Showing papers on "Fibrinoid necrosis published in 1985"

Vascular changes in radiation bowel disease

Abstract: A series of 20 cases of radiation bowel disease (RBD) was studied qualitatively and the arterial changes were studied quantitatively. A control series of 45 cases was studied. In the control cases there were positive correlations between the medial thickness of all vessels studied and the diastolic blood pressure as well as the incidence of intimal fibrosis in both intramural and extramural arteries. The medial thickness in all the arteries in cases of RBD was significantly higher than in the controls. This was probably due to the large number of fibrin thrombi which increased the vascular resistance. The degree of intimal fibrosis of the intramural arteries and arterioles was significantly greater than in the controls. Similarly the incidence of intimal fibrosis in all arterioles and intramural arteries was greater than the control group. The degree of intimal fibrosis was related to the dose of radiation received. The effect of radiation was an on-going process since the percentage of arterioles with intimal fibrosis increased with the time after radiotherapy. Blood pressure and age played no part in these correlations in RBD. The most consistently observed qualitative changes in RBD were in the arteries, arterioles and to a lesser extent the veins. These showed fibrin thrombi, fibrinoid necrosis, subendothelial oedema and fibrin. Various stages of healing were seen in the vessels. We believe that the blood vessels are the main site of injury in RBD and that the endothelial cell is the initial target for radiation damage.

Clinical and Histopathologic Spectrum of Necrotizing Vasculitis: Report of Findings in 101 Cases

Abstract: • Clinical and histopathologic features of 101 cases of necrotizing vasculitis were selected on the basis of the following histopathologic criteria: fibrinoid necrosis of blood vessel walls, endothelial cell hyperplasia, and an infiltrate within and around the blood vessel walls predominantly of polymorphonuclear leukocytes. There were three clinical patterns of vasculitis: (1) associated with other coexistent disease, (2) associated with known precipitating events, and (3) idiopathic. Two histologic features were particularly notable in view of the clinical findings. First, vasculitis extending deep into the reticular dermis or subcutaneous tissue seemed to be associated more often with systemic disease such as malignancy or connective tissue disease. Second, in biopsy specimens from patients with hypocomplementemia, the inflammatory infiltrate was composed almost exclusively of neutrophils, as compared with the mixed infiltrate seen in normocomplementemic vasculitis. ( Arch Dermatol 1985;121:220-224)

Eosinophilic angiocentric fibrosis of the upper respiratory tract: a mucosal variant of granuloma faciale? A report of three cases.

Abstract: Three patients with an unusual stenosing lesion affecting the upper respiratory tract are described. The lesion involved the mucosa of the nasal septum and lateral nasal wall in two cases and the mucosa of the sub-glottic region of the larynx in one. The lesion leads to thickening of the sub-mucosal connective tissues by an usual pathological process. It begins as a focal peri-vascular sub-epithelial exudate of eosinophils accompanied by collections of plasma cells and lymphocytes without fibrinoid necrosis. These foci progress to form extensive areas of peri-vascular fibrosis showing a characteristic angiocentric whorling with an 'onion-skin' pattern. This process leads to thickening and matting of the mucosa which becomes adherent to the underlying structures. As fibrosis progresses, the lympho-plasmacytic component regresses but the eosinophils remain. The fibrosis does not resolve and the consequent stenosis requires surgical relief. No other site appears to be affected by this process, but one case was associated with granuloma faciale. The cause is unknown. We have given the term 'eosinophilic angiocentric fibrosis of the upper respiratory tract' to this condition to encompass its cardinal features.

Comparison of primary plexogenic arteriopathy in adults and children. A morphometric study in 40 patients.

