Preeclampsia is becoming an increasingly common diagnosis in the developed world and remains a high cause of maternal and fetal morbidity and mortality in the developing world. Delay in childbearing in the developed world feeds into the risk factors associated with preeclampsia, which include older maternal age, obesity, and/or vascular diseases. Inadequate prenatal care partially explains the persistent high prevalence in the developing world. In this review, we begin by presenting the most recent concepts in the pathogenesis of preeclampsia. Upstream triggers of the well described angiogenic pathways, such as the heme oxygenase and hydrogen sulfide pathways, as well as the roles of autoantibodies, misfolded proteins, nitric oxide, and oxidative stress will be described. We also detail updated definitions, classification schema, and treatment targets of hypertensive disorders of pregnancy put forth by obstetric and hypertensive societies throughout the world. The shift has been made to view preeclampsia as a systemic disease with widespread endothelial damage and the potential to affect future cardiovascular diseases rather than a selflimited occurrence. At the very least, we now know that preeclampsia does not end with delivery of the placenta. We conclude by summarizing the latest strategies for prevention and treatment of preeclampsia. A better understanding of this entity will help in the care of at-risk women before delivery and for decades after.
Giant cell reparative granuloma (GCRG) is an infrequent non-tumoural lesion affecting particularly the maxillary and mandibular bones and only rarely the cranial bones. The pathogenesis is still controversial and the differential diagnosis, especially from giant cell tumours of bone, is difficult. A case of GCRG of the sphenoid masquerading as an intracranial tumour is reported here. The relevant literature is reviewed.
While the wide belief is that monoclonal antibodies, due to their large size, would not be able to penetrate the blood-brain barrier, we present a rare case of aseptic meningitis induced by intravenous cetuximab administration. A 58-year-old man with tonsillar squamous cell cancer presented with headache and fever, which started approximately 1 h after his first dose of cetuximab (loading dose of 400 mg/m(2) equalling 800 mg). CT scan of the head was non-revealing and laboratory tests including complete blood count, serum comprehensive metabolic panel and coagulation profile were within normal limits. Aseptic meningitis in the setting of cetuximab therapy has been reported on 6 previous occasions. Consistent with these prior reports, it is interesting to note that this case also occurred after administration of the initial higher loading dose of Cetuximab. This is of interest as Cetuximab is more frequently being dosed at 500 mg/m(2) (higher dose) every 2 weeks in colorectal cancer.
Introduction: Acute pancreatitis (AP) is known to cause cascade of complex inflammatory response following an initial insult. Hence the scoring systems includes white blood cell count (WBC). This study analyse the inflammatory responses between gallstone pancreatitis (GP) versus non-galltone pancreatitis (NGP). Methods: All patients presented with AP between October 2016 to October 2017 were included in this study and relevant parameters were collected from an electronic patient documents. Total of 140 patients were analysed in this study. We have collected the WBC count and C-reactive protein (CRP) at admission, 24 hours and 72 hours to assess their response to AP. Results: Among 140 patients with acute pancreatitis, 33 patients had GP and remaining of 107 patients suffered NGP. The WBC count at admission, 24 hours and 72 hours in GP versus NGP were (11.6AE 5 versus 13.7AE17; P=.24), (12.6AE20 versus 10.1AE17;P=0.21) and (13.2AE22 versus 9.2AE4.7;P=0.15) respectively. But the CRP levels at admission, 24 hours and 72 hours were (30.4AE 73 versus 47.6AE79; P=0.25), (71.9AE20 versus 92.2AE97; P=0.35) and (89AE106 versus 122.7AE107; P=0.05) respectively. Conclusion: There was a significantly high CRP level was associated with non-biliary pancreatitis. Further investigation is needed to assess this response and perhaps this could shed on evolution of AP.
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