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)

There were adduced the results of studying of cellular and humoral factors of the immunity in a brief-lasting ischemia-reoxygenation of the extremities in 56 patients with surgical diseases and in 31 pupils, in whom the organism reactivity lowering was revealed. It was established, that changes in the ischemia-reoxygenation of the extremities are multifactorial and they are connected primarily with the immunocompetent cells activation. Nonmedicinal method of the "tourniquet" immunocorrection was proposed, which is recommended as a concurrent one - for the recovery acceleration or solely - in the treatment of inflammatory diseases. It may be prescribed as a health-improving method in a rapid fatigue, insomnia, weakness, loss of appetite and other signs of the organism reactivity lowering. Application of the method secures the morbidity lowering in frequently ill pupils.
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PMID:[The "tourniquet" ischemia-reoxygenation of the extremities as the method of nonmedicinal immunocorrection]. 1682 18

Oxidative stress is associated with muscle fatigue and weakness in skeletal muscle of ischemic heart disease patients. Recently, it was found that endurance training elevates protective heat shock proteins (HSPs) and antioxidant enzymes in skeletal muscle in healthy subjects and antioxidant enzymes in heart failure patients. However, it is unknown whether coronary ischemia and mild infarct without heart failure contributes to impairment of stress proteins and whether exercise training reverses those effects. We tested the hypothesis that exercise training would reverse alterations in muscle TNF-alpha, oxidative stress, HSP70, SOD (Mn-SOD, Cu,Zn-SOD), glutathione peroxidase (GPX), and catalase (CAT) due to chronic coronary occlusion of the left circumflex (CCO). Yucatan swine were divided into three groups (n = 6 each): sedentary with CCO (SCO); 12 wk of treadmill exercise training following CCO (ECO); and sham surgery controls (sham). Forelimb muscle mass-to-body mass ratio decreased by 27% with SCO but recovered with ECO. Exercise training reduced muscle TNF-alpha and oxidative stress (4-hydroxynonenal adducts) caused by CCO. HSP70 levels decreased with CCO (-45%), but were higher with exercise training (+348%). Mn-SOD activity, Mn-SOD protein expression, and Cu,Zn-SOD activity levels were higher in ECO than SCO by 72, 82, and 112%, respectively. GPX activity was 177% greater in ECO than in SCO. CAT trended higher (P = 0.059) in ECO compared with SCO. These data indicate that exercise training following onset of coronary artery occlusion results in recovery of critical stress proteins and reduces oxidative stress.
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PMID:Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion. 1687 55

A 27-yr-old woman recreationally inhaled cocaine. Several hours later, she noted chest tightness, back and neck pain, and later bilateral upper-extremity weakness. Physical examination revealed flaccid paresis of the upper extremities. Spasticity at 2 mos after injury, but no detectable weakness, developed in the lower extremities. Cocaine was detected in her urine. Magnetic resonance imaging showed hyperintensity in the anterior cervicothoracic spinal cord. Electrodiagnostic studies of the upper extremities were consistent with anterior horn cell death. Cocaine abuse is associated with cerebrovascular events; spinal cord effects are rarely reported. The patient seems to have an infarct in the anterior spinal artery distribution, with clinical, imaging, and electrodiagnostic findings of upper-extremity lower-motor neuron injury, accompanied by spasticity of the lower extremities. Gray matter has increased susceptibility to ischemia compared with white matter, producing flaccid weakness in the cervical region with isolated arm weakness. Although uncommon, cocaine abuse can cause spinal cord infarction.
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PMID:Spinal cord infarction secondary to cocaine use. 1716 48

