Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherosclerosis was diagnosed on necropsy in 21 dogs in a 14-year period. Nine dogs died and 12 were euthanatized because of complications associated with the disease. The mean age was 8.5 +/- 0.5 years; 18 dogs were male. Three breeds (Miniature Schnauzer, Doberman Pinscher, and Labrador Retriever) had a higher prevalence of the disease than other breeds in the canine necropsy population of The Animal Medical Center. Most common clinical signs were lethargy, anorexia, weakness, dyspnea, collapse, and vomiting. Hypercholesterolemia, lipidemia, and hypothyroidism were common in affected dogs tested, and protein electrophoresis revealed high values for alpha 2 and beta fractions in all dogs tested. Electrocardiography indicated conduction abnormalities and myocardial infarction in 3 of 7 dogs. Necropsy revealed that affected arteries (including coronary, myocardial, renal, carotid, thyroidal, intestinal, pancreatic, splenic, gastric, prostatic, cerebral, and mesenteric) were yellow-white, thick and nodular, and had narrow lumens. Myocardial fibrosis and infarction also were observed in the myocardium. Histologically, affected arterial walls contained foamy cells or vacuoles, cystic spaces, mineralized material, debris with or without eroded intima, and degenerated muscle cells.
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PMID:Clinical and pathologic findings in dogs with atherosclerosis: 21 cases (1970-1983). 374 84

From 1967 to 1979, 25 patients (pts) were operated on for fibromuscular disease (FMD) of the internal carotid artery (ICA). Eleven patients (44%) had transient weakness of an extremity, 4 had amaurosis fugax and 6 (24%) had an asymptomatic carotid bruit. Bilateral carotid arteriography showed significant stenotic lesions in 23 pts (92%) (bilateral in 10), arterial dissection in 1, and severe associated atherosclerosis with ICA endarterectomy and graduated internal dilatation (GID) (9 bilateral); 2 underwent GID with ICA endarterectomy and patch graft: 1 pt had tube graft replacement of the ICA. There was no operative mortality. One pt had a stroke during operation after tube graft replacement of the ICA. Of the 19 pts followed for 2 to 12 years (mean 7.3 years), 2 had late recurrence of mild symptoms. One pt required GID of the contralateral ICA recurrence of symptoms 4 years postoperatively. Graduated internal dilatation of fibromuscular disease of the internal carotid artery can produce long term relief of symptoms; recurrence is rare.
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PMID:Fibromuscular disease of carotid arteries: long term results of graduated internal dilatation. 723 63

A 50-year-old man was admitted to our hospital, because of weakness in his right leg. On admission, he had generalized hyperreflexia and positive Babinski signs bilaterally. After admission, weakness in his left leg and confusion developed. A cerebrospinal fluid examination revealed increases in cell counts and protein but was negative for malignant cells. Blood chemistry was normal except for elevated LDH. A bone marrow biopsy yielded lymphoma cells. Successive T2-weighted cranial MRI showed a progressively expanding high signal area in the right parieto-occipital lobe. His confusional state improved after chemotherapy; however, two months later another cranial CT showed multiple enhanced mass lesions. The patient died 20 months after the onset of illness. Postmortem examination revealed widespread intravascular aggregates of malignant lymphomatous cells in the cerebrum, lungs and kidney, as well as multiple infarcts without atherosclerosis in the cerebrum. These pathological findings are compatible with those of intravascular malignant lymphomatosis. In addition, extravascularly expanding tumor cells formed multiple nodular lesions in the cerebral hemisphere. An immunohistochemical study showed that the tumor cells were positive for B-cell marker L26. Intracranial lymphomatous mass lesion rarely occurs in cases of intravascular malignant lymphomatosis. In the present case, tumor cells were presumably restricted to intravascular spaces, occluded them and resulted in ischemic lesions in the cerebrum in the early phase, but they expanded extravascularly and developed mass lesions in the terminal stages. In conclusion, intravascular malignant lymphomatosis is considered to be phenotypes of malignant lymphoma. This is the first case of intravascular malignant lymphomatosis associated with intracranial lymphomatous mass lesions in Japan.
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PMID:[An autopsy case of intravascular malignant lymphomatosis with intracranial lymphomatous mass lesions]. 778 Dec 32

A 39-year-old woman with long-standing anorexia nervosa was admitted to our hospital because of extreme weakness and cachexia. During a hyperalimentation therapy, she developed chest pain, revealing the electrocardiogram and cardiac enzymes a myocardial infarction of the inferior wall. We suggest that anorexia nervosa does not 'protect' against coronary atherosclerosis, and that some of the cases of sudden death could be related to myocardial ischemia.
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PMID:Anorexia nervosa and myocardial infarction. 796 Feb 53

