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)

Gastrointestinal involvement occurs in most patients with systemic sclerosis and is subclinical in about one third. Early pathology is characterized by vasculopathy, resulting in tissue ischemia and progressive dysfunction. Noninvasive esophageal studies using semisolid bolus scintigraphy are sensitive but lack specificity. Long-term treatment of reflux with high-dose proton pump inhibitors appears safe and effective for symptom relief and may prevent recurrence of esophagitis and stricture. Dyspepsia may result from gastroparesis and antral distension. Gastric antral vascular ectasia is a vascular manifestation, and bleeding may be controlled endoscopically. Prokinetic agents effective in pseudoobstruction include metoclopramide, domperidone, cisapride, octreotide, and erythromycin. Patients with intestinal neuropathy or response to bolus octreotide are more probable long-term responders. The combination of octreotide and erythromycin may be particularly effective in systemic sclerosis. The combination of cisapride and erythromycin may cause serious cardiac arrhythmia and is contraindicated. Omeprazole may predispose to small intestinal bacterial overgrowth. Malabsorption not responding to antibiotic therapy should be investigated with small-bowel biopsy to rule out more unusual causes. Pneumatosis cystoides intestinalis may be due to excessive hydrogen production by intestinal bacteria altering the partial pressure of nitrogen in the intestinal wall. In selected cases, surgery for intestinal failure is an option with resection or bypass of affected segments or placement of enterostomy tubes for feeding or decompression. Careful preoperative characterization of intestinal segments is required.
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PMID:Gastrointestinal features of scleroderma. 901 61

Through a discussion of the etiology and pathology of diabetic foot lesions with particular emphasis on ulceration and osteoarthropathy, the author will develop a plan for treatment and prevention using a multidisciplinary approach to such problems. Underlying risk factors including neuropathy, ischemia, infection, and, especially high pressures must be evaluated and appropriately ameliorated in order to promote resolution and avoidance of recidivism. Accordingly, conservative management with pressure-relieving devices, topical therapies, and prophylactic surgery on structural deformities plays an integral part in the overall podiatric management of the high-risk foot in diabetes mellitus.
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PMID:Team approach toward lower extremity amputation prevention in diabetes. 924 72

Oxidative stress is present in the diabetic state. Our work has focused on its presence in peripheral nerves. Antioxidant enzymes are reduced in peripheral nerves and are further reduced in diabetic nerves. That lipid peroxidation will cause neuropathy is supported by evidence of the development of neuropathy de novo when normal nerves are rendered alpha-tocopherol deficient and by the augmentation of the conduction deficit in diabetic nerves subjected to this insult. Oxidative stress appears to be primarily due to the processes of nerve ischemia and hyperglycemia auto-oxidation. The indexes of oxidative stress include an increase in nerve, dorsal root, and sympathetic ganglia lipid hydroperoxides and conjugated dienes. The most reliable and sensitive index, however, is a reduction in reduced glutathione. Experimental diabetic neuropathy results in myelinopathy of dorsal roots and a vacuolar neuropathy of dorsal root ganglion. The vacuoles are mitochondrial; we posit that lipid peroxidation causes mitochondrial DNA mutations that increase reduced oxygen species, causing further damage to mitochondrial respiratory chain and function and resulting in a sensory neuropathy. Alpha-lipoic acid is a potent antioxidant that prevents lipid peroxidation in vitro and in vivo. We evaluated the efficacy of the drug in doses of 20, 50, and 100 mg/kg administered intraperitoneally in preventing the biochemical, electrophysiological, and nerve blood flow deficits in the peripheral nerves of experimental diabetic neuropathy. Alpha-lipoic acid dose- and time-dependently prevented the deficits in nerve conduction and nerve blood flow and biochemical abnormalities (reductions in reduced glutathione and lipid peroxidation). The nerve blood flow deficit was 50% (P < 0.001). Supplementation dose-dependently prevented the deficit; at the highest concentration, nerve blood flow was not different from that of control nerves. Digital nerve conduction underwent a dose-dependent improvement at 1 month (P < 0.05). By 3 months, all treated groups had lost their deficit. The antioxidant drug is potentially efficacious for human diabetic sensory neuropathy.
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PMID:The roles of oxidative stress and antioxidant treatment in experimental diabetic neuropathy. 928 97

Anterior ischemic optic neuropathy is the most common cause of persistent monocular visual loss in persons over the age of 50. At the heart of this form of optic neuropathy is a sequence of cytoplasmic and membrane events that culminate in axonal destruction. Early depletion of ATP is followed by membrane depolarization, influx of Na+ and Ca2+ via specific voltage-gated channels and reverse operation of the Na+/Ca2+ exchange protein. Toxic Ca2+ overload is the ultimate consequence of these events. Preventing or modulating any of these well-defined steps mitigates against the development of anoxic injury. Translating these molecular insights about how optic nerve axons are damaged by ischemia-like conditions into clinical gains remains the challenge for the future.
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PMID:Ischemic injury of optic nerve axons: the nuts and bolts. 929 51

