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 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An eighty-four-year-old man was admitted to the hospital because of pain at rest in the lower extremities. On physical examination, trophic changes of the skin and petechiae in the limbs were observed. Computed tomographic scan of the abdomen showed focal renal infarctions and calcification of the descending aorta. Moreover, radionuclide imaging of the arterial system revealed complete obstructions of the two right iliac arteries and the left external iliac artery, where collateral flows were observed. Laboratory examination showed a severe thrombocytopenia caused by immunoglobulin G (IgG)-type autoantibody against platelets. He was diagnosed as having arteriosclerosis obliterans complicated by idiopathic thrombocytopenic purpura, although no known risk factors promoting atherosclerosis other than age were evident. In such a case with hemorrhagic diathesis, a hemorheologic agent and the vasodilator prostaglandin could confer advantages in relieving and controlling the ischemic leg pain without hemorrhagic complications. Moreover, small doses of the initial prednisolone therapy for ITP might also be recommended to avoid thrombus formations in the atherosclerotic lesions.
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PMID:A rare case of arteriosclerosis obliterans without prominent risk factors complicated by idiopathic thrombocytopenic purpura. A case report. 861 16

Arteriosclerosis obliterance (ASO) is defined as the ischemic status of lower extremity produced by a stenotic and/or occlusive lesion of lumens of major arterial stress based on the pathology of atherosclerotic change. The sign and symptom of ASO are usually thought to be progressed slowly by natural progression process of atherosclerosis, however, in certain occasion, the progression of clinicopathological status of leg ischemia is acute as well as grave, so as to manifest rest pain or necrosis of the lower extremity. The basic mechanism of acute exacerbation of lower leg ischemia is attributed to the acute extended thrombus formation in arterial lumen. The factors influencing to the thrombus formation are represented as Virchow's Trias such as the changes in arterial wall, the stasis of blood flow and the coagulability of blood. One of the characteristic feature associated with massive and extended ischemia of lower leg is myonephropathic metabolic syndrome proposed by Haimovich in 1960. This syndrome is particularly seen immediately following the restoration of blood flow to the severely damaged leg and characterized by renal as well as systemic organs disorder. The relationship between the extent of muscle damage and the duration of ischemia is analysed through our data.
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PMID:[The clinico-pathological aspects of acute exacerbation of arteriosclerosis obliterance]. 880 10

The diagnosis of arteriosclerosis obliterans of the lower extremities can be made by the history alone or by the physical examination alone in the most patients. It is very important to evaluate the hemodynamic study in determination of indication for operation and operative procedures. The two major symptoms, each of which diagnostic, are intermittent claudication and ischemic rest pain. Intermittent claudication is pain or fatigue that occurs in a muscle or muscle group on repititive use. The anatomical level of claudication is significant. When aorto-iliac artery is obstructed, pain may occur first in the hip or thighs. Pain occurs in the calf in the occlusion of the femoral artery and foot pain indicates the occlusion of distal popliteal artery. Ischemic rest pain indicates an advanced stage of the disease. Fontaine classification is usually used as the stage of ischemia on the extremity. There are many laboratory evaluations of circulatory insufficiency in the diagnosis of arteriosclerotic obliterans. Measurement of segmental blood pressure is most valuable and useful among various measurements. We can get critical informations of circulatory insufficiency in the leg using segmental blood pressure. In order to differentiate from arteriosclerotic obliterans there are thromboanyitis obliterans aortitis syndrome, popliteal arterial entrapment syndrome, spinal canal stenosis, and diabetic arterial occlusive disease.
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PMID:[Clinical diagnosis of arteriosclerosis obliterans]. 880 11

In the last decade, the indications, risks and limitations of arteriography were dramatically changed because of the improvement of contrast agents and the advent of digital subtraction angiography (DSA). The most widely used contrast agents, at present, are nonionic monomers which have low osmolality and consequently cause less sensation of heat, vasodilatation and pain of injection. These alleviate the pain of angiography for patient and the serious complications were markedly decreased, however, the adverse effects of contrast mediums still remains, particularly the late onsets of adverse effects. The advent of DSA made it possible to perform arteriography in the outpatient department since the catheter size became thin and consequently less invasion for patients. Because the diagnostic procedure was specialized and individualized, the arteriography of lower extremities is often performed by radiologists. The arteriography for patients having arteriosclerosis obliterans (ASO) requires the precise understandings of pathophysiology and vascular anatomy. Therefore, the vascular surgeons and radiologists have to discuss before examinations, which could provide correct anatomical information and minimize the invasion.
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PMID:[Angiography of extremities]. 880 14

