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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The size of a thoracic aortic aneurysm (TAA) is an important factor of the operative indication. We experienced a ruptured TAA the diameter of which was only 4 cm. A 71 years old man was admitted due to the severe back pain under the shocked condition. We diagnosed him a ruptured TAA by CT scan. Because he had no progressive anemia and the hemodynamics was very stable, we followed him conservatively. Two months later, the operation was performed. We resected the aneurysm and inserted an aortic prosthetic graft. From the operative findings, the aneurysm was certified as a true aneurysm, and the maximal diameter was only 4 cm. First choice for the treatment of ruptured TAA is the emergent operation. But when the hemodynamics is extremely stable and the anemia does not progress at all, a conservative therapy can be selected. Even if the aneurysm is very small, the control of hypertension is quite important.
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PMID:[A ruptured thoracic aortic aneurysm with 4 cm diameter]. 148 39

A 71-year-old man was noted to habitually snore loudly at night and have a predisposition to somnolence during the daytime. While dozing during the day, he developed cardiac arrest at the time when snoring stopped, and was resuscitated. By means of a respiration monitor, he was diagnosed as having sleep apnea syndrome (SAS) with a combination of obstructive, central, and mixed type. However, neither respiratory insufficiency nor cardiac insufficiency was observed, and there were no abnormal findings on laboratory tests and bronchoscopy. SAS complicated by cardiac arrest is usually seen in cases with concomitant symptoms such as excessive obesity, hypertension, arrhythmia, right heart insufficiency, secondary polycythemia, or mental disorder. The present case abruptly developed cardiac arrest in the absence of such symptoms. This case therefore suggests the importance of screening tests using a respiration monitor during sleep in subjects who have a loud snore or a predisposition to somnolence during the daytime. Although treatment with UPPP alone had no noticeable effect, UPPP treatment combined with sleeping in the lateral position was effective in the present case. The efficacy rate of UPPP has been reported to be 50 to 60%. The early establishment of a method for precise evaluation of the site of obstruction as well as criteria for appropriate application of UPPP are urgently required.
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PMID:[A resuscitated case of sleep apnea syndrome with cardiac arrest]. 160 64

A 71-year-old man was admitted to the Wake Forest University/Baptist Hospital Medical Center on February 1, 1989, with pharyngitis and a cutaneous eruption that began that day. The past history was significant for a diagnosis of chronic lymphocytic leukemia (CLL) made in 1984, and for longstanding hypertension, severe coronary artery disease, and prostatic hypertrophy. The patient had required no therapy for his CLL until August, 1988, when he developed hemolytic anemia and was treated with oral chlorambucil, 4 mg/day, and a tapering course of prednisone. By December, 1988, the prednisone therapy had been discontinued, but the patient required hospital admission for pneumococcal pneumonia, which responded well to intravenous antibiotic therapy. One day prior to the current admission the patient complained of persistent fevers, sore throat, productive cough, and headache. He noted a new cutaneous eruption on the day of admission in February, 1989. The past history was positive for occasional herpes stomatitis. The patient did not know if he had previously been infected with varicella. Skin examination revealed multiple (greater than 20), single, and grouped vesicles in a generalized distribution involving the bilateral trunk, head, neck, arms, and legs. The heaviest involvement was on the right posterior auricular area and on the neck. A Tzanck preparation obtained from an early lesion was positive for multinucleated giant cells. Viral culture was negative at 24 hours and at 1 week. A skin biopsy of an early vesicular lesion was performed and revealed intraepidermal vesicles with acantholysis and giant cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Granuloma annulare and disseminated herpes zoster. 145 73