Abstract: Pulmonary vascular changes were studied in histological sections from 15 children and 25 adults with primary plexogenic arteriopathy. The severity of medial hypertrophy and degree of vasoconstriction were measured in histological sections and there was a close correlation between these two variables in both children and adults. More advanced arterial changes, expressed as an index of pulmonary vascular disease, were more common in adults, and their severity correlated positively with the degree of medial hypertrophy. No such correlation was found in children. There were similar numbers of plexiform lesions per square centimetre in children and adults, so that the differences in the indices of pulmonary vascular disease were mainly due to the intimal changes. Concentric laminar intimal fibrosis was more severe in adults. It is suggested that intensive spastic vasoconstriction results in the development of fibrinoid necrosis and subsequently of plexiform lesions and that this may happen irrespective of the presence of severe intimal fibrosis. This suggests that children with primary plexogenic arteriopathy in whom plexiform lesions have not yet developed are more likely to respond to vasodilator treatment than are adults in whom irreversible changes associated with intimal fibrosis have developed.

Pathophysiological events leading to the end-organ effects of acute hypertension

Abstract: The term "hypertensive crisis" refers to a group of acute hypertensive disorders that have, in common, evidence of end-organ dysfunction. From a pathophysiological viewpoint, these disorders may be classified into two major categories. In primary hypertensive disorders, the predominant pathophysiological events and subsequent end-organ failure are directly attributable to the uncontrolled hypertension. Secondary hypertensive crises have many similar features; however, the ultimate progression from onset of hypertension to end-organ failure tends to be modified by concurrent target-organ disease. The chain of events leading to the progression from benign to malignant hypertension centers around two general theories--the pressure hypothesis and the humoral hypothesis--both of which suggest that when a critical imbalance of pressure and/or humoral factors occurs, depending variously on etiological factors, rapidity, and degree and duration of blood pressure elevation, a series of pathological events ensue leading to myointimal proliferation and fibrinoid necrosis. The primary target-organ effects of severe hypertension generally affect the central nervous, renal, and cardiovascular systems and occur when the normal compensatory mechanisms are exceeded either by a breakthrough in autoregulation, as in the central nervous system, or by an imbalance in myocardial supply and demand. To a certain extent the pathophysiological events and target-organ susceptibility will determine the manner in which the hypertensive event presents. Although effective therapy is optimally tailored to the specific underlying disease process, in the acute setting, where important clinical data may be lacking, an appreciation of these underlying mechanisms will aid in the selection of a regimen that is both safe and effective.

Mastitis associated with ovine progressive pneumonia virus infection in sheep.

Abstract: Vasculitis, involving small muscular arteries and arterioles, was found in 5 of 18 sheep naturally infected with ovine progressive pneumonia (OPP) virus and in 5 of 11 sheep experimentally infected with OPP virus. In order of frequency, arterial lesions were seen in carpal joint capsules, kidneys, meninges, brains, lungs, and tracheas. The lesions were intramural edema and hemorrhage, mononuclear cell infiltration, fibrinoid necrosis of media, and thrombosis. The vascular lesions were frequently associated with interstitial pneumonitis, arthritis, and encephalitis also induced by OPP virus.

Open lung biopsies in congenital heart disease for evaluation of pulmonary vascular disease. Predictive value with regard to corrective operability.

Abstract: For evaluation of pulmonary vascular disease 140 open lung biopsies were performed in 137 patients with congenital heart disease in order to decide whether the state of the lung vessels would allow corrective surgery. As far as possible follow-up was obtained in patients who underwent a cardiac repair. From the study of these biopsy specimens it appeared that medial hypertrophy of pulmonary arteries and changes in pulmonary veins should not be considered an impediment for a corrective operation as long as more advanced changes are absent. The same is true for intimal thickening due to longitudinal smooth muscle, post-thrombotic changes or cellular proliferation. Concentric-laminar intimal fibrosis forms no contra-indication as long as it is mild but, if severe, it is likely that hypertensive pulmonary vascular disease will progress in spite of cardiac repair. In the presence of fibrinoid necrosis or plexiform lesions correction of a cardiac anomaly should not be attempted. The presence of dilatation lesions is more disputable but probably, as long as they are scarce and not accompanied by fibrinoid necrosis or plexiform lesions, corrective surgery may be attempted. This becomes very dubious when they are more numerous.

