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2.
AACE Clin Case Rep ; 5(2): e108-e111, 2019.
Article in English | MEDLINE | ID: mdl-31967013

ABSTRACT

OBJECTIVE: To describe a rare case of Wernicke encephalopathy (WE) as a result of hyperemesis gravidarum due to primary hyperparathyroidism (PHPT) in pregnancy. METHODS: We present the clinical presentation, supportive laboratory values, diagnostic dilemmas, treatment, clinical outcome, and supportive literature review of a patient with WE as a result of hyperemesis gravidarum due to PHPT in pregnancy. RESULTS: A 27-year-old previously healthy G1P0 female presented with initial symptoms of right upper-quadrant pain, nausea, vomiting, and paresthesias at 17.3 weeks of gestation. The patient later developed neurologic symptoms including acute encephalopathy, ataxia, and intranuclear ophthalmoplegia. The suspicion for WE was confirmed with characteristic findings on brain magnetic resonance imaging. WE was attributed to severe malnutrition from hyperemesis gravidarum and poor prenatal care. Hypercalcemia with an elevated parathyroid hormone level was identified following an unfortunate intrauterine fetal demise, raising suspicion for PHPT. PHPT was confirmed, and after undergoing successful parathyroidectomy, the patient regained normal neurologic function, with the exception of mild lower-extremity paresthesias. CONCLUSION: This case is an example where early recognition and treatment of hyperparathyroidism can be masked by severe malnutrition and present in an unusual way with neurologic symptoms of WE. Early recognition and suspicion are critical in preventing poor fetal outcomes and long-term consequences.

3.
J Cell Sci ; 123(Pt 2): 213-24, 2010 Jan 15.
Article in English | MEDLINE | ID: mdl-20048339

ABSTRACT

Lung development is the result of complex interactions between four tissues: epithelium, mesenchyme, mesothelium and endothelium. We marked the lineages experiencing Notch1 activation in these four cellular compartments during lung development and complemented this analysis by comparing the cell fate choices made in the absence of RBPjkappa, the essential DNA binding partner of all Notch receptors. In the mesenchyme, RBPjkappa was required for the recruitment and specification of arterial vascular smooth muscle cells (vSMC) and for regulating mesothelial epithelial-mesenchymal transition (EMT), but no adverse affects were observed in mice lacking mesenchymal RBPjkappa. We provide indirect evidence that this is due to vSMC rescue by endothelial-mesenchymal transition (EnMT). In the epithelium, we show that Notch1 activation was most probably induced by Foxj1-expressing cells, which suggests that Notch1-mediated lateral inhibition regulates the selection of Clara cells at the expense of ciliated cells. Unexpectedly, and in contrast to Pofut1-null epithelium, Hes1 expression was only marginally reduced in RBPjkappa-null epithelium, with a corresponding minimal effect on pulmonary neuroendocrine cell fate selection. Collectively, the primary roles for canonical Notch signaling in lung development are in selection of Clara cell fate and in vSMC recruitment. These analyses suggest that the impact of gamma-secretase inhibitors on branching in vitro reflect a non-cell autonomous contribution from endothelial or vSMC-derived signals.


Subject(s)
Arteries/cytology , Cell Lineage , Lung/blood supply , Lung/metabolism , Myocytes, Smooth Muscle/cytology , Receptors, Notch/metabolism , Signal Transduction , Aging/metabolism , Animals , Basic Helix-Loop-Helix Transcription Factors/metabolism , Cell Differentiation/drug effects , Cell Lineage/drug effects , Cilia/drug effects , Cilia/metabolism , Endothelial Cells/cytology , Endothelial Cells/drug effects , Endothelial Cells/metabolism , Epithelial Cells/cytology , Epithelial Cells/drug effects , Epithelial Cells/metabolism , Epithelium/drug effects , Epithelium/embryology , Epithelium/metabolism , Homeodomain Proteins/metabolism , Lung/cytology , Lung/embryology , Mesoderm/cytology , Mesoderm/drug effects , Mesoderm/metabolism , Mice , Myocytes, Smooth Muscle/drug effects , Myocytes, Smooth Muscle/metabolism , Signal Transduction/drug effects , Transcription Factor HES-1 , Transforming Growth Factor beta/pharmacology , Uteroglobin/metabolism
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