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)

Neutrophils, the most abundant leukocytes in the human body, are considered to be the first line of defense in the fight against microorganisms. In this fight neutrophils employ weaponry such as reactive oxygen species produced via the NADPH oxidase complex 2 together with the release of intracellular granules containing antimicrobial agents. The discovery that activated neutrophils release decondensed chromatin as DNase-sensitive neutrophil extracellular traps (NETs) lead to a renewed interest in these leukocytes and the function of NETs in vivo. In this review, we will focus on desirable as well as detrimental features of NETs by the example of gout and pancreatitis. In our models we observed that neutrophils drive the initiation of inflammation and are required for the resolution of inflammation.
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PMID:Neutrophils and neutrophil extracellular traps orchestrate initiation and resolution of inflammation. 2758 95

CA199 is a sialic acid containing glycan antigen found in both glycoproteins and glycolipids, which is recognized by monoclonal antibodies generated by hybridoma technology. The increased serum CA199 levels measured by using the monoclonal antibodies have been used as diagnostic or prognostic biomarker for pancreatic cancer. Even though increased serum CA199 levels are also observed in other cancers and noncancer diseases, it is largely unknown if CA199 levels could serve as biomarkers for other diseases as well. Therefore, in our current study, serum CA199 levels from 45,645 patients with 47 clinically defined diseases and 14,783 healthy controls who attended their annual physical examination were collected and measured by the clinical laboratory in the Affiliated Hospital of Qingdao University over the past 5 years. Based on the median, mean, and -Log10p values, we found that patients with pancreatic cancer, lung fibrosis, cirrhosis, liver cancer, hepatitis, and pancreatitis had the highest media and mean serum CA199 levels with statistical significance based on the -Log10p values. Unexpectedly, patients suffering from gout and anemia had significantly low CA199 levels compared to that of the healthy controls. These results showed that serum CA199 levels are not only increased in pancreatic and other cancer patients but also either increased or decreased in noncancer diseases. The overall data indicated that the abnormal serum CA199 level might be an indicator of system malfunction rather than a cancer biomarker in general.
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PMID:Serum CA199 levels are significantly increased in patients suffering from liver, lung, and other diseases. 3090 55

Background. Familial dysbetalipoproteinemia (also known as type 3 hyperlipoproteinemia) is typically associated with homozygosity for the apolipoprotein E2 isoform, but also sometimes with dominant rare missense variants in the APOE gene. Patients present with roughly equimolar elevations of cholesterol and triglyceride (TG) due to pathologic accumulation of remnant lipoprotein particles. Clinical features include tuberoeruptive xanthomas, palmar xanthomas, and premature vascular disease. Case. A 48-year-old male presented with severe combined dyslipidemia: total cholesterol and TG were 11.5 and 21.4 mmol/L, respectively. He had dyslipidemia since his early 20s, with tuberous xanthomas on his elbows and knees. His body mass index was 42 kg/m2. He also had treated hypertension, mild renal impairment, and a history of gout. He had no history of cardiovascular disease, peripheral arterial disease, or pancreatitis. Multiple medications had been advised including rosuvastatin, ezetimibe, fenofibrate, and alirocumab, but his lipid levels were never adequately controlled. Genetic Analysis. Targeted next-generation sequencing identified (1) the APOE E2/E2 homozygous genotype classically described with familial dysbetalipoproteinemia; (2) in addition, one APOE E2 allele contained the rare heterozygous missense variant p.G145D, previously termed apo E-Bethesda; (3) a rare heterozygous APOC2 nonsense variant p.Q92X; and (4) a high polygenic risk score for TG levels (16 out of 28 TG-raising alleles) at the 82nd percentile for age and sex. Conclusion. The multiple genetic "hits" on top of the classical APOE E2/E2 genotype likely explain the more severe dyslipidemia and refractory clinical phenotype.
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PMID:Severe Combined Dyslipidemia With a Complex Genetic Basis. 3153 26


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