Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Early in the acute phase of myocardial infarction the phenomenon of expansion may occur, with regional thinning and dilatation of necrotic region. This complication may be detected by echocardiography since the first hours of infarction. During the two subsequent weeks, an additional increase of left ventricular volume may occur, due to an increase of length of the infarcted segments and, as well, of the contractile segments which suffer a "volume overload hypertrophy". This is the phenomenon of remodeling. Finally during the first year post infarction, a progressive left ventricular dilatation may develop. This late dilatation seems to be due to an increase of perimeter of the contractile regions only. By the time this topographic changes have occurred, the left ventricle assumes a more spheric configuration. Left ventricular dilatation affects adversely cardiac function, with higher incidences of heart failure and death. Experimental and clinical studies show that, in selected patients, remodeling and ventricular dilatation may be attenuated by the administration of angiotensin-converting-enzyme inhibitors, with better indices of left ventricular function. Final results of several on-going multicenter studies are awaited for; they will allow a better definition of the role of ACE inhibitors on prevention and treatment of left ventricular dysfunction after myocardial infarction.
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PMID:[Expansion of infarction, dilatation and ventricular remodelling. Therapeutic potential of angiotensin-converting enzyme inhibitors]. 161 Jun 13

A collagen network, composed largely of type I and III fibrillar collagens, is found in the extracellular space of the myocardium. This network has multiple functions which includes a preservation of tissue architecture and chamber geometry. Given its tensile strength, collagen is a major determinant of tissue stiffness. Its disproportionate accumulation, in the form of either a reactive or a reparative fibrosis, further increases stiffness. A degradation of collagen tethers, on the other hand, is an anatomic requisite for a distortion in tissue architecture and a reduction in stiffness that can lead to chamber dilatation, wall thinning, and even rupture of the myocardium. Collagen turnover in the myocardium is dynamic. When synthesis exceeds degradation, an adverse accumulation of collagen appears to distort tissue structure. This is true for either the hypertrophied and/or nonhypertrophied ventricle. Factors that contribute to the appearance of myocardial fibrosis are largely different from those that promote cardiac myocyte growth. Included amongst these fibrogenic factors are effector hormones of the reinin-angiotensin-aldosterone system (RAAS). Studies conducted both in intact animals (relative to dietary sodium intake) and in cultured adult cardiac fibroblasts have pointed toward the association between collagen accumulation and chronic elevations in circulating angiotensin II and aldosterone. A tissue hormonal system involving angiotensin II, endothelins and bradykinin, may likewise regulate fibrogenesis. In this regard, angiotensin converting enzyme is found in connective tissue of the normal heart, including the matrix of heart valves and the adventitia of the intramural coronary arteries, and fibrous tissue that forms following infarction or with chronic RAAS activation. The importance of ACE in the regulation of local angiotensin II and bradykinin levels and their contribution to collagen turnover is a fruitful area of research with important clinical implications. The myocardium also contains a proteolytic system, including collagenase. The characteristics and regulation of matrix metalloproteinases and their tissue inhibitors in various cardiovascular disease states requires further investigation.
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PMID:Collagen network of the myocardium: function, structural remodeling and regulatory mechanisms. 802 11

We encountered a case of granulomatous tubulointerstitial nephritis in a patient with sarcoidosis, who was also found to show an elevated serum titer of anti-glomerular basement membrane (GBM) antibody. The serum creatinine level had been documented to be within normal range 8 months before the first visit. Gallium scintigraphy revealed bilateral kidney uptake, but no uptake in the pulmonary hilum. No typical findings of sarcoidosis, e.g., bilateral hilar adenopathy, uveitis or elevated serum ACE level were recognized in the early stage. Echocardiography showed basal thinning of the interventricular septum, a specific feature of cardiac sarcoidosis, and hilar lymph node uptake on gallium scintigraphy and anterior uveitis appeared during the disease course. Active tuberculosis, fungal infection, vasculitis and malignancy were clinically excluded. We performed a renal biopsy. Light microscopy revealed non-caseating granulomatous tubulointerstitial nephritis with multinucleated giant cells and normal glomeruli. Inflammatory reaction was seen only within the interstitial tubules. The serum creatinine level had increased to 4.52 mg/dl. The patient was administered methylprednisolone pulse therapy, followed by administration of oral prednisolone. The renal function improved immediately in response to this therapy. Based on the above, we made the final diagnosis of granulomatous tubulointerstitial nephritis associated with sarcoidosis. While the serum titer of anti- GBM antibody was elevated, to our surprise, renal biopsy did not reveal linear anti-GBM antibody staining in this case. Furthermore, interestingly, the serum anti-GBM antibody titer in our patient decreased in parallel with the clinical improvement of sarcoidosis. Severe and progressive renal dysfunction was the most prominent clinical feature without other organ manifestations in our patient, which is a rare occurrence in sarcoidosis.
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PMID:A case of acute kidney injury caused by granulomatous tubulointerstitial nephritis associated with sarcoidosis and concomitant presence of anti-glomerular basement membrane antibody. 2684 5