Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of gout increases with age. Up to 7% of men > 65 and 3% of women > 85 have gout. Risk of gout increases significantly with increasing serum uric acid levels. Alcohol consumption and purine-rich foods such as red meat and seafood increase the risk of incident gout significantly. Loop and thiazide diuretics are also associated with increased risk. Gout is frequently associated with the metabolic syndrome. Dehydration, increasing creatinine levels, and surgery are also known to precipitate flares. Acute gout manifests as severe joint pain, of rapid onset, reaching maximal intensity within a few hours. Gout has a predilection for lower extremity joints. It often starts at the first metatarsophalangeal joint, a condition termed podagra. Other common sites of gouty flares include: tarsal and subtalar joints; ankle; knee; wrist; small joints of the hands; Achilles tendon; and olecranon bursae. The joint affected is usually hot, red, swollen and very painful. This is often associated with skin erythema. Identification of MSU crystals in the synovial fluid of an inflamed joint or from tophi allows a definite diagnosis of gout to be made. Hyperuricaemia does not confirm or exclude gout as most people with hyperuricaemia are asymptomatic, while serum uric acid levels tend to decrease during acute attacks. Short-acting NSAIDs should be used at maximal dose as first drug of choice if not contraindicated. In patients at risk of GI complications, co-prescription of a proton pump inhibitor or the use of COX-2 selective agents should be considered. Colchicine can be particularly useful in patients with heart failure in whom NSAIDs are contraindicated but should be avoided in patients with severe renal impairment. Joint aspiration and injection of intra-articular steroids is one of the most effective ways of treating acute monoarthritic gout. Uric acid lowering therapy is initiated if a patient suffers two or more attacks in one year. Many rheumatologists will start this therapy in hyperuricaemic patients whose first attack is very severe or in polyarticular gout.
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PMID:Diagnosis and treatment of gout in primary care. 2227 26

Since it was proposed in 2007, molecular hydrogen therapy has been widely concerned and researched. Many animal experiments were carried out in a variety of disease fields, such as cerebral infarction, ischemia reperfusion injury, Parkinson syndrome, type 2 diabetes mellitus, metabolic syndrome, chronic kidney disease, radiation injury, chronic hepatitis, rheumatoid arthritis, stress ulcer, acute sports injuries, mitochondrial and inflammatory disease, and acute erythema skin disease and other pathological processes or diseases. Molecular hydrogen therapy is pointed out as there is protective effect for sepsis patients, too. The impact of molecular hydrogen therapy against sepsis is shown from the aspects of basic vital signs, organ functions (brain, lung, liver, kidney, small intestine, etc.), survival rate, and so forth. Molecular hydrogen therapy is able to significantly reduce the release of inflammatory factors and oxidative stress injury. Thereby it can reduce damage of various organ functions from sepsis and improve survival rate. Molecular hydrogen therapy is a prospective method against sepsis.
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PMID:Molecular Hydrogen Therapy Ameliorates Organ Damage Induced by Sepsis. 2741 21

The progression of liver disease is portrayed by several common, overarching signs and symptoms. Classically, these include findings such as spider angiomata, jaundice, palmar erythema, and as cirrhosis decompensates, ascites, variceal hemorrhage (VH), hepatic encephalopathy (HE), and hepatocellular carcinoma (HCC). Aside from these universal hallmarks among cirrhotics, patients with nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) harbor their own distinct systemic associations and manifestations. NAFLD is tightly linked to metabolic syndrome, which appears to be a driving force for a multitude of comorbidities, such as insulin resistance, cardiovascular disease, chronic kidney disease (CKD), obstructive sleep apnea (OSA), as well as increased malignancy risk. ALD also maintains a variety of comorbidities congruent with systemic effects of chronic alcohol use. These findings are highlighted by cardiovascular conditions, neuronal damage, myopathy, nutritional deficiencies, chronic pancreatitis, in addition to increased malignancy risk. While a general, guideline-driven management for all cirrhotic patients remains imperative for minimizing risk of complications, a tailored treatment strategy is useful for patients with NAFLD and ALD who entertain their own constellation of unique systemic manifestations.
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PMID:Nonalcoholic fatty liver disease and alcoholic liver disease: metabolic diseases with systemic manifestations. 3162 Jun 47

The complex regional pain syndrome (CRPS) is a neuropathic disorder, often precipitated by a fracture, injury of the soft tissue or a surgical procedure followed by extended immobilization. Clinical signs and symptoms of this syndrome include abnormalities of pain processing (mechanical and thermal allodynia, hyperalgesia and hyperpathia), skin changes regarding local temperature and the presence of erythema, cyanosis or mottled appearance, neurogenic edema, motor and trophic disorders. The CRPS has three evolutionary stages-acute, dystrophic and atrophic, and it is divided into two types, reflecting the absence or presence of nerve damage. The patient presented in this study was a female with a history of metabolic syndrome, diagnosed with polyarticular chronic gout, which despite the specific drug treatment administered, had multiple predisposing factors for the development of CRPS consecutive to the fracture of both bones of the right forearm. It is evident that the recovery period after injury is slightly different in each individual and depends on the severity of the injury and patient factors such as age, general condition and the presence of other comorbidities. The delay between the onset of symptoms and her presentation to the physician, conferred a poor prognosis for the developing pathology, with important functional and motor impairment.
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PMID:Posttraumatic Complex Regional Pain Syndrome and Related Comorbidities. 3204 62