Late Postpartum Eclampsia with Postpartum Angiopathy: An Uncommon Diagnosis in the Emergency Department.

BACKGROUND: Late postpartum eclampsia is defined as occurrence of eclampsia >48 h after delivery and is a rare clinical entity. The delayed onset and nonspecific symptoms at presentation make this entity a challenge to diagnose in patients presenting to the emergency department (ED); however, early recognition and timely interventions are the keys to reducing morbidity and mortality in patients with late postpartum eclampsia. CASE REPORT: A 28-year-old woman presented to our ED with a chief complaint of headache of 4 days duration, 8 days after an uncomplicated, normal vaginal delivery. Her past medical history was unremarkable and her entire pregnancy was without medical incident. The patient's examination was within normal limits other than a blood pressure of 152/111 mm Hg and pulse of 54 beats/min. Given her undifferentiated headache and the possibility of preeclampsia, the patient was treated with magnesium sulfate, which was subsequently stopped due to worsening bradycardia. Hydralazine was administered for blood pressure control. Three hours after the magnesium was stopped, the patient reported blurry vision, which was immediately followed by a generalized tonic-clonic seizure. After the seizure, lorazepam was given for control of seizures, and the patient was admitted to the medical intensive care unit. The patient was transferred to the postpartum floor 6 days later in stable condition and without any further seizure activity. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Patients with late postpartum eclampsia are infrequently encountered in the ED due to the rarity of this condition. Increased awareness of this entity among emergency physicians will lead to early interventions, which are crucial in decreasing morbidity and mortality in these patients.

Allelic diversity in the TGFB1 regulatory region: characterization of novel functional single nucleotide polymorphisms.

Altered TGF-beta1 expression due to polymorphisms affects a wide variety of normal cellular and disease processes such as T cell activation and proliferation, tumor progression, and asthma. In this study, a comprehensive examination of function and diversity was undertaken for the TGFB1 promoter region and exon 1 (-2,665 to +423). The known TGF-beta1 promoter was extended to encompass 463 bases by the identification of a strong enhancer activity for a distal segment (-2,665 to -2,204). Ten novel polymorphisms and 14 novel alleles were identified. Most single nucleotide polymorphisms (SNPs) appear to be randomly associated except c.-768_-769insC and c.+74G > C and a set of five novel polymorphisms present in a single allele in persons of African descent. The TGFB1 alleles clustered into three phylogenetic groups based on the common functional SNPs c.-1347C > T (commonly known as -509C-T) and c.+29T > C (commonly known as +869T-C) suggesting three phenotypic groups. Two SNPs unique to African-Americans affect the TGFB1 regulatory region. The c.-1287G > A SNP in the promoter alters the binding affinity of two unidentified transcription factor complexes which translates into a significant difference in reporter gene expression and the c.-387C > T SNP in the 5' UTR alters the binding of Stimulating protein 1 and 3. Thus, TGFB1 possesses a highly polymorphic, extensive regulatory region that likely impacts the pathogenesis of numerous TGF-beta1 related diseases.