Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 65-year-old man was admitted to our hospital because of thirstyness and left lower abdominal pain. On admission, he was found to have urolithiasis, renal insufficiency (BUN: 73 mg/dl, Crt: 4.4 mg/dl), and hypercalcemia (13.2 mg/dl). Chest X-ray films and computed tomograms showed enlargement and calcification of the hilar lymph nodes, and thickened interlobar fissures in both lungs. Levels of angiotensin converting enzyme (30.2 IU/l) and 1.25 (OH)2VitD3 (66.4 pg/ml) were elevated. Histologic examination of the specimen obtained from transbronchial lung biopsy showed non-caseous epithelioid cell granulomas. Because the level of parathyroid hormone was normal and no malignancies were detected, a diagnosis of sarcoidosis was made. Treatment with extracorporeal shock wave lithotripsy, transurethral lithotomy, saline infusion, and prednisolone (30 mg/day) alleviated the urolithiasis, renal insufficiency, and hypercalcemia. After discharge, the patient was followed up and given prednisolone therapy. About 1 month after the prednisolone dose had been tapered to 15 mg/day, the patient experienced dyspnea and facial and pedal edema. Because congestive heart failure was diagnosed, he was re-admitted to our hospital for a second time. Although he was then placed on intensive therapy, he died of ventricular tachycardia associated with sarcoidosis of the heart.
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PMID:[Sarcoidosis with hypercalcemia, urolithiasis, renal insufficiency, and heart failure]. 1048 65

This case presented the scenario of a patient who had severe bronchospasm from an unknown etiology. Further, she had difficulty speaking and denied any past medical history, which made a diagnosis more difficult. Prehospital providers were challenged with determining the differential diagnosis for bronchospasm and hypoxemia. Was the patient experiencing an anaphylactic reaction, acute asthmatic attack or something else? The key here, once again, is conducting a thorough assessment and patient history. Remember, all that wheezes is not asthma; therefore, providers in this case had to determine if the patient was suffering something such as anaphylaxis, asthma, bronchitis, pneumonia or even congestive heart failure (CHF). Typically, anaphylaxis and asthma affect ventilation, not oxygenation, so until the late stages of anaphylaxis or asthma, the patient will have difficulty moving air, but will be oxygenating OK. We understand that many respiratory conditions can cause wheezing, but CHF? Yes: As left ventricular function diminishes and leads to increased pulmonary pressure, serum begins to leak out of the pulmonary vessels and into the interstitial space. As the interstitial pressure increases, it causes narrowing of the bronchioles, and air traveling through the narrowed bronchioles causes the wheezing sound. Fluid may also be leaking out of the pulmonary capillaries and occupying space in the alveolar sacs. When the interstitial pressure is high and the bronchioles continue to narrow, providers may initially hear only the wheezing and not the crackles from the smaller airways. In these conditions, oxygen is not exchanged adequately into the blood, and the patient becomes hypoxemic. Good assessment and patient history will guide the EMS provider to the cause of bronchospasm. For example, does the patient have a history of asthma? If yes, asthma is likely to be the cause. Does the patient have any rash, hives or swelling? If yes, anaphylaxis is likely the cause. Is the patient elderly, and does he/she show pedal edema, JVD, hypoxemia and/or distended neck veins? If yes, CHF may be the cause. [table: see text] There are questions regarding the use of bronchodilators in patients suffering CHF. If a CHF patient is wheezing (bronchospasm), then a beta-2 selective breathing treatment may be appropriate, along with nitrates and diuretics. Oxygenation is the critical problem in CHF, and hypoxemia will continue to worsen cardiac function. Remember, both bronchoconstriction and alveolar sacs filling with fluid will impair oxygenation of the RBCs and ultimately the vital organs. Focused prehospital management of CHF is aggressive in restoring oxygenation. For example, many agencies are now using oxygen, nitrates, ACE inhibitors and CPAP. By better understanding the pathophysiology of respiratory emergencies and their differential diagnosis, we will improve patient outcomes.
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PMID:Breathless. 1196 14

Hypertension is one of the most common conditions seen in primary care and a major public health problem in India. It can lead to various complications if not detected early and treated appropriately. As per the latest Eighth Joint National Committee (JNC 8) the goal BP in most hypertensive patients age <60 years should be <140/90 mmHg and treatment can be started by selecting drugs from among 4 specific medication classes i.e. angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB), calcium channel blocker (CCB) or diuretics. CCB is one of the first line drugs in the management of hypertension. Among CCB, Cilnidipine is a unique Ca2+ channel blocker as it has inhibitory action on the sympathetic N-type Ca2+ channels along with its effect on L-type Ca2+ channels. This article focuses on the current status of cilnidipine in the management of hypertension and co-morbidities. Cilnidipine by attenuating norepinephrine release from sympathetic nerve endings leads to vasodilatation, decreases heart rate and increases renal blood flow. Cilnidipine has an advantage of causing less reflex tachycardia, less pedal edema and better control of proteinuria in comparison to L-type CCB. By causing dilatation of efferent arteriole, it causes less damage to glomeruli and suppresses podocyte injury. Cilnidipine also increases insulin sensitivity. Therefore, cilnidipine as CCB can be a good choice in hypertensive patients with diabetes, chronic kidney disease and in patients developing pedal edema with other CCB.
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PMID:Cilnidipine: Next Generation Calcium Channel Blocker. 2773 56

Bilateral pitting edema is rare adverse drug reaction observed in the psychiatry department. Drug related pedal edema is most commonly seen with ACE inhibitors, non-steroidal antiinflammatory drug, and calcium channel blockers. But pitting edema with Sodium valproate is very rare. Here, we report two cases of Sodium valproate-induced bilateral pitting edema.
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PMID:Sodium Valproate-Induced Bilateral Pitting Pedal Edema - A Case Report. 2878 77