Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Labetalol has been successful in treating hypertension, and few side effects have been reported, although there have been cases of muscle pain during treatment. A patient with essential hypertension treated with labetalol 600 mg daily complained of muscle pains, particularly in the legs. No neurological abnormality was found, but the activity of muscle enzymes in the blood was high. Findings on electromyography were compatible with myositis and electron microscopical findings suggested toxic myopathy. Labetalol was stopped for 10 days, and the muscle pain disappeared and enzyme activity returned to normal. When labetalol was restarted the pain returned and enzyme activities rose. Myopathy should be considered in patients experiencing muscle pain after treatment with labetalol.
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PMID:Labetalol-induced toxic myopathy. 678 36

Reference is made to the picture observed in two patients with flaccid tetraparesis, severe hypopotassaemia, and myoglobinuric muscle necrosis (hypokalaemic myopathy). Recent onset of hypertension was a feature of both cases. Initially, however, no reason could be assigned for this, nor for the massive loss of potassium. Numerous investigations in the first case (and relatively quick verification in the second) incriminated a steroid, 9-alpha-fluoroprednisolone acetate, in a nasal spray. This has often been reported as the cause of an iatrogenic syndrome due to excess of mineral corticoids, with hypertension, hypokalaemia and alkalosis, suppression of plasma renin activity, and reduction of blood and urinary aldosterone, all of which were observed in these two patients. Withdrawal of the drug and treatment with potassium chloride led to relatively rapid normalisation of the serum electrolytes. Recovery of muscle strength took place after about 20 days, almost at the same time as the normalisation of muscle enzymes. Hypertension, on the other hand, regressed slowly. The nexus between chronic use of the spray and the occurrence of hypokalaemic muscle necrosis is examined in detail. Stress is laid on the importance of specific investigation of the prior use of intranasal steroids in the differentiation of muscle disturbances due to potassium depletion.
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PMID:[Hypokalemic myopathy caused by fluoroprednisolone in a nasal spray. Observations 2 cases]. 685 55

A retrospective study of 112 cases of lupus erythematosus, 103 acute disseminated lupus erythematosus (ADLE) and 9 chronic discoid lupus (CDL), was conducted to determine the incidence of disorders of conduction (DC), and to study their prognosis and discuss their pathogenicity. The mean age of the group was 38 +/- 16 years, and the mean follow-up period after discovery of the DC was 53 months. Cardiac lesions were present in 49.5 p. cent of the 103 patients with ADLE : pericarditis in 27 p. cent, murmur from lupus endocarditis or cardiomyopathy in 23 p. cent, heart failure in 4.8 p. cent, and hypertension in 17 p. cent. Disorders of conduction were present in 18 (17.5 p. cent) of the 112 patients studied. These included 5 partial right bundle-branch blocks (no complete right bundle-branch block), 2 complete and 3 partial left bundle-branch blocks, 5 complete, 2 first degree, and 1 second degree atrioventricular blocks (AVB). The atrioventricular blocks were usually located in the truncal or fascicular regions, but in 2 cases they were nodal in origin. The 5 complete AVB were associated with ADLE in two cases and CDL in the three other cases. The AVB in the ADLE cases appeared 9 to 20 years after the onset of the lupus, these two patients developing pericardiomyocarditis unaccompanied by disorders of conduction. The three complete AVB occurring during CDL were detected 9 to 18 months after the diagnosis. A fatal outcome was noted in 13 (12.5 p. cent) of the ADLE patients and one of the 9 cases of CDL. Ten-year survival curves showed no difference in prognosis for the groups with or without disorders of conduction, but mortality increased in patients with DC after 10 years. As disorders of conduction were more frequently observed in patients with lupus than in a control population, they can be attributed to either a lupus myocarditis or prolonged administration of synthetic antimalarial agents. Disorders of conduction, and particularly complete AVB are, in fact, observed in patients without pericardiomyocardial lesions, and when they exist usually develop a long time after the onset of the cardiac lesion. All patients had been treated with antimalarials, however, and the onset of the DC was associated with a chloroquine myopathy in some of them. Three of the five complete AVB were observed during the course of CDL in patients without cardiac lesions, this being a supplementary argument for implicating synthetic antimalarials.
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PMID:[Disorders of conduction in lupus erythematosus : frequency and incidence in a group of 112 patients (author's transl)]. 730 72

Amoxapine is a second-generation tricyclic antidepressant structurally related to the neuroleptic loxapine. It was previously marketed as an alternative to traditional tricyclic antidepressants because of alleged shorter onset of action and fewer cardiotoxic effects. However, various adverse reactions, including cardiac dysrhythmias, renal failure, coma, seizures, and neuroleptic malignant syndrome, were reported during therapy or after acute overdose. A 14-year-old boy ingested 1900 mg of amoxapine and developed seizures, hypertension, hyperpyrexia, altered mental status, myoglobinuria, renal failure, and transient magnetic resonance imaging (MRI) changes suggestive of hypertensive encephalopathy and neuroleptic malignant syndrome. Since mitochondrial disorders can cause multisystem failure, including encephalopathy, renal tubular dysfunction, and myopathy, a transient, toxic disorder of mitochondrial function was considered as the basis for the patient's clinical and MRI changes.
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PMID:Amoxapine overdose in a young man: a transient mitochondrial abnormality? 747 9

