Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: CAS:7440-70-2 (calcium)
 333,191 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolation of the causative agent remains the "gold standard" for the early diagnosis of pertussis. For this purpose, the nasopharynx is swabbed with a calcium alginate swab. Cephalexin-containing charcoal horse blood medium is used for the transport of the swabs to the bacteriology laboratory. As an alternative, the isolation of bordetellae can be performed at the paediatrician's office by direct inoculation of charcoal horse blood agar plates. Long-lasting cough of unknown aetiology is the main field for pertussis serology (ELISA). Even today, severe courses of whooping cough requiring hospitalization are not rare, especially in infants. Erythromycin (given in high doses for 14 days) is the antibiotic of choice for pertussis. As an alternative to the macrolides, cotrimoxazole may be administered or amoxycillin. Salbutamol and the corticosteroids have been shown to be useful for the symptomatic treatment of severe pertussis in infants.
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PMID:[Pertussis: diagnosis, clinical aspects and therapy]. 219 59

Recently there has been extensive development of orally active angiotensin converting enzyme (ACE) inhibitors in addition to those already marketed, for example, captopril, enalapril, lisinopril and ramipril. It was initially thought that ACE inhibitors were likely to be most useful as antihypertensive agents in conditions in which circulating renin and angiotensin II were elevated. However, it is now clear that they can also lower arterial pressure when plasma renin is not high. In addition, they have beneficial effects in cardiac failure. Thus, captopril, enalapril, lisinopril and ramipril can be used in the treatment of mild to moderate hypertension either alone or in conjunction with diuretics or calcium antagonists. Broadly speaking, efficacy appears to be similar to that of beta-blockers or diuretics. Unfortunately, however, there are no long term studies comparing one ACE inhibitor with another or with other classes of antihypertensive agents. Furthermore, there are no prognostic studies which show that use of ACE inhibitors reduces morbidity or mortality in hypertension. Many new ACE inhibitors are undergoing clinical assessment, including alacepril, cilazapril, fosenopril, perindopril, quinapril and ramipril. The drugs vary, in that some exist in the active form whereas others are prodrugs which are converted to the active agent following absorption. In addition they each possess one of several ligands, for example, carboxyl, phosphinyl or sulfhydryl groups, and so vary in their affinity for ACE. Although many of these agents are renally excreted, a small number are metabolised via the liver (e.g. quinapril and spirapril) and this may prove advantageous in the presence of renal impairment. In common with captopril and enalapril, the new ACE inhibitors inhibit the renin-angiotensin system and initial results suggest that they are effective in lowering blood pressure in essential hypertension. Furthermore, they reduce systemic vascular resistance in the absence of a reflex tachycardia. There are a number of adverse effects which are attributable to the pharmacological mechanism of the ACE inhibitors as a group; these include hypotension, particularly in patients with high renin levels, prior diuretic use, renal impairment or in the elderly. Additional adverse effects may relate to chemical structure. The high incidence of adverse effects noted in early studies related to excess dosage and to the presence of a sulfhydryl group, which the more recently developed ACE inhibitors lack. The adverse effects most commonly reported with established and new ACE inhibitors include headache and fatigue, cough, skin rashes, hypotension and diarrhoea. As a group, ACE inhibitors have an acceptable but not negligible adverse effect burden.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin converting enzyme inhibitors and moderate hypertension. 222 19

ACE inhibitors have antihypertensive efficacy similar to that of thiazides, beta-blockers and calcium antagonists. They are simple to prescribe and to take, and are relatively free from subjective side-effects apart from persistent dry cough. There are few specific concerns about safety, but experience of long-term use is still relatively limited. They are valuable additional or alternative antihypertensive drugs when standard therapy is contraindicated or fails to control blood pressure.
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PMID:The role of ACE inhibitors in the management of hypertension. 228 49

