Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was undertaken to investigate the antinociceptive and anti-inflammatory activities of the leaf and twig extracts of Dorstenia barteri (Moraceae) in mice. Both the leaf and twig extracts of Dorstenia barteri at 50, 100 and 200 mg/kg showed significant (P < 0.05-0.01) antinociceptive activities in chemical-, mechanical- and thermal-induced pain test models. Intraperitoneal administration of the plant extracts at 50, 100 and 200 mg/kg significantly (P < 0.05-0.01) inhibited carrageenin-induced acute inflammation in oedema paw weight, pulmonary oedema and number of pleural leucocytes in a dose-dependent way. The twig extract was found to be more active than the leaf extract in all the experimental models used. The inhibitory effects of the plant extracts were comparable to those of the reference drugs acetylsalicyclic acid (ASA) and phenylbutazone (PBZ) at 100 mg/kg i.p. The significant reduction in acetic acid-induced abdominal contractions, the decrease in oedema paw weight as well as in the number of leucocytes in the pleural cavity exudates, and the significant increase in the reaction time and pain threshold of mice observed in this study suggest that Dorstenia barteri extracts possess both anti-inflammatory and antinociceptive activities. The present study, therefore, lend pharmacological support to the folkloric uses of Dorstenia barteri extracts in the treatment, control and/or management of arthritis, rheumatism, gout, headache and other forms of body pains in some parts of Africa.
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PMID:Antinociceptive and anti-inflammatory effects of Dorstenia barteri (Moraceae) leaf and twig extracts in mice. 1537

The study was held in order to analyze the main causes of death in cases of rheumatic diseases (RD) in Moscow. The authors studied the pathology records of autopsies performed in 1999-2002 in two pathology departments of Moscow clinics. Cases with RD were selected. The study found 165 cases of RD, which constituted 2% of all autopsies performed in these departments. There were 99 cases (60%) of rheumatic heart disease (RHD), 4 cases (2.4%) of rheumatic fever (RF) relapse, 28 cases (17%) of rheumatoid arthritis (RA), 8 cases (4.8%) of systemic lupus erythematosus (SLE), 3 cases (1.8%) of scleroderma systematica (SS), 2 cases (1.2%) of ankylosing spondylitis (AS), 2 cases (1.2%) of systemic vasculitis (SPV), 11 cases (7.3%) of osteoarthrosis, 3 cases (1.8%) of gout, 1 case (0.6%) of polymyositis. The death of patients with RHD had been caused by hemodynamic decompensation (HD) in 54% of the cases, acute cardiovascular collapse (ACC) in 14% of the cases, 6% of the patients had died from thromboembolism (TE) and 26%--from other conditions (intoxication, uremia, brain and lung edema etc). The death of patients with RF was caused by TE in 2 cases, by HD in 1 case and by ACC in 1 case. Secondary amyloidosis resulting in chronic renal failure and uremia occurred in 5 out of 28 cases of RA, HD--in 3, ACC--in 7, TE--in 1, infectious complications--in 5, other complications--in 7 cases. Patients with SLE died from various conditions: uremia in 2 cases, acute adrenal failure in 1 case, infectious complications in 2, ACC--in 2, brain edema--in 1 case. The complications of SS were uremia and intoxication. ACC was the cause of death in cases of gout and SS. The majority of RD cases were patients with RHD. The main cause of death in RD was cardiovascular disorders.
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PMID:[The causes of death of patients with rheumatic diseases in Moscow]. 1575 89

We report an unusual case of delayed death due to sepsis following closed blunt injury to the neck. The victim was a 71-year-old male with a clinical history of hypertension, diabetes and gout. He was found dead about three weeks after being assaulted. He had not consulted a hospital after the assault. Forensic autopsy demonstrated a large liquefied subcutaneous hematoma on the right side of the neck, peri- and thrombophlebitis of the right internal jugular vein. Otherwise, there was no evidence of trauma. Histological examination showed dermal vesicles in the skin covering the hematoma, accompanied by marked inflammatory cell infiltration phagocytosing gram-positive streptococci, subcutaneous edema, panphlebitis with partially organized thrombi and bacterial colonies, pulmonary edema and multiple pulmonary microthrombi involving bacterial aggregates. Postmortem serum C-reactive protein and neopterin levels were markedly elevated. These findings suggest sepsis as the cause of death, induced by infected internal jugular vein thrombophlebitis following blunt neck injury involving impaired skin barrier.
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PMID:An autopsy case of internal jugular vein thrombophlebitis involving sepsis following blunt neck injury. 1820 29