A 59-year-old man with an 8-years history of diabetes mellitus had an acute onset of sharp pain in the anterior part of right lower leg. One month later, the pain changed to deep dull nature in the deeper site of the peroneal region. The pain increased, when he stood up, walked, and stayed in the cold room and decreased by rest. It was more painful in the evening than in the morning. The first sharp pain was thought to be caused by ischemia due to diabetic vascular neuropathy. The next dull pain was considered to be originated from ephaptic transmission between sympathetic efferent fibers to group IV and afferent ones from the skeletal muscle. The latter dull pain was selectively suppressed by nerve block when it became effective to the branch of deep peroneal nerve to extensor digitorum longus muscle. The hypothesis of ephaptic transmission was supported by meaningful decrease of muscle sympathetic activity detected by microneurography before and after the dosage of L-DOPS, which effectively suppressed the pain as well as other alpha-stimulant, midodrine hydrochloride. We concluded that the ephaptic pain caused by muscle sympathetic activity could be suppressed by the vasoconstrictive drugs through the mechanism of baroreflex control.
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PMID:[Pain caused by ephaptic transmission occurring in the recovery phase of diabetic vascular mononeuropathy was effectively suppressed with L-threo-3,4-dihydroxyphenyl-serine]. 959 2

The management of lower extremity diabetic ulceration exacts enormous emotional and economic costs from patients, their family members and caregivers, and society. A team approach to wound healing has proved effective, but efforts at prevention have been less successful. The etiology of lower extremity diabetic ulcers includes injury complicated by underlying neuropathy, ischemia, or both. Prevention of primary and recurrent ulcers can be increased through programs to educate patients and caregivers. Proper management begins with thorough assessment and continues with various forms of medical and surgical therapy, and timely referral to specialists when appropriate. The use of recombinant growth factors is becoming more widespread as more is learned about their essential role in wound healing. Monitoring the wound while it is being treated is as important as initial assessment. Across the United States and Canada, wound care clinics are being established to provide intensive care directed by specially trained multidisciplinary care teams. Less populated areas must rely on proper education of ET nurses, home care nurses, visiting nurses, podiatrists/chiropodists, and allied healthcare professionals. Challenges for the future include the development of protocols for comprehensive assessment and care, better methods of prevention, a greater understanding of the role of growth factors in wound healing, and optimizing wound care.
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PMID:Diabetic ulcers of the lower extremity: a review of comprehensive management. 961 7

Vasculitis involving peripheral nerves usually presents as an acute asymmetrical axonal neuropathy. We report a 67-year-old man with a symmetrical subacute neuropathy in which nerve conduction studies showed prominent conduction block, a finding indicative of demyelination. Sural nerve biopsy showed a vasculitic neuropathy with invasion of blood vessel walls by inflammatory cells and a mixture of nerve fiber loss and demyelination. The demyelination in this case was presumably a consequence of subinfarctive nerve ischemia.
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PMID:Conduction block in vasculitic neuropathy. 1039 22

Diabetic polyneuropathy is a complication, that affects most patients with longstanding diabetes mellitus, deteriorating their quality of life. In the last few years, new therapeutic approaches have been developed that can improve symptoms and neurologic function, and which may prevent and in some cases stop nerve damage, and even, promote nerve fiber regeneration. These treatments are supported by several investigations in animals and humans: a) thigh glycemic control (insulin), b) aldose reductase inhibition (tolrestat), c) prevention of protein glycation (amino-guanidine), d) improvement of nerve ischemia (vaso-dilators, gamma-linolenic acid), and e) administration of neurotrophic factors (gangliosides). Most evidence support the usefulness for glycemic control. Early treatment is suggested, because marked nerve fiber loss is present in advanced neuropathy.
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PMID:[Treatment of diabetic neuropathy]. 965

Neuropathy and ischemia, two common complications of diabetes mellitus, are the primary underlying risk factors for the development of foot ulcers and their complications. The presence of symmetric distal polyneuropathy, encompassing motor, sensory, and autonomic involvement, is one of the most important factors in the development of diabetic foot ulcers. Perhaps one third of diabetic foot ulcers have a mixed neuropathic and ischemic etiology. Although neuropathy and ischemia are the primary predisposing factors in the formation of diabetic foot ulcers, an initiating factor, such as physical or mechanical stress, is required for an ulcer to develop. Ischemic ulcers develop as a result of low perfusion pressure in a foot with inadequate blood supply, whereas neuropathic ulcers result from higher pressures in a foot with adequate blood supply but loss of protective sensation. In addition to increasing the risk of ulceration, diabetes mellitus also increases the risk of infection by impairing the body's ability to eliminate bacteria. The processes by which ulcers develop are reviewed here.
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PMID:The development and complications of diabetic foot ulcers. 977 68

Feet lesions are the most important cause of diabetic's consultation in general surgery. A retrospective study was conducted in Ouagadougou National Teaching Hospital, in order to analyse epidemiology, clinic, and evolutive aspects of this affection. In the same period, 222 cases of diabetes mellitus were admitted in general surgery and internal medicine. We noticed 42 cases of feet lesions. The mean age of patients was 53 years. Anterior knowledge of diabetes has not been a factor of early consultation. Consultation mean delay was a month. In 28 cases, feet lesions were 4 or 5 Wagner grade. The role of ischemia and neuropathy have not been evaluated, but sepsis was highly determinant factor. Insulin has been used in 83.3% of cases. Amputation concerned 19 patients. Mean length of hospital stay was 16.6 days and mortality rate was 38.1%. Prevention of complications can be much more effective if it is applied as a part of global approach to diabetes mellitus management.
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PMID:[Management of the diabetic foot, apropos of 42 cases at the Ougadougou University Hospital Center]. 982 68


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