Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Olfactory dysfunction has been reported in individuals with diabetes mellitus, but the etiology is unknown. Diabetes is often complicated by serious medical conditions which could be related to the development of decreased olfactory ability. Overall, our 111 subjects with diabetes showed deficiencies in their ability to identify odorants measured with the Odorant Confusion Matrix (mean = 67.8% correct). The presence of macrovascular disease was found to be associated with olfactory dysfunction. Glycemic control as well as the type and duration of diabetes were not related to olfactory ability. Also, there was no distinct association with the presence of neuropathy, retinopathy, nephropathy, hypertension, or impotence. Consistent with previous studies utilizing measures of odorant identification, performance decreased with increased age, females were somewhat superior to males, and smoking had a deleterious effect. Other nondiabetes-related medical conditions and medications had no apparent effect on the olfactory ability of our subjects. These results suggest that the sequelae associated with macrovascular disease, such as perhaps, ischemia, to the olfactory area, impact negatively on olfactory ability.
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PMID:Olfactory dysfunction in diabetes mellitus. 843 58

When a melito-diabetic patient presents trophic infected injury on the limb, it is essential an evaluation of the circulatory conditions for therapeutic procedures orientation. In some circumstances, although arterial pulsation is absent, there is no ischemia of tissues. In these cases, the maintenance treatment, with eventual resection of the necrosed and infected tissues may be adopted. Evolution of 70 diabetic patients with trophic injuries on extremities were submitted to a maintenance treatment. Age of patients varied from 28 to 88 years, with an average of 56.8. The most occurrence was verified in women, with 42 cases. Diabetes non-dependent on insulin (type II) was observed in 64 patients (91.5%), being the remaining 6 patients of type I. Diabetic retinopathy was observed in 14 (20%) of the patients, neuropathy in 22 (31%) and nephropathy in 8 patients (11.4%). All the patients presented arterial pulsation until the popliteal region. They were divided in 2 groups, considering trunk arteries of legs: Group I, pervial legs arteries, composed by 48 patients; Group II, occluded legs arteries, with 22 patients. In what refers to the anatomic local of the injuries, patients were classified in three groups: Group A, formed by 32 patients (45.7%), presenting injuries in one or two toes only, without affecting the metatarsic region; Group B, formed by 16 patients (22.9%), trophic injuries affecting the metatarsic region and Group C, formed by 22 patients (31.4%), injuries affecting the calcaneous region. Injuries in both of the groups were caused by mechanical traumatism. Duration of the injury in the inferior member varied from 7 to 48 days, resulting in a 12 days average.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Maintenance treatment of diabetic patients, associating arterial obstructive tibio-peroneal disease. 857 80

This study involved elderly patients with Meniere's disease with incapacitating vertigo. Several of these patients underwent surgery for relief of symptoms that was tailored to the individual's general health and degree of physical activity. Factors that might affect postoperative rehabilitation and recovery were considered, including vision, vertebrobasilar ischemia, proprioception (such as neuropathy resulting from diabetes), and basal ganglia disease. The postoperative results of this tailored approach have been completely satisfactory.
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PMID:Labyrinthectomy in the elderly. 857 66

Early and accurate diagnosis of infection or neuropathy of the diabetic foot is the key to successful management. Angiopathy leads to ischemia which, in combination with peripheral neuropathy, predisposes to pedal skin ulceration, the precursor of osteomyelitis. Chronic hyperglycemia promotes production of glycosylated end products which accumulate on endothelial proteins, causing ischemia of the vasa nervorum. When combined with axonal degeneration of the sensory nerves, the result is hypertrophic neuroarthropathy. Should the sympathetic nerve fibers also be damaged, the resultant loss of vasoconstrictive impulses leads to hyperemia and atrophic neuroarthropathy. Plain radiography, although less sensitive than radionuclide, magnetic resonance (MR), and computed tomographic examinations, should be the initial procedure for imaging suspected osteomyelitis in the diabetic patient. If the radiographs are normal but the clinical suspicion of osteomyelitis is strong, a three-phase 99mTc-MDP scan or MR imaging is recommended. An equivocal 99mTc-MDP scan should be followed by MR imaging. To exclude osteomyelitis at a site of neuroarthropathy, a 111In white blood cell scan is preferable. To obtain a specimen of bone for bacteriological studies, percutaneous core biopsy is the procedure of choice, with the entrance of the needle well beyond the edge of the subjacent ulcer.
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PMID:Imaging the diabetic foot. 861 54

An abnormal axonal membrane conductance might contribute to human diabetic neuropathy. To test this idea, we have compared the threshold changes produced by long-lasting (100-200 ms) de- and hyperpolarizing currents applied to median motor and sensory axons at the wrist in 63 diabetic patients with those from 50 normal controls and 27 amyotrophic lateral sclerosis (ALS) patients. Averages of the threshold electrotonus plots for motor and sensory axons of diabetic patients showed more subexcitability during, and slower recovery following, the application of hyperpolarizing currents. Such alterations have been previously found in isolated rat nerves after inhibition of axonal inward rectification by means of cesium ions. The abnormalities in diabetics were positively correlated with the age of patients and the presence of neuropathy. Threshold electrotonus seen in diabetes differed strongly from the effects of acute ischemia and were unlike changes recorded in ALS. The data indicate that an abnormal inward rectification of peripheral axons is associated with diabetic neuropathy. A better understanding of the neurobiology of this conductance might provide information about the pathophysiology of this disease.
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PMID:Abnormal axonal inward rectification in diabetic neuropathy. 880 52

