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)

Case 1, a 60-year-old man and case 2, a 70-year-old man had several year history of chronic renal failure with hypertension and hyperlipidemia due to diabetes mellitus. Treatment of hyperlipidemia was started by oral bezafibrate intake 1,200 mg per day in case 1 and 400 mg per day in case 2 respectively. Three to fourteen days later, both patients noticed symmetrical muscle pain and weakness. Then the symptoms worsened and they were hospitalized. At the time of admission, both patients revealed weakness in the proximal muscles of their upper and lower limbs and the serum creatine kinase and myoglobin levels were remarkably elevated. Myoglobinuria was also noted. Routine light microscopic examination of biopsied quadriceps femoris muscles of two patients showed scattered necrotic muscle fibers, some of which were under phagocytosis. The symptoms of the patients were immediately resolved after the drug was discontinued. Serum concentration of bezafibrate was remarkably elevated during treatment. Thus the diagnosis was established as having bezafibrate induced myopathy and, as far as we know, this is the first report of bezafibrate induced myopathy in Japan. On the basis of the above description, bezafibrate may induce muscle damage if dose is excess over the renal capacity. Extreme caution is warranted when the patient is placed on bezafibrate and has renal dysfunction. Strict dose adjustment is necessary in taking account of renal function to avoid muscle damage including rhabdomyolysis.
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PMID:[Bezafibrate myopathy in two patients with chronic renal failure]. 129 Nov 64

Chronic (12 weeks) peroral administration of cadmium chloride to albino rats in a dose of 2.5 mg/100 g body weight results in arterial hypertension characterized by the increase in systolic blood pressure up to 148 +/- 1.8 mm Hg (vs. 115.4 +/- 1.5 mm Hg in the control animals); the increase in vascular resistance, left ventricular cardiomyocyte hypertrophy, as well as by hypertrophy of arterial walls, the decrease in the ventricular index, the activation of synthesizing function of atrial endocrine cardiomyocytes; enhanced secretion of ANP; a more than two-fold increase in plasma myoglobin concentration, as well as by the development of cadmium-induced nephropathy. In the rehabilitation period (9 weeks) a relatively quick fall in the blood pressure is observed, as well as morphological features of myocardial and renal function recovery, suggesting the nonpersistent nature of cadmium-induced hypertension.
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PMID:[Morphofunctional characteristics of cadmium-induced arterial hypertension]. 189 57

Malignant hyperthermia (MH) is a pharmacogenetic disease in man and animals. It primarily involves skeletal muscle tissue, but other tissues might be affected to a lesser degree. Calcium homeostasis in muscle cells is upset in susceptible individuals, so that various agents and circumstances can increase the free, ionised intracellular calcium concentration to damaging levels. The primary defect is not known at present, but is believed to involve an abnormally sensitive calcium-induced calcium release mechanism. Thus small, localised increases in calcium concentration releases more calcium so that a vicious cycle is triggered. The increased calcium concentration causes multiple effects in the muscles by stimulating contraction and a hypermetabolic state, clinically observed as rigidity and fever. If demands on the homeostatic mechanisms to lower the calcium concentration become exhausted, and metabolism is insufficient to supply enough phosphocreatine and ATP, membrane potentials cannot be maintained, and permeability of the cell membranes increase. This causes loss of phosphate and H+ as well as K+ and Mg++, and later myoglobin and creatine kinase. Thereby oxidative metabolism is further impeded with formation of lactate as a result. The ensuing acidosis stimulates sympathetic innervation, resulting in tachycardia, high blood pressure, and vasoconstriction. Hyperkalemia causes arrhythmia. Dantrolene inhibits the release of calcium and can halt the process if given before depletion of the energy rich phosphates is too advanced.
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PMID:Pathophysiology of malignant hyperthermia. 269 55

