Severe Hyperlipidemia Induced Hemorrhagic Pancreatitis during Pregnancy

Background. We report a case of familial hyperlipidemia in pregnancy that resulted in hemorrhagic pancreatitis. Case. A patient at 27-week gestation was admitted for recurrent pancreatitis secondary to severe hyperlipidemia. With conservative care, the patient improved but on the fourth day of admission she experienced a sudden onset of hypotension and was diagnosed with hemorrhagic pancreatitis. Conclusion. Pancreatitis caused by hyperlipidemia is an uncommon event during pregnancy. A familiarity with the severe complications associated with this potentially life-threatening condition is important

Impact of genetic counseling on primary and preventive care in obstetrics and gynecology

OBJECTIVE: To evaluate the utility of the prenatal three-generation pedigree in assessment of the obstetric patient\u27s primary medical risks. STUDY DESIGN: In a case series, 250 charts of patients referred for amniocentesis on the basis of advanced maternal age were reviewed for a significant genetic risk of a primary care disorder. RESULTS: A total of 40 patients (16%) were at significantly increased risk for a primary care disorder. Thirty-eight patients (15.2%) were at increased risk for medical conditions for which early screening, detection and/or intervention are established. CONCLUSION: For the advanced maternal age population, formal genetic risk assessment performed prior to amniocentesis can be beneficial in primary care risk assessment

The Importance of Genetic Counseling before Amniocentesis

OBJECTIVE: To determine the adequacy of genetic risk assessment among primary care providers and to evaluate the efficacy of genetic counseling before routine genetic amniocentesis. STUDY DESIGN: A retrospective cohort study was undertaken. Charts of 275 consecutive patients referred for genetic counseling and amniocentesis on the basis of advanced maternal age (AMA) were compared with charts of 103 consecutive patients referred for an abnormal maternal serum alpha-fetoprotein (MSAFP) finding. Pedigree information obtained during counseling of these patients was compared with the family histories charted by the referring physician. RESULTS: In 35.6% of pedigrees evaluated, a significant genetic risk was discovered during genetic consultation that had not been noted by the referring physician. Furthermore, 9.8% of AMA patients and 10.7% of patients with abnormal MSAFP results underwent additional genetic testing or screening on the basis of genetic counseling. Additional genetic testing of 0.8% of amniotic fluid specimens was done on the basis of the genetic risk assessment elicited during counseling. Although a significant difference in increased genetic risk was observed between the AMA and abnormal MSAFP groups (AMA 30.8% positive, MSAFP 48.5% positive; relative risk 0.81, confidence limit 0.70 to 0.93), no significant difference was observed between the two groups with regard to patient interventions (relative risk 0.97, confidence limit 0.79 to 1.21) or amniotic fluid testing (p = 0.57, not significant). CONCLUSIONS: The data support the importance of genetic counseling before amniocentesis. Furthermore, the findings support the relevancy and usefulness of genetic counseling in more accurately ascertaining genetic risk and in maximizing the benefits of genetic evaluation of patients seemingly at low risk for other genetic diseases

Circulating T-Cell Subsets, Monocytes, and Natural Killer Cells in Peripartum Cardiomyopathy: Results From the Multicenter IPAC Study

•Immune cell subsets were examined in healthy postpartum and peripartum cardiomyopathy (PPCM) women.•In the early postpartum, PPCM women had lower NK and higher CD3+CD4–CD8–CD38+ T cell levels.•Levels largely normalized by 6 months postpartum. The aim of this work was to evaluate the hypothesis that the distribution of circulating immune cell subsets, or their activation state, is significantly different between peripartum cardiomyopathy (PPCM) and healthy postpartum (HP) women. PPCM is a major cause of maternal morbidity and mortality, and an immune-mediated etiology has been hypothesized. Cellular immunity, altered in pregnancy and the peripartum period, has been proposed to play a role in PPCM pathogenesis. The Investigation of Pregnancy-Associated Cardiomyopathy (IPAC) study enrolled 100 women presenting with a left ventricular ejection fraction of <0.45 within 2 months of delivery. Peripheral T-cell subsets, natural killer (NK) cells, and cellular activation markers were assessed by flow cytometry in PPCM women early (<6 wk), 2 months, and 6 months postpartum and compared with those of HP women and women with non–pregnancy-associated recent-onset cardiomyopathy (ROCM). Entry NK cell levels (CD3–CD56+CD16+; reported as % of CD3– cells) were significantly (P < .0003) reduced in PPCM (6.6 ± 4.9% of CD3– cells) compared to HP (11.9 ± 5%). Of T-cell subtypes, CD3+CD4–CD8–CD38+ cells differed significantly (P < .004) between PPCM (24.5 ± 12.5% of CD3+CD4–CD8– cells) and HP (12.5 ± 6.4%). PPCM patients demonstrated a rapid recovery of NK and CD3+CD4–CD8–CD38+ cell levels. However, black women had a delayed recovery of NK cells. A similar reduction of NK cells was observed in women with ROCM. Compared with HP control women, early postpartum PPCM women show significantly reduced NK cells, and higher CD3+CD4–CD8–CD38+ cells, which both normalize over time postpartum. The mechanistic role of NK cells and “double negative” (CD4–CD8–) T regulatory cells in PPCM requires further investigation