ATP-sensitive potassium channels (K(ATP)) couple cell metabolism to electrical activity by regulating potassium movement across the membrane. These channels are octameric complex with two kind of subunits: four regulatory sulfonylurea receptor (SUR) embracing four poreforming inwardly rectifying potassium channel (Kir). Several isoforms exist for each type of subunits: SUR1 is found in the pancreatic beta-cell and neurons, whereas SUR2A is in heart cells and SUR2B in smooth muscle; Kir6.2 is in the majority of tissues as pancreatic beta-cells, brain, heart and skeletal muscle, and Kir6.1 can be found in smooth vascular muscle and astrocytes. The K(ATP) channels play multiple physiological roles in the glucose metabolism regulation, especially in beta-cells where it regulates insulin secretion, in response to an increase in ATP concentration. They also seem to be critical metabolic sensors in protection against metabolic stress as hypo or hyperglycemia, hypoxia, ischemia. Persistent hyperinsulinemic hypoglycaemia (HI) of infancy is a heterogeneous disorder which may be divided into two histopathological forms (diffuse and focal lesions). Different inactivating mutations have been implicated in both forms: the permanent inactivation of the K(ATP) channels provokes inappropriate insulin secretion, despite low ATP. Diazoxide, used efficiently in certain cases of HI, opens the K(ATP) channels and therefore overpass the mutation effect on the insulin secretion. Conversely, several studies reported sequencing of KCNJ11, coding for Kir6.2, in patients with permanent neonatal diabetes mellitus and found different mutations in 30 to 50% of the cases. More than 28 heterozygous activating mutations have now been identified, the most frequent mutation being in the aminoacid R201. These mutations result in reduced ATP-sensitivity of the K(ATP) channels compared with the wild-types and the level of channel block is responsible for different clinical features: the "mild" form confers isolated permanent neonatal diabetes whereas the severe form combines diabetes and neurological symptoms such as epilepsy, deve-lopmental delay, muscle weakness and mild dimorphic features. Sulfonylureas close K(ATP) channels by binding with high affinity to SUR suggesting they could replace insulin in these patients. Subsequently, more than 50 patients have been reported as successfully and safely switched from subcutaneous insulin injections to oral sulfonylurea therapy, with an improvement in their glycated hemoglobin. We therefore designed a protocol to transfer and evaluate children who have insulin treated neonatal diabetes due to KCNJ11 mutation, from insulin to sulfonylurea. The transfer from insulin injections to oral glibenclamide therapy seems highly effective for most patients and safe. This shows how the molecular understan-ding of some monogenic form of diabetes may lead to an unexpected change of the treatment in children. This is a spectacular example by which a pharmacogenomic approach improves the quality of life of our young diabetic patients in a tremendous way.
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PMID:Diabetes and hypoglycaemia in young children and mutations in the Kir6.2 subunit of the potassium channel: therapeutic consequences. 1729 10

Rhabdomyolysis is defined as a pathological condition of skeletal muscle cell damage leading to the release of toxic intracellular material into the blood circulation. Its major causes include trauma, ischemia, drugs, toxins, metabolic disorders, and infections. The pathophysiological hallmark of the syndrome is an increase in intracellular free ionized calcium due to either cellular energy depletion, or direct plasma membrane rupture. The increased intracellular calcium activates several proteases, intensifies skeletal muscle cell contractility, induces mitochondrial dysfunction, and increases the production of reactive oxygen species, ultimately resulting in skeletal muscle cell death. Clinically, the syndrome presents with severe muscular pain, weakness and myoglobinuria. Increased myoglobin and creatine phosphokinase as a consequence of muscular cell death are the major laboratory findings, which, in combination with the clinical presentation, lead the clinician to the final diagnosis of the syndrome.
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PMID:The syndrome of rhabdomyolysis: Pathophysiology and diagnosis. 1733 59

Intra-aortic balloon pump (IABP)-related neuropathy is an infrequent complication, and the development of motor deficits is even rarer in such cases. We report a 37-year-old man with anterior ST-elevation myocardial infarction who received emergent percutaneous coronary intervention and IABP counterpulsation. Weakness and numbness developed after IABP removal despite lack of evidence of ischemia in the involved extremity. Nerve conduction velocity study and electromyogram led to the diagnosis of femoral nerve neuropathy. The neurologic deficits recovered after 6 months of rehabilitation. This case illustrates the importance of bedside neurologic examination of the involved extremity for early detection of possible injury to the femoral nerve in patients after IABP treatment and insertion of larger bore catheter.
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PMID:Isolated femoral nerve neuropathy after intra-aortic balloon pump treatment. 1749 6

Lymphoma is a systemic disease. It is not uncommon to be found involved in digestive or central nervous system. However, lymphoma involved in these two systems at the same time is rare. The clinical feature of a case of lymphoma with gastrointestinal bleeding and limbs weakness was investigated and the literature was reviewed. The patient came to our hospital with melena and hematemesis. She was diagnosed as gastric ulcer by gastroscopy and biopsy showed lymphoma. Two days after she came to hospital, the patient presented with progressing limbs weakness. Magnetic resonance imaging (MRI) showed irregular abnormal signals in T2-T4 vertebra, which was enhanced obviously. A strip abnormal signal could be seen in spinal cord and involved in neighboring centrum and ribbing. The lesion extended to paravertebral tissue. The final diagnosis was lymphoma involved in stomach and spinal cord. Diseases presented with both upper digestive tract bleeding and symptoms of central nervous system were rare, including malignancies, virus infection and some therapy. Lymphoma was one of the causes. On the other hand, spinal cord ischemia might occur after gastrointestinal bleeding. Thus, doctors should examine the patients carefully to diagnose these diseases.
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PMID:[A case of upper gastrointestinal bleeding and paraplegia]. 1765 79

