Pathology Of Gout Research Articles

Imaging in gout

Imaging has the potential to assess various pathological manifestations of gout, including monosodium urate (MSU) crystal deposition, tophus formation and cartilage, soft tissue, and bone pathology. This review discusses recent research examining the role of imaging to assess the manifestations of disease. Various imaging techniques are used in the assessment of gout, including plain radiography, ultrasonography, conventional computed tomography (CT), dual energy computed tomography (DECT), and MRI. Potential roles for ultrasonography are MSU crystal detection, measurement of tophi, and assessment of disease complications. Ultrasonography may allow detection of MSU crystals in patients with hyperuricaemia, prior to development of clinically apparent gout. Conventional CT allows excellent visualization of tophi and bone erosion. DECT is a promising method of noninvasive MSU crystal detection. MRI allows assessment of tophi, synovial and soft tissue disease, and bone pathology. The relative absence of MRI bone marrow oedema in gout suggests that the mechanisms of bone erosion in gout are quite different from those in other erosive arthropathies. Imaging modalities have provided important insights into the pathology of gout. The role of various imaging techniques in gout diagnosis, monitoring, and prediction of outcome is rapidly developing.

Acute Gout: The Inflammasome

Gout is one of the most common and painful forms of arthritis in humans with a growing incidence and prevalence over the last decades. Recent studies into the pathophysiology of acute gout have revealed that MSU (monosodium urate), the crystalline form of uric acid, is recognized by immune cells as a danger signal and can initiate an inflammatory response. This response is orchestrated by the intracellular pattern-recognition receptor NLRP3, which upon exposure to MSU, forms a cytosolic multiprotein-complex called the inflammasome, leading to the activation of caspase- 1. Caspase-1 then cleaves the highly pro-inflammatory cytokines interleukin (IL)-1β and IL-18, leading to the secretion of their biologically active forms and culminating in an acute gout attack. This newfound molecular understanding of the pathology of gout has seen the introduction of IL-1 inhibitors as an improved treatment for acute gout with reduced side effects compared to conventional gout therapies.

The inflammatory process of gout and its treatment

Gouty arthritis is a characteristically intense acute inflammatory reaction that erupts in response to articular deposits of monosodium urate (MSU) crystals. Important recent molecular biologic advances in this field have given us a clear picture of the mechanistic basis of gouty inflammation. The innate immune inflammatory response is critically involved in the pathology of gout. Specifically, MSU crystals promote inflammation directly by stimulating cells via Toll-like receptor signaling and by providing a surface for cleavage of C5 and formation of complement membrane attack complex (C5b-9), culminating in secretion of cytokines, chemokines, and other inflammatory mediators with a dramatic influx of neutrophils into the joint. Despite the detailed mechanistic picture for gouty inflammation, there are no placebo-controlled, randomized clinical studies for any of the therapies commonly used, although comparative studies have demonstrated that many nonsteroidal anti-inflammatory drugs are equivalent to indomethacin with respect to controlling acute gouty attacks. In general, the first line of anti-inflammatory therapy for acute gout is nonsteroidal anti-inflammatory drugs, and the selective cyclo-oxygenase-2 inhibitor celecoxib can be used where appropriate. The second line of treatment is glucocorticosteroids, given systemically (oral, intravenous, or intramuscular) or intra-articularly. Alternatively, synthetic adrenocorticotropic hormone is effective, partly via induction of adrenal glucocorticosteroids and partly via rapid peripheral suppression of leukocyte activation by melatonin receptor 3 signaling. The third line of treatment is oral colchicine, which is highly effective when given early in an acute gouty attack, but it is poorly tolerated because of predictable gastrointestinal side effects.

Pathology of Gout

Pathology of Gout

THE ETIOLOGY AND PATHOLOGY OF GOUT.

THE ETIOLOGY AND PATHOLOGY OF GOUT.

THE ETIOLOGY AND PATHOLOGY OF GOUT.