Cardiovascular lesions in collagen-vascular diseases.

Abstract: In this review, the cardiac lesions which develop in association with the various collagen-vascular diseases are described. In rheumatoid arthritis, the most frequent lesions are: fibrous obliterative pericarditis, with pericardial deposits of calcium, fibrin, cholesterol, and rheumatoid granulomas; granulomatous or nonspecific myocarditis; valvulitis, vasculitis, and amyloid deposits. In ankylosing spondylitis, the lesions involve mainly the valves (aortic and mitral valves) and the aorta. In systemic lupus erythematosus, the predominant cardiovascular lesions are: pericarditis, Libman-Sacks endocarditis, nonspecific myocarditis, vasculitis with fibrinoid necrosis, and acceleration of atherosclerosis. In scleroderma, the main cardiac lesion is fibrosis with only scanty inflammatory cells; pericarditis and nonbacterial thrombotic endocarditis also occur. In dermatomyositis/polymyositis, fibrous or fibrinous pericarditis can occur, as well as myocarditis with infiltrates of lymphocytes and plasma cells and with degeneration and necrosis of myocytes; valvulitis is uncommon except when the disease is related to mucinous adenocarcinoma. In polyarteritis nodosa, various stages of necrotizing vasculitis involve all layers of the arterial walls; foci of myocardial necrosis of various sizes can occur in association with these lesions; cardiac hypertrophy related to hypertension and pericarditis related to uremia, may also be found. In Wegener's granulomatosis, pericarditis, inflammatory infiltrates, necrotizing granulomas, and vasculitis have been observed in the heart.

Cerebral arteries in hypertension: structural and hemodynamic aspects.

Abstract: Chronic hypertension is associated with structural alterations in the cerebrovascular bed, with increased vessel wall thickness and media/lumen ratio over a large range of arterial sizes. In the relaxed cortical surface arteries of spontaneously hypertensive rats and in some segments of the basal arteries, the enlarged media encroaches on the lumen. The altered vessel geometry increases the steepness of the resistance curve and enables the blood vessels to withstand higher intraluminal pressure. On the other hand, the risk for ischemic complications is increased because of an elevated minimal resistance. Pathological, degenerative changes occur when the compensatory mechanisms are insufficient to protect the microvessels from the pressure increases. Small intraparenchymatous cerebral arteries develop hyaline degeneration, fibrinoid necrosis, and microaneurysms with the appearance of hemorrhages and lacunae. Hypertension predisposes for atherosclerosis in the cervicocranial and intracranial basal arteries, increasing the risk for large hemispheric infarcts and transitory ischemic attacks. Stenosis/occlusion of the arteries and embolization from an atheromatous plaque might have a larger impact on the hypertensive than the normotensive brain because of less efficient collateral circulation related to the altered vessel geometry.

Necrotising glomerulonephritis associated with cholesterol microemboli.

Abstract: Embolisation of cholesterol in the kidneys may result in severe, irreversible renal failure. Antemortem diagnosis can sometimes be established by renal biopsy when characteristic crystalline clefts are seen in arterial lumens and ischaemic changes in the renal parenchyma. Although fibrinoid necrosis of small vessels has been associated with microemboli of cholesterol, necrotising angiitis in the kidney has not been reported as a manifestation of cholesterol embolisation. We describe a case of necrotising glomerulonephritis associated with cholesterol microemboli in an elderly man with extensive aortic atheromatosis.

Chronic ophthalmic Wegener's granulomatosis.

Abstract: A case of Wegener's granulomatosis is reported which manifested episcleritis followed by scleritis, and followed in turn by separate episodes of right and left orbital pseudotumor spanning 15 years prior to respiratory tract disease. The unusually protracted progression of symptoms in this case may be explained on the basis of the histopathological findings. Areas of fibrinoid necrosis of connective tissue occurred alone or alternated with areas of nongranulomatous fibrinoid necrosis of blood vessel walls. Granulomatours vasculitis was not observed. This histopathological picture is pathognomic of early cases of Wegener's granulomatosis which run especially protracted courses.