Thoracic outlet syndrome (TOS) is a nonspecific label. When employing it, one should define the type of TOS as arterial TOS, venous TOS, or neurogenic TOS. Each type has different symptoms and physical findings by which the three types can easily be identified. Neurogenic TOS (NTOS) is by far the most common, comprising well over 90% of all TOS patients. Arterial TOS is the least common accounting for no more than 1%. Many patients are erroneously diagnosed as "vascular" TOS, a nonspecific misnomer, whereas they really have NTOS. The Adson Test of noting a radial pulse deficit in provocative positions has been shown to be of no clinical value and should not be relied upon to make the diagnosis of any of the three types. The test is normal in most patients with NTOS and at the same time can be positive in many control volunteers. Arterial TOS is caused by emboli arising from subclavian artery stenosis or aneurysms. Symptoms are those of arterial ischemia and x-rays almost always disclose a cervical rib or anomalous first rib. Venous TOS presents with arm swelling, cyanosis, and pain due to subclavian vein obstruction, with or without thrombosis. Neurogenic TOS is due to brachial plexus compression usually from scarred scalene muscles secondary to neck trauma, whiplash injuries being the most common. Symptoms include extremity paresthesia, pain, and weakness as well as neck pain and occipital headache. Physical exam is most important and includes several provocative maneuvers including neck rotation and head tilting, which elicit symptoms in the contralateral extremity; the upper limb tension test, which is comparable to straight leg raising; and abducting the arms to 90 degrees in external rotation, which usually brings on symptoms within 60 seconds.
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PMID:Diagnosis of thoracic outlet syndrome. 1782 54

Constructing vascular access for hemodialysis causes changes in blood flow to the extremity, which can lead to distal ischemia. Ischemic steal syndrome is manifested by pain; weakness; pallor; and, in severe cases, ulceration and tissue loss. Severe ischemia, requiring reintervention, has an incidence of 4%, although some degree of ischemia causing pain or parasthesias occurs in 10% to 20% of patients following access construction. Pathophysiology may be on the basis of inadequate arterial collateral inflow due to occlusive disease, particularly involving the medium-sized vessels, or high flow in a fistula exceeding the inflow capacity in the absence of intrinsic occlusive disease of the inflow arteries. Predicting steal remains difficult, although certain patient characteristics and preoperative techniques can help identify those patients in whom arteriovenous fistulas have an increased risk of causing steal. Patients with diabetes, multiple access procedures, and constructions based on proximal arteries are more prone to ischemia. Ultrasonography and digital-brachial indices measured by photoplethysmography or Doppler techniques have been used to predict fistulas that are more likely to cause ischemia, but these fall short of reliability. Operative techniques for correcting steal include arteriovenous fistula ligation, percutaneous transluminal angioplasty, banding or restrictive procedures, and distal revascularization interval ligation or modifications of this technique. Operative intervention for ischemic steal syndrome successfully resolves ischemia in 80% to 95% of patients. Some patients can have persistent pain despite healing of ulceration.
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PMID:Strategies for management of ischemic steal syndrome. 1788 20

Myasthenia gravis (MG) is a rare, autoimmune neuromuscular junction disorder. Contemporary prevalence rates approach 1/5,000. MG presents with painless, fluctuating, fatigable weakness involving specific muscle groups. Ocular weakness with asymmetric ptosis and binocular diplopia is the most typical initial presentation, while early or isolated oropharyngeal or limb weakness is less common. The course is variable, and most patients with initial ocular weakness develop bulbar or limb weakness within three years of initial symptom onset. MG results from antibody-mediated, T cell-dependent immunologic attack on the endplate region of the postsynaptic membrane. In patients with fatigable muscle weakness, the diagnosis of MG is supported by: 1. pharmacologic testing with edrophonium chloride that elicits unequivocal improvement in strength; 2. electrophysiologic testing with repetitive nerve stimulation (RNS) studies and/or single-fiber electromyography (SFEMG) that demonstrates a primary postsynaptic neuromuscular junctional disorder; and 3. serologic demonstration of acetylcholine receptor (AChR) or muscle-specific tyrosine kinase (MuSK) antibodies. Differential diagnosis includes congenital myasthenic syndromes, Lambert Eaton syndrome, botulism, organophosphate intoxication, mitochondrial disorders involving progressive external ophthalmoplegia, acute inflammatory demyelinating polyradiculoneuropathy (AIDP), motor neuron disease, and brainstem ischemia. Treatment must be individualized, and may include symptomatic treatment with cholinesterase inhibitors and immune modulation with corticosteroids, azathioprine, cyclosporine, and mycophenolate mofetil. Rapid, temporary improvement may be achieved for myasthenic crises and exacerbations with plasma exchange (PEX) or intravenous immunoglobulin (IVIg). Owing to improved diagnostic testing, immunotherapy, and intensive care, the contemporary prognosis is favorable with less than five percent mortality and nearly normal life expectancy.
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PMID:Myasthenia gravis. 1798 28


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