A 78-year-old man was hospitalized because of muscular weakness and acute renal failure. He had been taking glycyrrhizin (280 mg/day) for the last 7 years. Hypertension was noted in his history. Serum potassium was 1.9 mEq/l with metabolic alkalosis. There was hyporeninemic hypoaldosteronism. Serum enzymes, including GOT, LDH and CPK were markedly elevated. In addition, serum myoglobin was as high as 46 micrograms/ml with massive myoglobinuria. Oliguria occurred and blood urea nitrogen and serum creatinine rapidly elevated from 20.9 to 87 mg/dl and from 1.3 to 6.7 mg/dl, respectively. Profound calcium deposition was found in the damaged skeletal muscles, including the quadriceps femoris, axillar, neck, and cardiac muscles. These results indicate that licorice-induced pseudoaldosteronism produces hypokalemic rhabdomyolysis, resulting in acute renal failure and profound deposition of calcium into the damaged skeletal and cardiac muscles.
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PMID:An autopsy case of licorice-induced hypokalemic rhabdomyolysis associated with acute renal failure: special reference to profound calcium deposition in skeletal and cardiac muscle. 785 65

Hypertension produces myocyte hypertrophy and increases the extracellular matrix. In order to determine the composition of the extracellular matrix we studied the hearts from 14 hypertensive patients by immunohistochemistry using antibodies against collagen I, III, IV and V, fibronectin, myoglobin, muscular specific actin, Factor VIII, CD 34 and vimentin. The myocardium showed a focal increase in fibronectin, collagen I and III and diffuse deposition of laminin, collagen IV and V. Cells positive for vimentin, Factor VIII and CD 34 were also increased, but with considerable variation from case to case. We found no relation between matrix variation and the degree of hypertension or the time elapsed from the beginning of the disease. We conclude that the main role of the matrix in hypertension may be remodelling of the heart so that it entraps muscle fibres and increases their contractility.
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PMID:Alterations in the extracellular matrix of the myocardium in essential hypertension. 828 55

Ten cases of acute renal failure (ARF) were seen in the period from July 1990 to August 1991 in the Nephrology Department of the SIMS Hospital, Srinagar. All were males in the age group of 18-28 years and in apparent good health when apprehended by the police. There was alleged history of physical torture of different types. All had been beaten on the buttocks, back and limbs; in addition, 2 cases had been given repeated electric shocks and 1 case put to 'sit-and-stand' exercise for about 3 h. The interval between the first day of torture till they came to our observation varied from 4 to 11 days. The main clinical features at the time of presentation were generalized aches and weakness (10), oligoanuria (9), vomiting (8), hypertension (6), acidosis (10), facial puffiness and pedal edema (6), fever and shivering (3), pulmonary edema (2), stupor (4), and hyperkalemia (5). All the cases had an established ARF (serum creatinine 668-1,997 mumol/l and serum urea 21.8-71.8 mmol/l) when first seen. Muscle enzymes, creatine phosphokinase, lactic dehydrogenase and serum glutamic oxaloacetic transaminase were all significantly raised indicating rhabdomyolysis. All showed evidence of myoglobin casts in urine. Nine had oliguric and 1 had nonoliguric ARF. All except the 1 case with nonoliguric ARF were managed with peritoneal dialysis and/or hemodialysis. All recovered. Early recognition of ARF is important since the main attention in such cases is directed towards the surgical aspect.
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PMID:Acute renal failure following physical torture. 845 79

Molecular evidence, using DNA fingerprint analyses, of extensive genetic heterogeneity between spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) and even within some of the WKY colonies has been reported. Thus we investigated the genetic relations between Dahl S and R rats newly inbred by Dr. Iwai. Genomic DNA was isolated from the liver of four Dahl S and four Dahl R rats, digested with the restriction enzyme HinfI or AluI, and separated in 1.2% agarose gel by electrophoresis. Then, DNA fingerprinting was performed by Southern blot analysis using the human myoglobin 33.6 minisatellite probe. Bands were detected in an alkaline phosphatase reaction system. Within the same strains, there was no heterogeneity of these fingerprinting patterns. The S and R rats shared 82% of the bands in the HinfI-digested DNA and 93% of those in the AluI-digested DNA. These shared values were much greater than the reported value (54%) between SHR and WKY from Charles River Laboratories. These newly inbred Dahl S and R rats may be appropriate, although still limited, experimental animals for investigating the pathophysiology of salt-sensitive hypertension.
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PMID:Analysis of molecular heterogeneity of Dahl/Iwai salt-sensitive rats and salt-resistant rats. 916 Jul 90