Coronary arterial lesions in Mg-deficient hamsters.

Abstract: Dietary Mg deficiency is thought to promote coronary artery spasm, probably through Ca overloading of vascular smooth muscle (VSM) cells. We now report the demonstration of a coronary arteriopathy in hamsters fed a Mg-deficient diet for 10 days or more. Affected arteries showed endothelial and VSM cell hyperplasia and pleomorphism, chronic inflammation of the media and adventitia, and fibrinoid necrosis. Lesions of myocardial ischemia, distinct from the well-known lesions of myocardial necrosis and calcification common in Mg deficient animals, were also present. Von Kossa positive granules were found in the VSM of Mg-deficient, but not control, hamsters. This vasculopathy is a new factor to be considered in the pathophysiology of Mg deficiency. It is consistent with the view that Ca loading of VSM plays an important role in this condition and could be related to the occurrence of coronary artery spasm.

Cardiac lesions of selenium-vitamin E deficiency in animals.

Abstract: Necrosis of myocardium and skeletal muscle is a consistent finding in the numerous animal species in which spontaneous or experimental selenium-vitamin E (Se-E) deficiency has been described. Etiologic factors in the development of these lesions include: low dietary levels of Se, vitamin E, and sulfur-containing amino acids; high dietary concentrations of polyunsaturated fats; exposure to prooxidant conditions (toxicity by O2, O3, Fe, doxorubicin, and radiation injury); and intake of Se antagonists (Ag, Cu, Co, Cd, Te, Sb, and Zn). Myocardial lesions in Se-E deficient animals are most frequently seen in calves, lambs, turkey poults, and ducklings. In calves and lambs with cardiac lesions, the clinical finding usually is sudden death after vigorous exercise. At necropsy, affected calves have areas of necrosis and calcification in the left ventricular free wall and ventricular septum, while in lambs these lesions are seen in the right ventricular subendocardium. Histologically, areas of myocardial damage have hyaline necrosis with or without calcification, subsequent macrophagic invasion, and eventual fibrosis. In growing pigs, the hearts may have scattered pale streaks in the ventricular myocardium, but the most striking alterations are widespread epicardial and myocardial hemorrhages ("mulberry heart"). Histologically, both vascular and myocyte lesions are present. Vascular changes include fibrinoid necrosis of small arteries and arterioles and fibrin microthrombi in capillaries. The myocyte lesions in pigs and in birds consist of multifocal hyaline necrosis with calcification, followed by macrophagic invasion and fibrosis. Ultrastructural study of these lesions reveals myocyte alterations, which include mitochondrial swelling and mineralization, myofibrillar lysis, and necrosis with contraction bands.

Immunohistochemical findings in rheumatoid nodules.

Abstract: Eighteen nodules from patients with rheumatoid disease were studied histologically and immunohistochemically A continuum of microscopic changes was observed with varying degrees of fibrinoid necrosis, mononuclear cell infiltration and healing by fibrous scarring In two cases there was focal evidence of arteritis Fibrin was plentiful in the necrotic areas of nodules Small amounts of immunoglobulin were identified in plasma cells and as irregular extracellular deposits in and around areas of necrosis In a single small vein abnormal IgG was detected Mononuclear cells surrounding areas of necrosis stained strongly with antisera to ferritin and a cytoplasmic macrophage antigen, stained variably with muramidase (lysozyme) and negatively with alpha-1 antitrypsin antibodies Perls' stain for ferric iron was almost entirely negative and ultrastructural x-ray microanalysis indicated that the cytoplasm of these cells were entirely free of iron These findings confirm the chronic inflammatory nature of rheumatoid nodules but provide no support for the view that they originate in areas of vasculitis A relative lack of cytoplasmic antiprotease along with a strong expression of ferritin appears to be a characteristic feature of macrophages in rheumatoid tissue

Necrotic changes of the spinal cord with immune-complex-mediated disseminated vasculitis in a case of atypical allergic encephalomyelitis.