The treatment of hypertension in patients with airway dysfunction is a delicate problem. This article focuses on the airway effects of some antihypertensive drugs. Early on, the beta-adrenoceptor antagonists were shown to be hazardous in patients with asthma. Nonselective beta-blockers could induce severe asthma attacks and the bronchodilating effect of beta-agonists was totally blocked. Also, the beta-blockers with partial agonist activity totally blocked the effect of bronchodilating beta-agonists. The selective beta 1-adrenoceptor antagonists were shown to have less pronounced effects on the airways, and it was possible to overcome the beta-blockade in the airways with high doses of beta-agonists. beta-Blockers are contraindicated in asthma patients, even if it is possible to give selective beta 1-adrenoceptor antagonists in some patients together with high doses of beta 2-agonists. Angiotensin converting enzyme (ACE)-inhibitors were recently shown to induce cough and bronchial hyperresponsiveness in some patients. This is probably due to an increased inflammation in the bronchial mucosa as substances (e.g., bradykinin) are not metabolized. Therefore, ACE inhibitors could be hazardous in asthmatic patients, as they can increase the underlying bronchial hyperresponsiveness. Calcium channel blockers were earlier considered to be beneficial in asthma, as it was shown that they had a small relaxant effect on bronchial tone, and could amplify the effect of bronchodilators. In studies of provoked bronchoconstriction, calcium channel blockers were shown to have some protective effect against allergens, histamine, methacholine, or exercise-induced bronchoconstriction. Calcium channel blockers do not have a major place in asthma treatment, but as they have no severe side effects on the airways, they could preferably be given to hypertensive patients with airways disease instead of other antihypertensive agents.
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PMID:Antihypertensive drugs and airway function, with special reference to calcium channel blockade. 248 71

The respective prevalence of hypertension and asthma is sufficient for their combined existence to be far from rare. The effects of certain antihypertensive drugs, e.g., alpha 2-adrenoceptor agonists, on the bronchi may be either harmful or beneficial. When inhaled, alpha 2-agonists reduce the immediate bronchial response to allergens, whereas when ingested they aggravate the bronchial response to histamine and all the more so when their effect on the central nervous system is greater. Therefore, there has been much interest in agents such as the new oxazoline derivative, rilmenidine, which has less central effects than clonidine, an imidazoline compound of reference. Calcium antagonists inhibit smooth muscle contraction and release of mast cell inflammatory mediators. In asthmatic subjects, their short-term administration leads to a modest improvement in spontaneous bronchial obstruction, has only a partial protective action against various nonspecific or allergenic stimuli, and slightly reinforces the beneficial effect of beta 2-agonists. Beta-adrenoceptor antagonists aggravate bronchial obstruction and nonspecific bronchial hyperreactivity in asthmatic subjects. These harmful effects are dose-dependent, have even been reported after the administration of eyedrops, and are common to all beta-blockers. Angiotensin-converting enzyme inhibitors increase bronchial hyperreactivity in patients who develop cough during treatment and may, in certain cases, worsen or even induce asthma, probably by opposing inactivation by hydrolysis of tachykinins and of bradykinins.
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PMID:Bronchial effects of alpha 2-adrenoceptor agonists and of other antihypertensive agents in asthma. 257 Dec 93

A patient with long-standing, asymptomatic, primary hyperparathyroidism developed pain in the anterior neck area, with cough, dysphagia and increasing shortness of breath. This led to respiratory insufficiency, which required endotracheal intubation and respirator assistance. During the ensuing hours the patient developed an area of ecchymosis on the anterior chest. Chest x-ray showed widening of the superior mediastinum, and CT scan showed a large mass with a fluid level. Surgery revealed a large hematoma originating from a mediastinal parathyroid adenoma with a hemorrhagic infarct. Serum calcium, previously elevated, decreased to normal with the onset of neck pain, and the patient remains normocalcemic. Previous reported cases of this rare complication of parathyroid adenomas are reviewed. Hemorrhagic infarct of a parathyroid adenoma may present with a rapidly enlarging mediastinal mass, and/or hypercalcemic crisis. Surgical removal of the infarcted adenoma can return the serum calcium to normal.
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PMID:Spontaneous hematoma of a parathyroid adenoma. 265 47

The respective prevalence of arterial hypertension and of asthma is sufficient that their association is far from unusual. Antihypertensive medications may have deleterious or beneficial effects on the bronchi. Calcium inhibitors oppose the contraction of smooth muscle and the liberation of inflammatory mediators from mast cells. In asthmatics, their acute administration has a modest beneficial effect on spontaneous bronchial obstruction, only exerts a partial protective action against numerous non-specific or allergic stimuli, and weakly reinforces the beneficial effects of beta-2 agonists. The antagonists of beta-adrenergic receptors worsen bronchial obstruction and non-specific bronchial hyperreactivity in asthmatics. These deleterious effects increase with the dose and have been observed even after administration of eye drops and apply to all beta blockers. Inhibitors of angiotensin converting enzymes increase bronchial hyperreactivity in patients developing cough during treatment and may indeed, even in a few cases, trigger an asthmatic attack, probably by opposing the inactivation by hydrolysis of tachykinins and bradykinins. The effects of alpha-2 adrenergics are controversial. Inhaled, they reduce the early allergic bronchial response, even when ingested they aggravate the bronchial response to histamine, all the more so as their effect on the central nervous system is greater. The alpha-1 adrenergic antagonists, frusemide and ketanserin have an overall beneficial effect.
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PMID:[Asthma and antihypertensive treatment]. 267 23