A 73-year-old man presented with pain in lower limbs, lower abdomen, and anterior chest. His past medical history includes inferior myocardial infarction 3 years ago and hypertension. Electrocardiogram revealed ST elevation in II, III, and aVF indicating inferior myocardial reinfarction and angiography showed abdominal aortic embolism. Axillobifemoral bypass was performed urgently under general anesthesia. Because the patient developed acute renal failure and furosemide did not show diuretic effect, hemodialysis was used. The patient needed circulatory support with dopamine, dobutamine, epinephrine, and lidocaine intraoperatively. Approximately 90 minutes after the start of the operation, the patient developed ventricular fibrillation. The cardiac rhythm returned to normal after 2 minutes of cardiopulmonary resuscitation. The operation was performed successfully. An increase in serum potassium and metabolic acidosis were not noted postoperatively. However, weaning from the catecolamines was very difficult, and the patient died on 29th postoperative day. In this case, we employed general anesthesia without epidural anesthesia, because intraoperative hypotension might be the major cause for perioperative cardiac complications. Increase in serum potassium and myoglobin and metabolic acidosis were reported to occur after revascularization. Because the patient developed acute renal failure, intraoperative hemodialysis was valuable for preventing adverse effects due to reperfusion.
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PMID:[Perioperative management for acute abdominal aortic obstruction in a patient with acute myocardial reinfarction associated with acute renal failure]. 931 Dec 11

We evaluated whether recent cocaine use alters the specificity of CK-MB, myoglobin, and cardiac troponin I for acute myocardial infarction (AMI) in patients who are seen in the emergency department for chest pain. Patients <60 years old with potential myocardial ischemia underwent a standardized history and physical examination and routine CK-MB assays every 8 to 12 hours and had study serum obtained at presentation for CK-MB, myoglobin, and cardiac troponin I immunoassays, as well as benzoylecgonine, cocaine's main metabolite. We enrolled 97 patients, 19 (20%) of whom had recent used cocaine. Patients with and without cocaine use were similar with regards to sex, race, renal and muscular disease, diabetes, family history, and hypertension and rate of AMI (12% vs 11%, p = 1.0). In patients without MI, the mean myoglobin level was higher in cocaine users than noncocaine users (179 vs 74 ng/ml; Mann-Whitney p = 0.003), but the mean values were similar for CK-MB (2.2 vs 2.1 ng/ml; Mann-Whitney p = 0.58) and for cardiac troponin-I (0.02 vs 0.02 ng/ml; Mann-Whitney p = 0.87). The specificities of the markers in patients with and without cocaine use were as follows: cardiac troponin I, 94% vs 94%, (p = 1.0); CK-MB, 75% vs 88% (p = 0.24); and myoglobin, 50% vs 82%, (p = 0.02), respectively. Our data demonstrate that the specificity of myoglobin was altered by recent cocaine use. The specificity of CK-MB was affected less and the specificity of cardiac troponin I was not affected by recent cocaine use.
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PMID:Effect of recent cocaine use on the specificity of cardiac markers for diagnosis of acute myocardial infarction. 948 72

Experimental hibernating-model investigations of animals have shown that myocardial necrosis can be induced by longer-term intracoronary dobutamine infusion. This study was designed to determine whether myocardial infarction could be ascertained in patients with chronic regional wall motion abnormalities and greater than 75% stenosis in the supplying coronary artery through dobutamine stress echocardiography. Twenty patients with coronary artery disease and regional resting wall motion abnormalities were examined with a standard dobutamine protocol (5 to 50 microg/kg/min). Exclusion criteria were an acute coronary syndrome, severe heart failure, and severe hypertension. Creatine kinase (CK, CKMB), myoglobin, and troponine-I were measured before and at each of the first 7 hours after beginning of infusion. Fourteen of these 20 patients exhibited viable myocardium. The serum markers CK, CKMB, myoglobin, and troponin-I demonstrated no increase beyond the reference range, suggesting that with this protocol, no myocardial necrosis was induced.
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PMID:Does dobutamine stress echocardiography induce damage during viability diagnosis of patients with chronic regional dysfunction after myocardial infarction? 951 57


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