Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 66-year-old woman with SLE who recently started oral steroid was admitted to our hospital because of subacute numbness of the bilateral legs and gait disturbance, despite of the stable symptoms of SLE and its serology. Blood tests revealed hyperglycemia. Nerve conduction study showed decreased nerve conduction velocities consistent with demyelinative neuropathy. On initiation of insulin to control hyperglycemia, conduction velocities were rapidly increased in one week, suggesting hyperglycemic neuropathy. The rapid improvement of the conduction velocities was argued against mechanical "demyelination", rather suggesting axonal dysfunction, possibly associated with impaired function of Na(+)-K(+)-ATPase in hyperglycemic state.
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PMID:[A case of hyperglycemic neuropathy with possible dysfunction of axonal excitability]. 1715 32

Current Clinical Management Guidelines of Diabetic Peripheral Neuropathy (DPN) are based on adequate glucose control and symptomatic pain relief. However, meticulous glycemic control could delay the onset or slow the progression of diabetic neuropathy in patients with DM type 2, but it does not completely prevent the progression of the disease. Complications of DPN as it continues its natural course, produce increasing pain and discomfort, loss of sensation, ulcers, infections, amputations and even death. In addition to the increased suffering, disability and loss of productivity, there is a very significant economic impact related to the treatment of DPN and its complications. In USA alone, it has been estimated that there are more than 5,000,000 patients suffering from DPN and the total annual cost of treating the disease and its complications is over $10,000 million dollars. In order to be able to reduce complications of DPN, it is crucial to improve or correct the metabolic conditions that lead to the pathology present in this condition. Pathophysiologic mechanisms implicated in diabetic neuropathy include: increased polyol pathway with accumulation of sorbitol and reduced Na+/K+-ATPase activity, microvascular damage and hypoxia due to nitric oxide deficit and increased oxygen free radical activity. Moreover, there is a decrease in glutathione and increase in homocysteine. Clinical trials in the last two decades have demonstrated that the use of specific nutrients can correct some of these metabolic derangements, improving symptom control and providing further benefits such as improved sensorium, blood flow and nerve regeneration. We will discuss the evidence on lipoic acid, acetyl-L-carnitine, benfotiamine and the combination of active B vitamins L-methylfolate, methylcobalamin and piridoxal-6-phosphate. In addition, we discuss the role of metformin, an important drug in the management of diabetes, and the presence of specific polymorphic genes, in the risk of developing DPN and how metabolic correction can reduce these risks.
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PMID:Metabolic correction in the management of diabetic peripheral neuropathy: improving clinical results beyond symptom control. 2208 24