(B) URIC-ACID METABOLISM IN GOUT AND THE THEORIES OF GOUT PRODUCTION. There is undoubtedly marked disturbance of nitrogenous metabolism in gout. Since the adoption of the classification of purins into the endogenous and varieties, too little time has elapsed and too few researches have been published to draw absolute conclusions as to how the metabolism of each is affected in this disease. The studies of Reach, Kaufmann, Vogt and Chalmers Watson show that in gout the exogenous nuclein is more slowly excreted than in health, and that in some cases there is a distinct retention. Vogt compared the results of rich purin-holding food on a gouty patient and a healthy individual at the same time. The gouty patient showed retention and delayed excretion of the purin bodies. It can be safely admitted, therefore, that exogenous purins lead to the excess of nuclein derivatives in the blood stream. It

A STUDY OF GOUT.

That the pathology of gout has not kept pace with the lines of distinction that have clinically been drawn, is much to be regretted, but we do know that it is the fibrous element which is most affected in chronic rheumatism, the synovial membrane with degeneration later on in the cartilage and bone in arthritis deformane, and the kidneys and blood primarily in gouty affections causing deposits of urates in the joints. If one should say that it was the uric acid in excess in the blood, in the form of urates, that was the cause of gout, he would very rightly be met with the assertion that there were other diseases with excess of urates in the blood and which did not have the manifestations of gout. A similar wrong conclusion would be to attribute the cause of arthritis deformane to micro-organisms, for it is known that the investigators

Recent Literature Gout: its Pathology and Treatment . Founded on the Gulstonian Lectures on "The Chemistry and Pathology of Gout," delivered by the Author before the Royal College of Physicians of London in 1897; with the Addition of some Recent Investigations concerning the Treatment of Gout, anda Detailed Account of the Treatment of the Various Forms of Gout. By Arthur

Recent Literature Gout: its Pathology and Treatment . Founded on the Gulstonian Lectures on "The Chemistry and Pathology of Gout," delivered by the Author before the Royal College of Physicians of London in 1897; with the Addition of some Recent Investigations concerning the Treatment of Gout, anda Detailed Account of the Treatment of the Various Forms of Gout. By Arthur

Gout, Its Pathology and Treatment.

The first part of this book is mainly a reproduction of the Goulstonian Lectures on "The Chemistry and Pathology of Gout," delivered in 1897. The second part discusses the causes, pathology, diagnosis and prognosis. The third is the important part of the book, in which the author gives the results of a large number of experiments made by himself to disprove many of the old theories believed in as to the cause of gout. Especially, he attempts to disprove the loss of alkalinity of the blood, as a cause, and shows that not only is the blood normal as to this condition, but that if it were not so it would not be conducive to the solubility of the sodium biurate. While he apparently shows by his experiments the untenableness of the older theories, he does not very satisfactorily give us anything in their stead. He discusses the effect of

The Chemistry and Pathology of Gout — Medical Notes

The Chemistry and Pathology of Gout — Medical Notes

The Goulstonian Lectures on the Chemistry and Pathology of Gout: Delivered before the Royal College of Physicians, March, 1897

The Goulstonian Lectures on the Chemistry and Pathology of Gout: Delivered before the Royal College of Physicians, March, 1897

The Goulstonian Lectures in the Chemistry and Pathology of Gout: Delivered before the Royal College of Physicians, March, 1897

The Goulstonian Lectures in the Chemistry and Pathology of Gout: Delivered before the Royal College of Physicians, March, 1897

The Goulstonian Lectures ON THE CHEMISTRY AND PATHOLOGY OF GOUT.

The Goulstonian Lectures ON THE CHEMISTRY AND PATHOLOGY OF GOUT.

The Goulstonian Lectures ON THE CHEMISTRY AND PATHOLOGY OF GOUT.

The Goulstonian Lectures ON THE CHEMISTRY AND PATHOLOGY OF GOUT.

The Goulstonian Lectures on the Chemistry and Pathology of Gout: Delivered before the Royal College of Physicians, March, 1897

The Goulstonian Lectures on the Chemistry and Pathology of Gout: Delivered before the Royal College of Physicians, March, 1897

The Goulstonian Lectures: ON THE CHEMISTRY AND PATHOLOGY OF GOUT

The Goulstonian Lectures: ON THE CHEMISTRY AND PATHOLOGY OF GOUT