Thirty-four patients with end-stage renal disease requiring hemodialysis developed over the course of 7 years (1987-1994) severe ischemia in the extremity carrying the angioaccess secondary to arterial 'steal'. Seven of these patients were treated with access ligation, 4 with banding reducing the flow through the access, and 23 with ligation of the artery distal to the inflow of the arteriovenous fistula and establishing of an arterial bypass from a point 5 cm proximal to the fistula to the distal artery. Of the 7 patients who underwent ligation, 5 had complete resolution of symptoms, 1 had persistent pain, and 1 patient had residual ischemic neuropathy. Of the 4 patients who underwent banding, 3 lost their access due to thrombosis shortly after the banding procedure, and in 1 patient partial resolution of symptoms was achieved. Of the 23 patients who underwent arterial ligation-bypass procedure, all showed immediate signs of improvement. One patient who presented with advanced gangrene eventually required amputation, and 3 patients had some residual symptoms. The cumulative patency of the access with this procedure was 73% at 1 year and 45.5% at 2 years. The patency for the bypass was 95.6% at 1 and 2 years. The arterial ligation-bypass procedure is currently the treatment of choice for patients developing severe ischemia secondary to 'steal' following construction of an arteriovenous fistula for dialysis.
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PMID:Pathogenesis and management of upper-extremity ischemia following angioaccess surgery. 889 30

Significant morbidity and mortality occur during the acute phase of the eosinophilia-myalgia syndrome (EMS), and many patients still have chronic manifestations of the disease. Although the precise etiologic agent or agents within implicated batches of L-tryptophan remain uncertain, histopathologic studies support a role for a cell mediated immune response underlying the pathophysiology of EMS. The cellular immune response seems to lead to a microangiopathy and release of cytokines that can induce eosinophilia and fibrosis. Such responses are most marked within the dermis, subcutis, fascia, and connective tissue in and around muscles, nerves, and other tissues. The pathophysiology of the chronic symptoms is poorly understood but may involve ischemia, neuropathy, and metabolic abnormalities.
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PMID:Pathophysiology of the eosinophilia-myalgia syndrome. 889 79

The aim of this study was to determine the frequency and characteristics of peripheral neuropathy associated to polycythemia vera. A prospective clinical and electrophysiological study was performed of 28 patients with polycythemia vera. Other causes of neuropathy were excluded. Eleven patients experienced paresthesiae, which were usually mild. In 13 (46%) patients, clinical examination revealed features suggesting polyneuropathy. Nerve conduction indexes were abnormal in 20 (71%) patients, suggesting the presence of a predominantly sensory axonal polyneuropathy. In the somatosensory evoked potentials a delay of the P40 wave was seen in 17 patients, while 11 exhibited a delay of the N20 wave. Three of these patients also showed bilateral increases in the I-III, I-V and III-V intervals of brain-stem evoked potentials. In most cases, the delay was moderate and symmetrical. No differences in sex, age, duration of disease, hematocrit values, or platelet counts were found between patients with or without clinical or electrophysiological polyneuropathy. A high percentage of patients with polycythemia vera present clinical or electrophysiological signs of predominantly sensory axonal polyneuropathy which is probably secondary to ischemia, due to increased blood viscosity and platelet dysfunction.
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PMID:Peripheral neuropathy associated with polycythemia vera. 895 Aug 63

Pathologic study of nerve tissue is especially useful for the recognition of interstitial events such as inflammation or vascular alterations that cannot be inferred from clinical or electrophysiologic findings and may provide insight into an underlying mechanism or cause. Considerable variation in the natural history and pathologic alterations among diabetic neuropathies suggests that they are heterogeneous. For diabetic polyneuropathy, two mechanisms need to be considered. The first assumes that hyperglycemia induces metabolic derangements that directly affect Schwann cells (or myelin), nodes of Ranvier, or axons. The second assumes that hyperglycemia and metabolic derangement affect the structure and function of endoneurial microvessels, which then induce fiber changes by altering the blood-nerve barrier, inducing hypoxia or ischemia, or by unknown mechanisms. In proximal diabetic neuropathy, there is increasing evidence that the characteristic lesion is an inflammatory (immune) vasculitis that induces ischemic nerve fiber degeneration. Truncal radiculopathy may be due to an inflammatory polyganglionopathy. In cranial nerve III neuropathy, the monophasic course and the pathologic alterations of ischemia suggest that localized vasculitis should be excluded in future cases. Many upper limb mononeuropathies in diabetes mellitus are from carpal tunnel syndrome. Repetitive shear forces, anatomic factors, and excessive stiffness of connective tissues may cause these mononeuropathies.
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PMID:Pathologic alterations in the diabetic neuropathies of humans: a review. 910 Jun 76

A 61-year-old man developed fever and a urinary tract infection followed five days later by acute visual loss in the right eye. Funduscopic examination was normal. A retrobulbar optic neuropathy was diagnosed but careful consideration was given to choroidal ischemia as an etiology. A sphenoidal mucocele was found on emergent MRI scan and drained expeditiously, with marked improvement in visual function. The diagnosis of giant cell arteritis should always be entertained when dealing with visual loss in the elderly.
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PMID:Acute unilateral visual loss in the elderly due to retrobulbar optic neuropathy. 897 Feb 41


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