Of 2,130 consecutive patients admitted to two hospitals with acute brain infarction, we examined 11 patients (0.52%) with medial medullary infarction. The infarcts documented by MRI were unilateral in 9 patients and bilateral in 2 patients, and located in the anteromedial arterial territory of the upper or middle part of the medulla. Atherosclerosis of the vertebral arteries was the predominant vascular pathology. The vertebral artery was occluded at its terminal portion in 7 patients. Nine patients had hypertension, and 8 of these had additional risk factors. Male gender (10 patients) and smoking habits (7 patients) were more prevalent compared with patients with pontine infarction. One patient had a medial medullary infarction attributed to dissection of the vertebral arteries following blunt head injury. Limb weakness was the major symptom in all patients, and gaze-evoked nystagmus was also frequent (6 patients). Tongue weakness ipsilateral to the infarct, the classic sign of medial medullary syndrome, was evident in only 3 patients. The outcome was usually excellent.
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PMID:Medial medullary infarction: analyses of eleven patients. 890 19

We report a 91-year-old man who had a stroke and died of renal failure. He had been treated for hypertension since 20 years before the onset of the present illness. In addition, he was operated on a gastric cancer 17 years previously. Otherwise he was doing well until May 29, 1991 (when he was 87-year-old) when he had sudden onset of dysarthria and right facial weakness. He was admitted to our hospital. On admission, general physical examination was unremarkable, and neurologic examination revealed a mentally sound man with slight dysarthria, right facial weakness, orolingual dyskinesia, and dysequilibrium in which he showed difficulty in tandem gait; however, no cerebellar ataxia was noted. A cranial CT scan revealed leukoaraiosis with multiple low density areas in the cerebral white matter. His BUN was 37 mg/dl and Cr 2.2 mg/dl. His neurologic symptoms cleared within the next few weeks and he was discharged with ticlopidine 100 mg q.d.. He had been doing well after the discharge except for gradual worsening of his renal function; his BUN was 65 mg/dl and Cr 3.27 mg/dl in April of 1994. On March 10, 1995, he fell down and hit his back; he became unable to walk because of pain, and he was admitted again on March 16, 1995. On admission, his blood pressure was 170/80 mmHg. There was an 1 + pitting pretibial edema; otherwise general physical examination was unremarkable. Neurologic examination revealed an alert and oriented man, however, Hasegawa's dementia scale was 23/30. Higher cerebral functions as well as cranial nerves were intact. He showed some unsteadiness of gait, however, no motor weakness or ataxia was noted. Deep tendon reflexes were diminished, but Chaddock sign was positive bilaterally. Vibration was diminished in the feet, however, pain and touch sensations were intact. Laboratory examination revealed a compression fracture of the twelfth thoracic vertebra. Blood count and chemistries were as follows; Hb 7.6 g/dl, Hct 23.3%, TP 6.0 g/dl, Alb 3.6 g/dl, BUN 87 mg/dl, Cr 4.53 mg/dl, T-Chol 174 mg/dl, HDL-Chol 49 mg/dl, Glu 156 mg/dl, Na 142 mEq/L, K 5.4 mEq/L, Cl 115 mEq/L. A urine specimen contained 1 + protein and 1 + glucose, and the sediments contained hyaline casts. A cranial CT scan was essentially same as that taken four years ago. His hospital course was complicated with pneumonia, congestive heart failure, and progressive renal failure. He was treated with intravenous fluid, chemotherapy, and other supportive measures, however, he expired from respiratory failure on April 30, 1995. He was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had Binswanger's disease in the brain, benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. Opinions were divided regarding the question as to whether or not this patient had Binswanger's disease. Although his cranial CT scan revealed leukoaraiosis, his dementia and gait disturbance was only mild until his fall on March, 1995. Clinical features did not conform to those of Binswanger's disease. Postmortem examination of the right hemisphere revealed wide spread atherosclerosis and arteriolosclerosis. The kidney showed benign nephrosclerosis due to arteriolosclerosis. Sclerotic changes were also seen in the coronary arteries and the left middle cerebral artery with 70% stenosis. Myelin stain showed diffuse myelin pallor of the cerebral white matters with scattered small infarcts. Arterioles in the white matter showed arteriolosclerosis. Small infarcts were also seen in the putamen and in the thalamus. This patient appeared to have had circulatory disturbance of the white matter which is the basic abnormality causing Binswanger's disease. However, white matter changes in this patient were not quite severe enough to make a pathologic diagnosis of Binswanger's disease.
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PMID:[A 91-year-old man with a stroke, hypertension, and renal failure]. 899 Apr 84