Despite intensive efforts to cure breast cancer, treatment generally fails, as evidenced by the age-adjusted mortality rate for breast cancer. For 60 years, breast cancer mortality remained virtually constant. As treatment failed to improve the life prospect of the average patient, it is based on false premises, e.g. Halsted's hypothesis, according to which the tumor is the only threat to the patient. Yet there is more to cancer than just the tumor. Two hallmarks of cancer, cachexia, and paraneoplasia, are usually ignored, since it is assumed that they are caused by the tumor. But what if it is the other way round, and cancer is first of all a cachexia accompanied by a tumor? At least this could explain why, in most cancers, treatment fails. Cancer is a chronic systemic disease with local manifestations like arteriosclerosis, which is also systemic and manifested solely by its local manifestations, e.g. stroke and myocardial infarction. In the same way as treatment of an ailing heart does not cure the underlying arteriosclerosis, tumor removal does not cure cancer, as it is 'metabolically' systemic. It is proposed here that carcinogens deplete a vital substance and induce a metabolic deficiency that ends in cachexia. In order to survive, the organism grows a protective organ-the tumor-that replenishes the missing substance. During the preclinical phase of cancer, deficiency is slight and compensated only by a minute tumor. With time, it gets worse and the tumor has to grow more and more in order to make up for the loss, causing pain and secondary damage to vital functions. The patient seeks help and the disease starts its clinical course. When deficiency worsens, the patient becomes cachectic and dies. Such a metabolic relationship exists in pernicious anemia, which illustrates how a tumor might be protective. Cancer is viewed here as pernicious cachexia induced by the loss of a vital metabolite and compensated by the tumor. Until the discovery of the missing substance, treatment ought to preserve the tumor and alleviate its secondary manifestations.
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PMID:A new cancer hypothesis. 886 26

A population based study was carried out over a 25-year period (1972-1997) to disclose the clinical and pathological features of aortic dissection based on the analysis of 79 (71 acute and 8 chronic) consecutive cases of disease observed in an defined population of 106,000 inhabitants. Of the 79 patients 65 (82.3%) were admitted to hospital and 14 (17.7%) died out of hospital. Their ages ranged from 36 to 97 years (mean, 65.4 yrs), 49 (62.0%) were men and 30 (38.0%) were women with means 61.2 and 69.1 years, respectively. The male/female ration was 1.6:1. All but two operated patients died. The pain was the leading symptom. Every patients had some kind of cardiovascular and respiratory signs. Neurologic symptoms occurred in 27/65 (41.5%) patients. In five patients the clinical picture of abdominal catastrophe and in two patients renal failure occurred. The major vessels were affected in 32/75 (42.7%) autopsies. Aortic rupture were seen in 64/79 (81.0%) cases. Five spontaneous healings were observed. The hypertension, the advantaged age and the arteriosclerosis are regarded as the mean predisposing factors.
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PMID:[Clinicopathology of aortic dissection]. 971 88

Neurological sequelae reported after epidural anesthesia include epidural hematoma, spinal cord ischemic injury and lumbosacral nerve root injury. We describe here a case of monoplegia of the right lower limb associated with an ipsilateral loss of perception of pain and temperature following an epidural anesthesia. MRI was compatible with a right centrolateral infarction in the gray matter of the spinal cord below D8. Hypotension, vascular spasm, trauma, arteriosclerosis, pressure increase in the epidural space are potential causative mechanisms. Unilateral symptoms might result from injury to a sulcocommissural artery or an anterior spinal artery when duplicated.
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PMID:[Lower limb monoplegia and dissociated hypoesthesia after peridural anesthesia]. 1048 52

