Disseminated herpes simplex virus 2 (HSV-2) infection, is a rare but devastating infection in pregnancy women. We present the case of a 30-year-old gravida 3, para 2−0-0−2, at 26 weeks 2 days gestation who presented with eleven days of vague and indolent symptoms before a diagnosis of disseminated HSV-2 infection with associated hepatitis was made. While the patient clinically improved with empiric acyclovir treatment, possibility of significant harm to the fetus remained, and the patient request elective termination. The authors review the epidemiology, diagnosis, treatment, and prognosis of disseminated HSV-2 infection in pregnancy.
INTRODUCTION:
The role of uric acid in preeclampsia (PEC) is controversial. We hypothesize that women with PEC express a pro-inflammatory cytokine profile compared to controls related to uricemia.
METHODS:
In an IRB approved secondary analysis of a two-center prospective cohort study of women with PEC risk factors, maternal serum was collected in second and third trimesters. PEC cases were matched with controls on age, body mass index, fetal number, and chronic hypertension. Women with gestational hypertension (GHTN) were matched to PEC cases. Multiplex technology analyzed inflammatory cytokines at diagnosis and at delivery if delayed. Serum uric acid levels were extracted from the medical record.
RESULTS:
Of 258 subjects, 26 PEC and 15 GHTN cases were identified. Of PEC cases, 53.8% were diagnosed preterm and 30.8% had CHTN. PEC cases delivered earlier than controls (P=.020). Unadjusted linear regression showed significant decrease in interleukin-18 (IL-18) in PEC versus controls (P=.033) and in monocyte chemoattractant protein-1 (MCP-1) in PEC versus GHTN cases (P=.022). By multivariable regression, covariates of gestational age, diabetes, PEC history and parity were not significant confounders. Qualitatively, uric acid demonstrated linear increase over pregnancy in PEC whereas controls had more abrupt increases near term.
CONCLUSION:
PEC cases expressed different levels of MCP-1 and IL-18 compared to controls and GHTN, suggesting a unique inflammatory state of PEC. Contrary to our hypothesis, select pro-inflammatory markers were lower in PEC. A larger population may clarify whether differences in subgroups of PEC or timing of sampling relative to diagnosis could explain findings.
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