Chronic bronchopneumonia associated with microlithiasis was diagnosed in a 9-year-old domestic shorthair cat with a 3-month history of coughing and dyspnea. Thoracic radiography revealed multifocal patchy alveolar infiltrates in all lung fields. Numerous acellular, concentrically laminated, periodic acid-Schiff-positive microliths were seen in mucus from tracheal washing. Microliths were composed primarily of calcium carbonate. A definite cause could not be identified. There was no response to treatment and the cat was euthanatized. Marked type-II alveolar cell proliferation, peribronchiolar smooth muscle proliferation, and alveolar microlithiasis were seen histologically. Microliths are rarely encountered in tracheal washings from companion animals. Their pathophysiologic properties and meaning remain to be established.
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PMID:Microlithiasis associated with chronic bronchopneumonia in a cat. 270 8

The chemistry, pharmacology, pharmacokinetics, clinical use, adverse effects, and dosage of lisinopril are reviewed. Lisinopril, a new nonsulfhydryl angiotensin-converting-enzyme (ACE) inhibitor, is absorbed in its active form. Like the other ACE inhibitors, it lowers peripheral vascular resistance, with a resultant decrease in blood pressure. Approximately 29% of lisinopril is absorbed after oral administration. No measurable metabolism occurs, and excretion is primarily renal. Accumulation of lisinopril occurs in patients with renal dysfunction; however, dosage adjustment is necessary only when the creatinine clearance is less than 30 mL/min. Lisinopril has been shown to be an effective antihypertensive agent at doses of 10 to 80 mg given once daily in patients with essential and secondary hypertension caused by renal artery stenosis. The effectiveness of lisinopril is comparable to that with diuretics, beta blockers, and calcium-channel antagonists. In patients who are unresponsive to maximal doses of lisinopril alone, addition of another antihypertensive agent may be beneficial. Limited information suggests that lisinopril may be comparable to captopril for the treatment of congestive heart failure. Adverse effects associated with lisinopril are relatively minor and are comparable to those associated with enalapril. Hematological abnormalities have not been reported with lisinopril. Class-related adverse effects include cough, azotemia, angioedema, hypotension, and hyperkalemia. Lisinopril appears to be comparable to other ACE inhibitors for the treatment of hypertension and may be as effective as its predecessors for the treatment of congestive heart failure. Further study is needed to better define a therapeutic niche for lisinopril.
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PMID:Lisinopril: a nonsulfhydryl angiotensin-converting enzyme inhibitor. 285 60

Since their introduction in clinical practice in 1980, ACE inhibitors have been found useful in the treatment of hypertension and CHF. In hypertension, they are effective as monotherapy in 40% to 50% of the patients, and in combination with diuretics or calcium antagonists, they are effective in up to 85% of the patients. They are well tolerated, are not associated with depression, impotence, bronchospasm or metabolic derangements such as hypokalemia, hyperuricemia or hyperglycemia, and do not have adverse effects on the quality of life. As a result, they are preferred in hypertensive patients with CHF, left ventricular dysfunction, mental depression, older age, coronary artery disease, metabolic disorders, chronic destructive pulmonary disease, and peripheral vascular disease. In CHF they cause long-lasting hemodynamic and symptomatic improvement, improve exercise tolerance, and may lower mortality in certain patient subsets. Evolving new indications for ACE inhibitors include the diagnosis of renovascular hypertension, the prediction of surgical success, the treatment of scleroderma renal crisis, the reduction of proteinuria, renal protection, cardioprotection, the improvement of arterial compliance, in Bartter's syndrome and idiopathic edema, etc. ACE inhibitors are usually well tolerated but in some instances they may cause class-specific side effects such as hypotension; usually reversible azotemia or renal failure, especially in patients with renal artery stenosis or with CHF with low blood pressure; cough; angioedema; and hyperkalemia. Differences among ACE inhibitors are emerging and include chemical class (e.g., zinc ligand), biotransformation, potency, pharmacokinetics, prodrugs, tissue effects, additional pharmacologic properties, and drug interactions.
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PMID:Angiotensin converting enzyme inhibitors. II. Clinical use. 305 46


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