gout/phosphatase

Hyperuricemia and gout can be seen in patients with Paget's disease of bone (PD). This may be secondary to increased nucleic acid turnover in accelerated bone remodeling. It is unclear whether all PD patients should be evaluated for the presence of PD and gout in the same patient. In this report, I

Patients with hepatic glucose-6-phosphatase deficiency usually have a striking clinical syndrome during childhood and are readily diagnosed by the pediatrician. An adult patient had childhood manifestations of glucose-6-phosphatase deficiency that were mild and unrecognized; symptoms of tophaceous

1. GSD-I is described in a child with partial deficiency of hepatic glucose-6-phosphatase. 2. Growth retardation and hepatosplenomegaly were major clinical features. 3. Hyperlipidaemia, lactic acidaemia, hyperuricaemia and reduced uric acid clearance were major biochemical findings. 4. Although the

A group of 292 patients with diseases of the locomotor system was examined. Elevated activity of the liver isoenzyme of serum alkaline phosphatase was found in rheumatoid arthritis. Evaluation of the alkaline phosphatase isoenzyme in these states is especially important for studying nonspecific

BACKGROUND To assess the efficacy of fenofibrate treatment in combination with urate lowering agents in patients with gout. METHODS Fourteen male patients with chronic tophaceous or recurrent acute attacks of gout were evaluated in an open-label pilot study of the hypolipidemic agent, fenofibrate

In this review we consider diseases associated with pathological mineralization/ossification, namely, ankylosing spondylitis (AS), osteoarthritis (OA), generalized artery calcification of infancy (GACI), vascular calcification as well as chondrocalcinosis (CC) and pseudo gout. Deciphering the key

OBJECTIVE To analyze cellular mechanisms of bone erosion in gout. METHODS Peripheral blood mononuclear cells (PBMCs) and synovial fluid mononuclear cells (SFMCs) from patients with gout were analyzed for the presence of osteoclast precursors. Fixed tophus and bone samples were analyzed by

Gout is a chronic arthritis caused by the deposition of poorly soluble monosodium urate monohydrate (MSU) crystals in peripheral joints. Resident macrophages initiate inflammation in response to MSU mediated by NF-κB nuclear translocation and NLRP3 inflammasome activation. We investigated the role

AP isoenzymes were estimated in 292 patients with locomotor diseases and in 124 healthy controls. The diagnostic usefulness of AP determination is increased by estimation of isoenzymes. Investigations were made to study the biological profile of organ specific AP activities: 1. Rheumatoid arthritis

Type 1a glycogen storage disease (GSD 1a), or von Gierke disease, is a rare, autosomal-recessive disease caused by a deficiency of glucose-6-phosphatase, which leads to glycogen accumulation in the liver, kidney, and intestinal mucosa. Clinical manifestations include hypoglycemia, growth

Hyperuricemia is a well-known consequence of glucose-6-phosphatase (G6Pase) deficiency, the enzymatic abnormality that characterizes glycogen storage disease (GSD) Type Ia. However, acute gout as the presenting manifestation of GSD Type Ia has been reported in only a few patients. We report a new

Osteoarthritis or 'Joint Failure' is a multi-factorial disease with a final common pathway of cartilage degeneration and bone eburnation. The association of arthritic disease and joint degeneration with the deposition of sodium urate crystals in gout and calcium pyrophosphate crystals in pseudogout