Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

50 years old female patient, with history of diabetes mellitus and hypertension, receiving metformin (500 mg BID) and atenolol (50 mg BID), presented to the Emergency Room with asthenia and dizziness. The patient was also receiving alternative medication (Dragon Blanco) which contains no licorice. During the emergency workup she developed syncope and three episodes of ventricular fibrillation. She was electrically defibrillated and treated with amiodarone and potassium replacement. The patient was admitted to the Intensive Care Unit. Physical exam: BP: 160/90 mm Hg, RR: 15, Pulse: 83: Cardiovascular: grade II systolic murmur which irradiated to the neck. The rest of the examination was unremarkable. Labs: Na: 138 meg/dl, K: 1.6 meg/dl, Cl: 84 meg/dl, BUN: 17 mg/dl, Creat.: 1.1 mg/dl, Gluc.: 148 mg/dl, Renin: < 0.15 mcgr/ml, Aldosterone: 20.1 mcg%. Aldosterone-Renin ratio: 133. Chest X-Ray: cardiomegaly. EKG: RBBB, long QT segment and prominent broad "u" waves compatible with severe hypokalemia. A CT SCAN of the Abdomen/Pelvis showed a 3.2 cm right adrenal mass, most likely adenomatous. The patient was discharged with the diagnosis of primary aldosteronism. Due to the diagnosis of diabetes mellitus, hypertension and the three episodes of ventricular fibrillation, surgical treatment was postponed until stress tests and eventual coronary angiographic studies were performed. We found in our review of the medical literature 9 reports of fibrillation associated with hyperaldosteronism. Of those, only two were associated with primary aldosteronism, one of them with a fatal outcome. This case is highly unusual and emphasizes the importance of an adequate diagnosis of secondary hypertension.
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PMID:Ventricular fibrillation as the first manifestation of primary hyperaldosteronism. 1961 May 66

Renin inhibitors are antihypertensive drugs that block the first step in the renin-angiotensin system. Their mechanism of action differs from that of the angiotensin-converting enzyme inhibitors and angiotensin-receptor antagonists, but like these drugs, renin inhibitors interrupt the negative feedback effects of angiotensin II on renin secretion. The renin-angiotensin-aldosterone system (RAAS) has long been recognized to play a significant role in hypertension pathophysiology. Certain agents that modify the RAAS can control blood pressure and improve cardiovascular outcomes. Optimization of this compound by Novartis led to the development of aliskiren - the only direct renin inhibitor which is clinically used as an antihypertensive drug. Aliskiren is the first of a new class of antihypertensive agents. Aliskiren is a new renin inhibitor of a novel structural class that has recently been shown to be efficacious in hypertensive patients after once-daily oral dosing. In short-term studies, it was effective in lowering blood pressure either alone or in combination with valsartan and hydrochlorothiazide, and had a low incidence of serious adverse effects. It was approved by the Food and Drug Administration in 2007 for the use as a monotherapy or in combination with other antihypertensives. Greater reductions in blood pressure have been achieved when aliskiren was used in combination with hydrochlorothiazide or an angiotensin-receptor blocker. The most common adverse effects reported in clinical trials were headache, fatigue, dizziness, diarrhea, and nasopharyngitis. Aliskiren has not been studied in patients with moderate renal dysfunction; as an RAAS-acting drug, it should be prescribed for such patients only with caution.
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PMID:Aliskiren: An orally active renin inhibitor. 2168 46

Interstitial pneumonia was the first manifestation to be recognized as caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); however, in just a few weeks, it became clear that the coronavirus disease-2019 (COVID-19) overrun tissues and more body organs than just the lungs, so much so that it could be considered a systemic pathology. Several studies reported the involvement of the conjunctiva, the gut, the heart and its pace, and vascular injuries such as thromboembolic complications and Kawasaki disease in children and toddlers were also described. More recently, it was reported that in a sample of 214 SARS-CoV-2 positive patients, 36.4% complained of neurological symptoms ranging from non-specific manifestations (dizziness, headache, and seizures), to more specific symptoms such hyposmia or hypogeusia, and stroke. Older individuals, especially males with comorbidities, appear to be at the highest risk of developing such severe complications related to the Central Nervous System (CNS) involvement. Neuropsychiatric manifestations in COVID-19 appear to develop in patients with and without pre-existing neurological disorders. Growing evidence suggests that SARS-CoV-2 binds to the human Angiotensin-Converting Enzyme 2 (ACE2) for the attachment and entrance inside host cells. By describing ACE2 and the whole Renin Angiotensin Aldosterone System (RAAS) we may better understand whether specific cell types may be affected by SARS-CoV-2 and whether their functioning can be disrupted in case of an infection. Since clear evidences of neurological interest have already been shown, by clarifying the topographical distribution and density of ACE2, we will be able to speculate how SARS-CoV-2 may affect the CNS and what is the pathogenetic mechanism by which it contributes to the specific clinical manifestations of the disease. Based on such evidences, we finally hypothesize the process of SARS-CoV-2 invasion of the CNS and provide a possible explanation for the onset or the exacerbation of some common neuropsychiatric disorders in the elderly including cognitive impairment and Alzheimer disease.
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PMID:How Does SARS-CoV-2 Affect the Central Nervous System? A Working Hypothesis. 3330 84