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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Central retinal artery occlusion occurs most commonly between the ages of 50 and 70 years, and nearly one-half (45%) of patients also have carotid artery disease. Other causes of vision-threatening vascular disease include atherosclerosis, embolism, hypertension, diabetes mellitus, and valvular disease. Symptoms vary, depending on the ocular structures involved. The patient's symptoms are an important clue to the diagnosis of peripheral or posterior retinal vascular occlusion, macular blood vessel disease, intravitreal hemorrhage, optic nerve ischemia, and ocular ischemic syndrome. The patient's ocular symptoms should lead to investigation for clinical signs of ocular vascular disease (eg, hemorrhage, "hard" or "soft" exudates, neovascularization, retinal edema, pallor, emboli, vessel narrowing, or atriovenous crossing changes).
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PMID:Ocular vascular disease: in-office primary care diagnosis. 843 37

The hemolytic-uremic syndrome (HUS) is an acute disorder, characterized by the triad of microangiopathic hemolytic anemia, nephropathy and thrombocytopenia. The great majority of patients are children, usually under 4 years of age, although adults can be affected. The onset is abrupt and usually follows gastroenteritis or upper respiratory infection. Later, clinical manifestations based on the triad, such as pallor, jaundice, edema, hypertension and purpura soon develop. The urinary output is reduced and the urine may appear dark yellow or tea-colored. Laboratory tests of peripheral blood show severe hemolytic anemia associated with fragmented red blood cells and thrombocytopenia, usually below 50,000/microliters. The blood urea nitrogen, serum creatinine and lactate dehydrogenase concentrations are elevated. Proteinuria and microscopic hematuria, which are indicative of active glomerular damage are also seen. Profound understanding of these manifestations is sufficient to permit an early diagnosis of HUS.
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PMID:[Diagnosis and clinical features of hemolytic uremic syndrome]. 843 21

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

Hemolytic uremic syndrome spontaneously arises in a few patients with advanced cancer, but it is more commonly related to the use of certain chemotherapeutic agents. Mitomycin-C is, etiologically, the most common causative agent inducing hemolytic uremic syndrome, in a dose dependent manner. We report this syndrome, attributable to mitomycin-C at a cumulative dose of 40 mg/m2, in a gastric cancer patient. A 42-year-old female with stage III gastric cancer underwent radical gastrectomy and was given mitomycin-C at 10 mg/m2 intravenously every four weeks as adjuvant therapy. Hemolytic uremic syndrome was diagnosed three months after the last dose of mitomycin-C administration. The most prominent symptoms included pallor, hypertension and anasarca, with laboratory evidence of microangiopathic hemolytic anemia, azotemia and hyperkalemia. Her disease was progressive, but fortunately stabilized after staphylococcus column A dialysis. Her disease remained in remission for 24 months from the time of diagnosis, and then relapsed in the form of peritoneal carcinomatosis with partial intestinal obstruction.
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PMID:Mitomycin-C induced hemolytic uremic syndrome: a case report and literature review. 915 2

Pheochromocytomas are tumors that develop from chromaffin tissue of the embryonic sympathoadrenal system. These tumors may occur anywhere chromaffin tissue exists but most often develop in the adrenal medulla. Less than 50% of patients are diagnosed with pheochromocytomas while alive, and most of these tumors are found on autopsy. The classic signs and symptoms of pheochromocytomas are headache, perspiration, palpitations, pallor, and paroxysmal hypertension. Elevated levels of vanillylmandelic acid and metanephrines in patients' 24-hour urine collections are the most reliable diagnostic indicators of pheochromocytomas. Most patients with pheochromocytomas can be cured if diagnoses and surgical resections of tumors occur before irreversible cardiovascular disease and end-organ damage from hypertension develop.
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PMID:Surgical treatment of pheochromocytomas. 918 52

-According to the "epinephrine hypothesis," circulating epinephrine taken up by sympathetic nerves is coreleased with norepinephrine during sympathetic stimulation and binding of coreleased epinephrine to presynaptic beta-adrenoceptors augments exocytotic release of norepinephrine, contributing to high blood pressure. This study examined whether infusion of a physiologically active amount of epinephrine affects subsequent vascular responses and the estimated rate of entry of norepinephrine into regional venous plasma (norepinephrine spillover). Each of 3 experiments included intravenous infusion of 3H-norepinephrine, measurements of forearm vascular resistance, and intra-arterial infusion of epinephrine (3 ng/min per deciliter forearm volume). In experiment 1, subjects underwent lower body negative pressure (LBNP-25 mm Hg) before and after intra-arterial epinephrine; in experiment 2, LBNP and intra-arterial yohimbine before and after intra-arterial epinephrine; and in experiment 3, intravenous nitroprusside before and after intra-arterial epinephrine. In all subjects, intra-arterial epinephrine produced ipsilateral pallor and decreased forearm vascular resistance. Ipsilateral venous epinephrine increased by 10-fold. Epinephrine did not affect forearm vasoconstrictor responses to LBNP or vasodilator responses to intra-arterial yohimbine or intravenous nitroprusside; did not affect venous norepinephrine levels or norepinephrine spillover during LBNP, yohimbine, LBNP during yohimbine, or nitroprusside; and did not increase venous epinephrine levels during any of these manipulations. Loading of forearm sympathetic terminals with epinephrine therefore does not augment subsequent neurogenic vasoconstriction or norepinephrine release in the human forearm in response to sympathetic stimulation. The findings are inconsistent with the epinephrine hypothesis.
Hypertension 1999 Jan
PMID:A test of the "epinephrine hypothesis" in humans. 993 Oct 79

