transrectal ultrasound-guided prostate biopsy (TRUSPB) were documented, with special focus on cultures and susceptibility of isolates. We also evaluated the contribution of concomitant rectal cultures to the treatment of selective cases. Materials and Methods: Patients with sepsis after TRUSPB were followed prospectively. Manifestations and risk factors for antimicrobial resistance were documented. Results of urine and blood cultures and antimicrobial susceptibility were recorded for all participating patients. In 40 patients, rectal swab cultures were obtained concomitantly. Results: Ninety-five patients were consecutively studied. Sepsis symptoms started showing up within 48 h after biopsy in 93% of patients. At least one of the cultures was positive in 72 patients. E. coli grew in 70 cases; isolates were highly resistant: 67% displayed multidrug-resistance. Rectal cultures grew E. coli in 38 cases. In patients with positive E. coli in rectum and in at least one additional culture (blood and/or urine), the antibiogram was identical in all cases but one. Eight cases had negative cultures. Conclusion: The prevalence of antimicrobial resistance among E. coli isolates from patients with TRUSPB sepsis was alarming. Susceptibilities of rectal E. coli isolates used for deescalation of initial empiric treatment in culture-negative TRUSPB sepsis can contribute to the reduction of broad-spectrum antibiotics exposure.

OBJECTIVE: Somatic abnormalities involving chromosome 21, 18, and 13 are found in cancers and are detectable in circulating cfDNA. Previous publications have suggested increased risks of maternal neoplasm when multiple aneuploidies are detected on non-SNPbased NIPTs with normal fetal karyotypes. SNP-based NIPT distinguishes maternal/fetal cfDNA, allowing for CNV origin identification. This study reviewed maternal/fetal outcome SNP-based NIPT data to determine if multiple maternal copy number variants (CNVs) can predict increased risk of maternal neoplasms. STUDY DESIGN: Fetal/maternal outcomes were retrospectively collected for SNP-based NIPT cases accessioned from 7/1/2017 to 3/ 30/2021. Cases reported as unspecified atypical findings with data suggesting multiple maternal CNVs were included. RESULTS: Of 2,004,428 cases with results, 38 (0.002%) had unspecified atypical results with internal data consistent with maternal CNVs. Fetal/maternal health outcomes were obtained in 26/38 (68.4%) cases. A malignancy was diagnosed before, during, or after delivery in 14/26 cases. Positive predictive values (PPVs) for maternal neoplasm ranged from 39% (15/38 all cases) to 58% (15/26 known outcomes). One case of leiomyoma (1/26, 3.8%), and one case of lymphadenopathy (1/26, 3.8%) were observed. Fetal triploidy without reported maternal health issues was seen in 2 cases (2/26; 7.7%). 8/26 (30.8%) cases had no reported fetal/maternal health issues, including one with a family history of a BRCA mutation with patient mutation status unknown. (Table 1) CONCLUSION: SNP-based NIPT can incidentally identify maternal neoplasm presence/recurrence. When maternal CNVs are identified on SNP-based NIPT, our data suggests an increased risk of maternal neoplasm with PPVs ranging from 39-59%. Neoplasms in this cohort could be underdiagnosed due to limited follow-up time post NIPT (2-48 months). Reporting this incidental finding allows for better informed maternal clinical management, with possible earlier neoplasm detection.