This article confirms the existence of two variants of acute aortic pathology, the penetrating atherosclerotic ulcer (PAU) and the intramural hematoma (IMH), which are radiologically distinct from classic aortic dissection. Table 4 reviews the characteristics distinguishing PAU from classic aortic dissection and IMH. We took as a matter of definition that classic aortic dissection involves a flap which traverses the aortic lumen. We defined PAU and IMH as nonflap lesions, with PAU demonstrating a crater extending from the aortic lumen into the space surrounding the aortic lumen. This categorization can be summarized with the expression, "no flap, no dissection." With these definitions made, re-review of the imaging studies for the present report identified 36 such lesions out of 214 cases originally read as aortic dissection. Therefore, these variant lesions accounted for over 1 out of 8 acute aortic pathologies. Besides confirming the existence of the conditions, PAU and IMH, as distinct radiographic lesions, this series strongly suggests that these two conditions constitute distinct clinical entities as well. Table 4 summarizes the clinical patterns of these two entities as apparent from the present study, and contrasts them with classic aortic dissections. In particular, the following observations, some of which are consonant findings in smaller series, can be made regarding the typical patient profiles of PAU and IMH from the present study: The patients with PAU and IMH are distinctly older than those with type A aortic dissection (74.0 and 73.9 versus 56.5 years, P = 0.0001). Although not statistically significant, PAU and IMH patients tend to be older than patients with type B aortic dissections as well. For PAU and IMH, unlike aortic dissection, the concentration in the elderly is manifested in a very small standard deviation of the mean age (see Fig. 13); these two entities, PAU and IMH, are essentially diseases of the seventh, eighth, and ninth decades of life. Patients with PAU and IMH are almost invariably hypertensive (about 94% of cases). The pain of PAU and IMH mimics that of classic aortic dissection, with anterior symptoms in the ascending aortic lesions and intrascapular or back pain with descending aortic lesions. Unlike classic dissection, PAU and IMH do not produce branch vessel compromise or occlusion and do not result in ischemic manifestations in the extremities or visceral organs. PAU and IMH are more focal lesions than classic aortic dissection, which frequently propagates for much or the entire extent of the thoracoabdominal aorta. PAU is uniformly associated with severe aortic arteriosclerosis and calcification, whereas classic dissection often occurs in aortas with minimal arteriosclerosis and calcification. PAU and IMH tend to occur in even larger aortas than classic aortic dissection (6.2 and 5.5 versus 5.2 cm, P = 0.01). PAU and IMH are strongly associated with AAA, which is seen concomitantly in 42.1% of PAU patients and 29.4% of IMH patients. PAU and IMH are largely diseases of the descending aorta (90% for PAU and 71% for IMH). Although our pathology data is limited, we do feel that an inherent difference in the histologic intramural level of the hematoma may underlie the pathophysiologic process that determines which patient develops a typical dissection and which develops an intramural hematoma. In particular, we feel that the level of blood collection is more superficial, closer to the adventitia, in IMH than in typical aortic dissection. This may explain why the inner layer does not prolapse into the aorta on imaging studies or when the aorta is opened in the operating room. This more superficial location would also explain the high rupture rates as compared to classic aortic dissection (Fig. 14, Table 3). We did find PAU and IMH to behave much more malignantly than typical descending aortic dissection. As seen in Figure 6, the rupture rate is much higher than for aortic dissection. Docume
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PMID:Pathologic variants of thoracic aortic dissections. Penetrating atherosclerotic ulcers and intramural hematomas. 1058 37

Despite intensive effort to cure breast cancer, treatment generally fails, as evidenced by the age adjusted mortality from breast cancer. For 60 years, breast cancer mortality remained virtually constant. As treatment failed to improve the life prospect of the average patient, it is based on false premises, e.g., Halsted's hypothesis, according to which the tumor is the only threat to the patient. Yet there is more to cancer than just the tumor. Two hallmarks of cancer, cachexia, and paraneoplasia, are usually ignored, since it is assumed that they are caused by the tumor. But, what if it is the other way around, and cancer is first of all a cachexia accompanied by a tumor? At least this could explain why in most cancers treatment fails. Cancer is a chronic systemic disease with local manifestations. Like arteriosclerosis, that is also systemic and manifested solely by its local manifestations, e.g., stroke and myocardial infarction. In the same way as treatment of an ailing heart does not cure the underlying arteriosclerosis, tumor removal does not cure cancer, since being "metabolically" systemic. It is proposed here that carcinogens deplete a vital substance and induce a metabolic deficiency that ends in cachexia. In order to survive, the organism grows a protective organ, the tumor, that replenishes the missing substance. During pre-clinical phase of cancer, deficiency is slight and compensated even by a minute tumor. With time it gets worse and the tumor has to grow more and more in order to make up for the loss, causing pain and secondary damage to vital functions. The patient seeks help and the disease starts its clinical course. When deficiency worsens, the patient becomes cachectic and dies. Such a metabolic relationship exists in pernicious anemia, that illustrates how a tumor might be protective. Cancer is viewed here as pernicious cachexia induced by the loss of a vital metabolite and compensated by the tumor. Until the discovery of the missing substance, treatment ought to preserve the tumor and alleviate its secondary manifestations.
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PMID:Pernicious cachexia: a different view of cancer. 1069 3

Retroperitoneal fibrosis is a rare disease characterized by the formation of dense plaque of fibrous tissue covering the retroperitoneal structures. This disease is commonly presented as ureteral obstruction, but the involvement of duodenum is rare. We report a case of retroperitoneal fibrosis which was complicated with duodenal stenosis and was successfully treated with corticosteroids. A 58-yr-old man, who had history of aorto-iliac bypass graft due to arteriosclerosis obliterans with infrarenal aortic occlusion was admitted to the hospital with abdominal pain and a mass. Abdominal CT scan revealed the periaortic soft tissue mass encircling grafted aorta and stenosis of duodenal third portion. Retroperitoneal fibrosis with duodenal stenosis was diagnosed and prednisolone therapy was initiated. Follow-up CT scan showed that the patient responded to prednisolone therapy with eased pain, shrinking periaortic mass, and reduced duodenal stenosis.
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PMID:Retroperitoneal fibrosis with duodenal stenosis. 1141 Jul 4


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