Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0020473 (
hyperlipidemia
)
15,891
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Kyrle's disease (KD) is a dermatosis which was first described by Kyrle as "hyperkeratosis follicularis et parafollicularis in cutem penetrans" in 1916. Perforating dermatoses are a heterogeneous disorder group characterised by transepithelial elimination. KD has been seen in association with
multiple disorders
, including diabetes mellitus, renal and liver diseases, congestive heart failure,
hyperlipidaemia
, infective diseases and abnormal metabolism of vitamin A. This case report presents two patients with KD with associated systemic disease.
...
PMID:Kyrle's disease. 2442 45
Uric acid is the product of purine metabolism and its increased levels result in hyperuricemia. A number of epidemiological reports link hyperuricemia with
multiple disorders
, such as kidney diseases, cardiovascular diseases and diabetes. Recent studies also showed that expression and functional changes of urate transporters are associated with hyperuricemia. Uric acid transporters are divided into two categories: urate reabsorption transporters, including urate anion transporter 1 (URAT1), organic anion transporter 4 (OAT4) and glucose transporter 9 (GLUT9), and urate excretion transporetrs, including OAT1, OAT3, urate transporter (UAT), multidrug resistance protein 4 (MRP4/ABCC4), ABCG-2 and sodium-dependent phosphate transport protein. In the kidney, uric acid transporters decrease the reabsorption of urate and increase its secretion. These transporters' dysfunction would lead to hyperuricemia. As the function of urate transporters is important to control the level of serum uric acid, studies on the functional role of uric acid transporter may provide a new strategy to treat hyperuricemia associated diseases, such as gout, chronic kidney disease,
hyperlipidemia
, hypertension, coronary heart disease, diabetes and other disorders. This review article summarizes the physiology of urate reabsorption and excretion transporters and highlights the recent advances on their roles in hyperuricemia and various diseases.
...
PMID:Recent advances on uric acid transporters. 2924 27
Surgical treatment of coronary artery disease in the systemic lupus erythematosus (SLE) patients has not been comprehensively addressed. The present review aimed to give an overview of coronary artery disease in the SLE patients receiving coronary artery bypass grafting (CABG). The study materials were based on comprehensive literature retrieval, which recruited 17 pertinent articles with 30 patients. No differences were found in the graft patencies between the arterial and venous grafts; and between the early and late patency rates. Pathological inspections revealed that all graft vessels were normal with no signs of SLE-related atherosclerosis or vasculitis, one coronary artery was pathologically normal, and another coronary artery showed vasculitis. The
coexisting disorders
, including diabetes mellitus,
hyperlipidemia
, and nephropathy in the SLE patients cause early deterioration of the saphenous vein grafts. Early occlusion of the saphenous vein grafts was also observed in SLE patients. The left anterior descending coronary artery was most commonly affected by SLE and was the most common coronary artery requiring a CABG procedure. The graft vessels, both arterial and venous, rarely degenerated; whereas, early and late graft failure was usually caused by technical failures. The lack of vasculitis and atherosclerosis in the arterial grafts encourage surgeons to prefer to use the arterial grafts in SLE patients. Less invasive surgical technique would favour the patients in terms of long-term outcomes. Key Words: Coronary artery bypass grafting, Graft occlusion, Vascular, Systemic lupus erythematosus.
...
PMID:Coronary Artery Bypass Grafting in Patients with Systemic Lupus Erythematosus. 3303 82