The aortic dissection is an expanding intramural hematoma in the aortic wall separating its layers. That is the most common catastrophic condition of the aorta. Its incidence in Hungary about 3.0%/000/year may be appreciated. The mortality rate of the untreated cases exceeds the 90 per cent. The dissection begins by an intimal tear or by a medial hemorrhage, seldom. The progressing hematoma results in a false lumen running parallel with the true aortic lumen. On the basis of the location of the primary intimal tear the dissection may be proximal or distal. The inherited or acquired medial weakness and the hypertension are the main etiologic factors. Some pathological findings refer to predisposing role of the atherosclerosis. The ischemia caused by the dissection may damage any organ. The clinical picture is characterized by the polymorphism and the migration of the clinical signs. The suspicion of the disease may be raised on the basis of the anamnesis and the clinical picture. The diagnosis may be confirmed by the rutin chest roentgenograms and by the angiography, CT, MRI and ultrasonic examinations. The transoesophageal echocardiography is the best diagnostic tool. The treatment is medical and/or surgical. Advances in the surgical treatment brought turn in the very poor prognosis.
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PMID:[Aortic dissection]. 916 92

Several new approaches to the study of platelet activation have been developed. Logically, these should be combined with novel indices of coagulant function (60,61) to select rational targets for antithrombotic drugs. They may also be invaluable in dose-finding, which has been a particular weakness in this area of drug development (62,63). While activation of platelets and the coagulation cascade are virtually simultaneous events, markers of the atherosclerosis are also artificially segregated from those of the complicating thrombotic process. Oxidant stress has been implicated in both platelet activation (64) and atherogenesis (65), yet our ability to study this system has been so constrained that we are unsure of appropriate doses of antioxidant vitamins. Novel approaches to this problem promise the ability to study oxidative modification of proteins (46,66,67), lipids (57) and DNA (45,68) in clinical studies.
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PMID:Markers of platelet activation and oxidant stress in atherothrombotic disease. 919 67

Lumbar spine stenosis most commonly affects the middle-aged and elderly population. Entrapment of the cauda equina roots by hypertrophy of the osseous and soft tissue structures surrounding the lumbar spinal canal is often associated with incapacitating pain in the back and lower extremities, difficulty ambulating, leg paresthesias and weakness and, in severe cases, bowel or bladder disturbances. The characteristic syndrome associated with lumbar stenosis is termed neurogenic intermittent claudication. This condition must be differentiated from true claudication, which is caused by atherosclerosis of the pelvofemoral vessels. Although many conditions may be associated with lumbar canal stenosis, most cases are idiopathic. Imaging of the lumbar spine performed with computed tomography or magnetic resonance imaging often demonstrates narrowing of the lumbar canal with compression of the cauda equina nerve roots by thickened posterior vertebral elements, facet joints, marginal osteophytes or soft tissue structures such as the ligamentum flavum or herniated discs. Treatment for symptomatic lumbar stenosis is usually surgical decompression. Medical treatment alternatives, such as bed rest, pain management and physical therapy, should be reserved for use in debilitated patients or patients whose surgical risk is prohibitive as a result of concomitant medical conditions.
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PMID:Lumbar spine stenosis: a common cause of back and leg pain. 993 Jan 24

A 47-year-old man developed progressive muscular weakness in the left arm. MR images revealed low intensity signal lesions with ring enhancement by Gd-DTPA in right fronto-parietal lobes. At that time cerebral angiography was not performed because he refused. A tuberculin skin test showed strongly positive reaction and then administration of anti-tuberculous drugs was started. His symptom had remained stable for one year, but left facial palsy and dysarthria added about two years later. MR images revealed expansion of the lesions in right parietal lobe, adding cortical high intensity signal lesions with Gd-DTPA enhancement on T1-weighted images. Angiography disclosed tubular stenosis of right internal carotid artery at the portion of cervical to petrous segment and the local stenosis at right renal artery. These lesions were considered to be caused by fibromuscular dysplasia, but not atherosclerosis, because we could not find any atherosclerotic lesions in other arteries including right carotid bifurcation. His manifesting symptoms were ascribed to slowly progressive cerebral ischemia. And peculiar MRI findings in his early stage resembled those of inflammatory granulomatous diseases.
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PMID:[A peculiar MRI findings in a case with slowly progressive cerebral ischemia caused by internal carotid artery stenosis possibly due to fibromuscular dysplasia]. 1065 64


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