Background: Pheochromocytoma is a rare catecholamine-producing tumor of chromaffin cells in the adrenal medulla or of a paraganglion. Typically it presents with sustained or paroxysmal hypertension, severe headaches, palpitations and sweating due to hormone excess. However, the presentation can be variable and can mimic many other diseases. If left undiagnosed or untreated, it can lead to life-threatening consequences. Case Presentation:A 35 year old female with significant past medical history of migraine headaches, poorly controlled hypertension and a recent new onset seizure, presented with progressive worsening shortness of breath and persistent abdominal pain following a gastrointestinal illness. She also reported diaphoresis, cold fingers and toes, abnormal weight gain, and orthostatic symptoms that gradually worsened for two months prior to presentation. Laboratory evaluation revealed lactic acidosis, leukocytosis, and hypokalemia. Subsequently, a CT scan of the abdomen was performed that revealed an adrenal mass with significant elevation in urine metanephrines. As a result, the patient was diagnosed with pheochromocytoma and successfully treated with laparoscopic left adrenalectomy. Conclusion: Pheochromocytoma is a rare but can be life threatening if left undiagnosed. It is of utmost importance for clinicians to keep in mind such unusual presentation of a potentially life threatening tumor. To the best of our knowledge, this is an unusual presentation of Pheochromocytoma with severe lactic acidosis.
Most current mouse models Alzheimer’s disease (AD) exhibit pathological changes dependent on overexpression of mutant human genes linked to familial AD, and animal models that mirror late‐onset/age‐related AD (95% of AD cases) are lacking. Oxidative stress is considered a causative factor in age‐related AD, and Aldehyde dehydrogenase 2 (ALDH2) is important for the detoxification of endogenous aldehydes, such as 4‐hydroxynonenal (HNE), a lipid peroxidation product formed during periods of oxidative stress that can form protein adducts, altering cell function. HNE adducts accumulate in the brains of AD patients and are associated with AD pathology. Given this linkage, manipulations that increase HNE levels might be expected to result in biochemical and cognitive changes that mirror those found in AD. Accordingly, we followed the age‐related changes of a number of relevant AD markers over a 12 month period in hippocampal homogenates from Aldh2 null mice. Marked increases in HNE adduct formation occurred as early as 3 months, and there were age‐related increases in monomeric amyloid β (Aβ), phospho tau protein, and activated caspases 3 and 6. Also observed were age‐related decreases in PSD95 and synaptophysin (indicating synaptic loss) and of total and phosphorylated cAMP‐response element binding protein (CREB). Aldh2 null mice exhibit a graded, age‐related decrease in performance in recognition and spatial memory tasks beginning at 3 months of age and maximal at 6 months. These mice also exhibit dystrophic neurites and loss of dendritic spines, defects in cholinergic agonist‐induced CREB phosphorylation, endothelial dysfunction, and monomeric and oligomeric Aβ deposition in cerebral microvessels. Aldh2 null mice exhibit a wide spectrum of AD‐like pathological changes that are rarely observed together in current AD animal models, and may prove useful for assessing the efficacy of therapeutic agents for improving memory and for slowing, preventing, or reversing disease progression. Grant Funding Source: Botterell Foundation
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.