Sedative and neuromuscular blocking (NMB) drugs are used to facilitate care of head trauma patients requiring mechanical ventilation or therapy of intracranial hypertension. Because no specific regimen is appropriate in all patients, drug selection and utilization exhibit significant regional variation. Sedatives are used to decrease anxiety and diminish awareness of noxious stimuli. Propofol offers particular promise in neurosurgical intensive care. NMB drugs are used in 1% to 10% or more of critically ill patients. Increasingly more information is available to guide the use of NMB drugs for patients suffering head trauma. Broad concerns about these drugs include their use as adjunctive therapy to control intracranial hypertension, the incidence of prolonged weakness or myopathy, the potential for direct neurologic toxicity, and their effect on outcome. Resolution of these issues will improve the use of sedative and NMB drugs in intensive care.
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PMID:Sedative and neuromuscular blocking drug use in critically ill patients with head injuries. 749 55

A case of acute inflammatory myopathy associated with the use of pravastatin, a new hydrophilic 3-hydroxy-3 methylglutaril coenzyme A reductase inhibitor, is reported. The patient, a 69-year-old man was affected by non-insulin-dependent diabetes mellitus and hypertension. He assumed pravastatin (20 mg/day) because of hypercholesterolemia. He was admitted with acute myopathy of the lower limbs which resolved in a few days after pravastatin discontinuation. A previously unknown hypothyroidism, probably due to chronic autoimmune thyroiditis, was evidenced. Muscle biopsy (left gastrocnemius) revealed a perimysial and endomysial inflammatory infiltrate with a prevalence of CD4+ lymphocytes. While lovastatin and simvastatin have been associated with toxic myopathy, pravastatin-associated myopathy could represent a distinct, inflammatory entity.
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PMID:Pravastatin-associated myopathy. Report of a case. 760 76

The authors present the clinical history of a 70-year-old male with arterial hypertension who sought medical advice because of dyspnea on exertion, orthopnea and episodes of paroxysmal nocturnal dyspnea. The electrocardiogram showed left arterial hemiblock and abnormalities of ventricular repolarization compatible with a left lateral endocardiac lesion. Echocardiography revealed a hypertrophied left ventricle with a small ventricular cavity, compatible with an infiltrative-restrictive myopathy. Blood chemistry showed creatinine 4.9 mg/dl, BUN 133 mg/dl and alkaline phosphatase 204 i.v. The patient expired because of intractable heart failure. The histopathological examination of a piece of myocardium (authorized by the family) stained with Congo red confirmed the presence of abundant, diffuse deposits of amyloid, as had been suspected because of the echocardiographic findings.
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PMID:[Cardiac amyloidosis secondary to multiple myeloma detected by echocardiography]. 774 97

Glucocorticoids mainly act through binding to cytosolic receptors that translocate to the nucleus after ligand binding, and dimerize to affect gene transcription in multiple fashions. The liganded receptors may interact with DNA at specific glucocorticoid responsive-elements, may physically hinder the ability of other transcription-regulating proteins to interact with their own DNA response-elements, and may form intranuclear complexes with the transcription factor c-jun, thus changing the number of c-jun/c-fos heterodimers that bind at AP-1 sites. By these, and perhaps other, mechanisms, physiologic concentrations of glucocorticoids regulate normal tissue metabolism, and supraphysiologic concentrations cause Cushing's syndrome. Cushing's syndrome leaves virtually no body tissue untouched. Left untreated, it results in progressive adiposity, myopathy, dermopathy (atrophy, stria, purpura, and hirsutism), psychopathy, glucose intolerance, hypercholesterolemia, hypertension, atherosclerosis, immunosuppression, and, ultimately, death. The physiology underlying each of these effects of hypercortisolism has been reviewed. The differences in the presentation of Cushing's syndrome in children and adults have also been discussed. The goal of the clinician must be to identify individuals with Cushing's syndrome as early in the course of the disease as possible so as to avoid the devastating complications that result from prolonged hypercortisolism. In patients for whom screening tests are equivocal, or only intermittently elevated, it may be necessary to re-evaluate the patient over time to establish that the patient has hypercortisolism. Some clinical guidelines for which patients to screen for hypercortisolism have been presented. Once hypercortisolism is established, patients with mild hypercortisolism (urine free cortisol less than four-fold above the upper limit of normal) should undergo tests to differentiate true Cushing's syndrome from a pseudo-Cushing state.
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PMID:Glucocorticoid action and the clinical features of Cushing's syndrome. 780 50

The short-term clinical efficacies of furosemide, 25 mg/day, and torasemide, 10 mg/day, have been compared in 2 groups of 12 patients with severe heart failure. In each group there were similar numbers of patients in whom heart failure was due to coronary heart disease, high blood pressure, or idiopathic dilated cardiac myopathy. The design of the study was open and the diuretics were added to baseline treatment with digoxin. Treatment for 8 days with the 2 loop diuretics resulted in similar substantial and significant improvements in symptoms and exercise tolerance as judged by the increase in total body oxygen consumption, and reductions in radiographic evidence of pulmonary congestion and in right heart filling pressure as judged from the jugular venous pressure wave. The results of this short-term comparative study confirm that furosemide and torasemide are equally efficacious in inducing substantial improvements in the clinical status of patients in severe heart failure.
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PMID:Symptomatic achievements with diuretics in congestive heart failure. 795 35

Licorice abuse is a wellknown cause of high blood pressure, myopathy, and cardiac rhythm trouble. It should be considered as a cause of diffuse acute edema, as shown in the three following case-reports.
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PMID:[Generalized edema caused by licorice: a new syndrome. Apropos of 3 cases]. 800 77


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