Cerebral microcirculation has a series of complex relationships with arterial hypertension determined, on one hand, by the size and the location of the vessels involved, and on the other hand, by the chronic or acute nature of the hypertension. The small arterial vessels of the cerebral parenchyma react to the effects of chronic hypertension with irreversible structural changes, whose pathologic and radiological correlation is chronic ischemia of the white substance, shown by paleness of the white substance, together with small lacunar infarctions, with a clinical association of dementia, motor disorders and pseudo-bulbar syndrome. With the appearance of an acute rise in arterial pressure, these vessels react with generally reversible changes which lead to an increase in the permeability of the hematoencephalic barrier with formation of cerebral edema and a clinical association generally demonstrating the focal nature of the vascular abnormality (such as in hypertensive encephalopathy with changes in posterior hemispheric predominance) or its unilateral location in cases in which the process occurs in one of the carotid territories (post-endarterectomy).
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PMID:[Hypertensive vascular disease and cerebral microcirculation]. 1037 57

The pathologic features of silent hyperintense white matter lesions in T2-weighted images on MRI were studied in patients with no neurologic signs or symptoms. The small patchy hyperintense white matter lesions represented myelin pallor associated with vessels showing hypertension and arteriosclerotic changes. 'Caps' also showed myelin pallor with dilated perivascular spaces. There were no lacunar infarcts in these lesions. Some of 'caps' was shown to be elongated normal lateral ventricle. 'Rims' of early stage revealed subependymal gliosis that was a part of normal aging processes.
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PMID:Pathologic findings of silent hyperintense white matter lesions on MRI. 1052 52

Our aim was to establish the prevalence of Raynaud's phenomenon in a general practice in the east of Spain and compare our results with those of other studies performed in geographical areas with similar climatic characteristics. Two hundred and seventy-six subjects visiting their general practitioner for whatever reason were randomly selected from a particular area of the city of Valencia. Each was interviewed by their GP following the guidelines of a structured questionnaire to establish whether they had Raynaud's phenomenon or not. There were 205 women and 71 men. The mean age was 54.43, with a standard deviation of 18.22. Raynaud's phenomenon was present in nine subjects, two men and seven women, with a prevalence of 2.8% and 3.4%, respectively. Of the nine positives (mean age 60.56 years, standard deviation 16.38), two were diagnosed with hypertension and two with migraine. None of them usually took Raynaud's phenomenon-related drugs or performed physical exercise. No patient had a family history of Raynaud's phenomenon or had already been diagnosed with it. All the positive males were affected only by the pallor stage. This study shows lower prevalences than those of other studies performed in different geographical areas with similar climatic conditions.
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PMID:Prevalence of Raynaud's phenomenon in general practice in the east of Spain. 1134 37

Most pheochromocytomas can be cured by resection. In view of the unfavourable prognosis for surgical therapy in cases of late tumour detection and malignant tumours, the aim of the present study is to differentiate between typical signs and symptoms of malignant versus benign pheochromocytomas. We investigated the records of 133 patients retrospectively (1967-1998). In cases of benign tumours (104 of 133, mean age 42+/-15.8 years) tumour size was 5.9+/-3.4 cm, and history was 47.4+/-75.4 months. 7.7% of the tumours were extraadrenal, and 77% had paroxysmal manifestations. The other 29 patients (mean age: 39.2+/-21.9 years) had malignant lesions (tumour size: 9.4+/-5.9 cm (p=0.0022); history: 7.4+/-5.6 months (p=0.0137); extraadrenal: 24.1% (p=0.0219); paroxysmal: 37.9% (p=0.0012)). Symptoms of patients with benign tumours were hypertension (80%), headaches (42.3%), sweating (30.8%), tachycardia (26%) and pallor (24%) (Malignant: Hypertension 46%, p=0.0873; headaches 11%, p=0.0008; sweating 11%, p=0.0196; tachycardia 14%, p=0.1961 and pallor 0%, p=0.0010). Abdominal pain and dorsalgia occurred more frequently in malignant pheochromocytomas (26% versus 7%, p=0.0014). Unusually short histories and extraadrenal localization appear to be suspicious for malignancy. The "typical" clinical signs and symptoms occur more frequently in patients with benign tumours and can therefore be regarded as typical signs of benign pheochromocytomas.
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PMID:Clinical differences between benign and malignant pheochromocytomas. 1145 61


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