Traditional thinking suggests that pleural fluid develops on the basis of systemic venous hypertension or a primary pleural process. Recent investigations, however, indicate that both acute lung injury and pulmonary venous hypertension can be important in the pathogenesis of pleural effusions. To evaluate the role of acute lung injury in the formation of pleural effusions, we developed a model of acute, reversible lung injury in NZW rabbits. Intravenous ethchlorvynol (ECV), known to produce permeability edema in humans, was used to produce permeability pulmonary edema in rabbits. The injury was examined over 14 days with bronchoalveolar lavage, pleural fluid analysis, and morphologic analysis. Ethchlorvynol injection (40 mg/kg) produced a PMN-predominant, exudative alveolitis (2 h), alveolar hemorrhage (6 to 10 h), and pleural effusions by 2 h (peak, 10 h). Pathologic findings included a patchy, subpleural, hemorrhagic PMN inflammatory response, which peaked by 24 h, and an acute PMN vasculitis of small arterioles and capillaries; these changes resolved in 5 to 7 days. No parietal pleural abnormalities were observed. We conclude that ECV induces an acute, reversible parenchymal lung injury resulting in a capillary leak and that fluid moves from the interstitium of the lung into the pleural space along a pressure gradient through a relatively permeable mesothelium. The data support the concept that diffuse or localized lung injury can result in pleural effusions.
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PMID:Pleural effusions associated with ethchlorvynol lung injury result from visceral pleural leak. 278 46

A 71-year-old hypertensive patient experienced a severe hypertensive crisis. His blood pressure was 300/200 mm Hg three days after nifedipine therapy was discontinued. He had been taking nifedipine together with methyldopa. During five months on the combined treatment, his blood pressure had not risen higher than 170/100 mm Hg. A severe hypertensive crisis following abrupt nifedipine withdrawal has not been previously reported, to our knowledge. We recommend that caution be used when abrupt cessation of nifedipine therapy is considered in the treatment of hypertension.
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PMID:Hypertensive crisis associated with nifedipine withdrawal. 394

Tetrodotoxin, a violent neurotoxin, is present in puffer fish and may occur in a variety of marine animals. Outbreaks of human tetrodotoxin poisoning, following consumption of marine organisms other than puffer fish, has been rare. We here report an outbreak of tetrodotoxin poisoning following ingestion of gastropod molluscs and its clinical features are discussed. A 71-year-old woman was admitted with hypertension and other neurological symptoms developing after ingestion of some molluscs. A further 16 cases were also found to have typical symptoms of tetrodotoxication after mollusc consumption. Clinical features in these 17 cases were similar to those conventionally found in tetrodotoxin poisoning, except that there was hypertension in eight cases (47%). All except one case had mild poisoning and recovered well. The molluscs consumed comprised two different species: Nassarius castus and Nassarius conoidalis, both of which were shown to contain various amounts of tetrodotoxin. It is concluded that tetrodotoxin poisoning following mollusc consumption is a possibility. Hypertension, as an unusual feature in tetrodotoxication, is frequent in this outbreak, and should be looked for in future cases. The explanation of hypertension in tetrodotoxication may come either from an exaggerated response to sympathetic stimuli, or due to various responses of the vasomotor centre to a small dose of tetrodotoxin. Further studies are required to answer this question.
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PMID:An outbreak of tetrodotoxin poisoning following gastropod mollusc consumption. 761 8

We reported a case of neuroleptic malignant syndrome (NMS) associated with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). A 71-year-old woman, who had been diagnosed as hypertension and multiple cerebral infarction, was given sulpiride 150 mg daily for depressive state. Three days after started sulpiride, she developed fever, sweating, difficulty of movement and was admitted to the hospital. The white blood cell count rose to 16,300/mm3 and serum creatine kinase (CK) to 3,063 IU/L. Two days later CK rose to 20,050 IU/L regardless of stopping the drug, so she was transferred to our hospital for further investigation. On admission, it was the 6th day from the onset, she was mute and akinetic accompanied by muscle pain and rigidity in extremities. Serum CK was 1,831 IU/L, Na 122 mEq/L, osmolality 244 mOsm/kg, plasma antidiuretic hormone (ADH) level 6.5 pg/ml and urine Na was 101 mEq/L, osmolality 467 mOsm/kg. Renal and adrenal functions, plasma renin activity were normal. From the history, course and these data, diagnosis of NMS associated with SIADH was made. Intravenous sodium (130-200 mEq/day) and fluids (1,000-1,200 ml/day) were carefully infused. She became active, muscle pain disappeared and rigidity, akinesia decreased. CK, serum Na and osmolality gradually improved to normal. About the transient increase in ADH secretion, we considered that hypothalamic disturbance in NMS might induce leakage of stored ADH from neuroendocrine neurons in it.
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PMID:[Neuroleptic malignant syndrome associated with the syndrome of inappropriate secretion of antidiuretic hormone]. 778 Dec 36

The occurrence of familial dissecting aortic aneurysms without Marfan syndrome is rare. This report describes two aged siblings who underwent successful surgery for this disease. Neither patient had the clinical features of Marfan syndrome, and both had histories of systemic hypertension. Case 1: A 76-year-old man had dissecting aortic aneurysm, DeBakey type IIIa, which was localized and had multiple lumina with thrombi. Case 2: A 71-year-old man (younger brother of case 1) had retrograde dissecting aortic aneurysm, DeBakey type IIIa. Histological examinations of the aortae showed cystic medial necrosis in both cases, and also showed atherosclerotic changes in case 1. These two siblings had no familial history of cardiovascular incidents and were much older than previously reported cases. Therefore it may be possible that the dissecting aortic aneurysms of these two cases occurred coincidently rather than due to hereditary factors.
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PMID:[Dissecting aortic aneurysms that occurred in aged brothers without Marfan syndrome]. 783 22

A 71 years old man, ex-smoker, moderate drinker, with a history of diabetes mellitus (type II), moderate arterial hypertension, mild aortic stenosis and moderate uniform left ventricular hypertrophy echographically documented, developed a non Hodgkin low malignancy cavum lymphoma. He has underwent chemotherapy for two years (adriamycin and other chemotherapy drugs) at moderate dosages. A complete remission of the lymphoma followed the treatment, but an initial deterioration of left ventricular function, with heart dilatation and congestive heart failure, was found. The patient improved by medical treatment, returning to the previously stable clinical condition. However a ventricular dilatation reoccurred and a paroxysmal complete atrio-ventricular block developed, necessitating the implantation of a pace maker. The patient died suddenly, during sleep, at home. This is a unique case, because of the numerous cardiac factors associated (chemotherapy and clinical findings). More probably the combination of these multiple factors and their interrelationship could explain the unique non-linear evolution of the left ventricular hypertrophy. In conclusion in these patients a very strict clinical and pharmacological follow up with serial echocardiographical examinations is fundamental and highly recommended.
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PMID:[Normalization of left ventricular function and subsequent recurrence of dilatation and pump failure in a patient with hypertensive heart disease in dilated phase after treatment with anthracycline]. 792 84

Two patients with non-insulin-dependent diabetes mellitus (NIDDM) and moderate chronic renal failure experienced a worsening of glycaemic control when recombinant human erythropoietin (r-HuEPO) was introduced, leading to insulin therapy. A 71-year-old woman with a 20-year history of NIDDM had presented histologically documented diabetic nephropathy for 2 years during which glucose control was stabilized by a diet and glibenclamide 10 mg. In the 6 months following introduction of r-HuEPO, hyperglycaemic symptoms developed, and HbA1C increased from 8.9% to 12.3%. During this period, no intercurrent events occurred, except epistaxis due to accelerated hypertension one month after r-HuEPO was started. A 62-year-old man had a 15-year history of NIDDM, with proliferative retinopathy, macroproteinuria and chronic renal failure for 4 years. The day after the first injection of r-HuEPO, capillary glucose level rose dramatically. In both of these cases, antihypertensive treatment was increased and insulin introduced. The role of r-HuEPO in hyperglycaemia was probable in the first case and highly probable in the second. Reports about the effects of r-HuEPO on glucose metabolism in uraemic patients are conflicting. Short- and long-term effects can differ, although long-term benefit is likely. The fact that our patients were not dialized may have been important. Clinicians should be aware that glucose control may deteriorate with r-HuEPO, requiring some uraemic NIDDM patients to undergo insulin therapy.
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PMID:Erythropoietin can deteriorate glucose control in uraemic non-insulin-dependent diabetic patients. 953 11


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