Abstract: A 42-year-old woman demonstrated recurrent, progressive neurological symptoms of peripheral and central nervous system damage of undefined infectious origin. Laboratory investigations showed abnormalities in the CSF and serum, suggesting subacute viral infection. Neuropathological examination revealed complete, widespread necrosis in the cervical and thoracic segments of the spinal cord with mononuclear and microglial infiltrations. There was pronounced thickening and fibrinoid necrosis of the vessel walls with mononuclear cuffs along the spinal cord. Dispersed, similar but less intensive inflammatory changes were present in the medulla oblongata, midbrain and basal ganglia. Surprisingly, there was diffuse demyelination with only slight glial and inflammatory reactions throughout the white matter of both hemispheres. The finding of coarse- and fine-grained deposits of IgG and C3 component of complement in the vessel walls of the spinal cord and vasa nervorum of cervical roots and peripheral spinal nerves, together with positive heterologous complement binding and the results of glycine-HC1 buffer elution, suggested immune-complex-mediated disseminated vasculomyelinopathy of the CNS and PNS. Consequent local ischemic changes and hypersensitivity phenomena led to frank necrosis of the cervical spinal cord and to extreme white matter demyelination in the brain. The case was diagnosed as allergic encephalomyelitis in which diffuse demyelination occurred coincidentally with spinal cord necrosis.

Echocardiographic manifestations of nonrheumatic aortic regurgitation

Abstract: Recently, the frequency of nonrheumatic aortic regurgitation (AR) has apparently increased, accompanied by a decrease in frequency of rheumatic fever. The purpose of the present study was to ascertain the echocardiographic features of nonrheumatic AR. We had 24 surgically- or autopsy-proven cases of nonrheumatic AR admitted during a two year period. These were 10 cases of infective endocarditis (IE), five with ventricular septal defect of type I, three with syphilis, and two with prosthetic valve malfunctions, and the remainder five were difficult to diagnose clinically. These five were three men and two women, whose ages ranged from 40 to 67 years and averaged 50 years, and their final diagnoses were annulo-aortic ectasia (AAE), Behcet's disease, and the aortitis syndrome (Takayasu's arteritis), and two other cases were of unknown etiology. The echocardiographic manifestations were compared with the operative, autopsy, and pathological findings. Echocardiographically, there were few or no increased intensities of aortic valvular echoes, and aortic roots had a tendency to dilate, leading to the failure of coaptation of valve leaflets, for a relative lack of valvular surface area to cross-sectional area of the aortic ring. Three of the five had flail aortic valves and three had associated MVP. Three were diagnosed as floppy aortic valves at the time of surgery. Excised valves revealed little hyperplasia or sclerosis grossly. Fibrinoid necrosis or mucoid degeneration were noted by light microscopy. Some specimens of aortic walls also revealed cystic medial necrosis or disruption of elastic fibers. All these findings were based on degenerative processes of connective tissue, and not on inflammatory processes. These pathological findings and the coexistence of mitral valve prolapse (MVP), which were not regarded as coincidental, suggest that connective tissue fragility--congenital or acquired--may play an important role in the genesis of nonrheumatic AR.

[Intestinal involvement in Behçet's syndrome].

Abstract: Intestinal lesions in Behcet's syndrome are much more common in Japan than in the Western World Colonic or ileo-colonic lesions develop after several years of recurrent aphthae and are manifested by acute complications, such as perforation or massive haemorrhage, or by protracted haemorrhagic diarrhoea with progressive deterioration of the patient's general condition Radiological and endoscopic findings are similar to those of severe acute colitis, such as ulcerative colitis or Crohn's disease The diagnosis of Behcet's syndrome involving the bowel rests on the presence of numerous extra-intestinal lesions and of extensive colonic ulceration often located in otherwise healthy parts of the mucosa Histology shows, beside a non-specific inflammatory infiltrate affecting the entire wall of the colon, lesions of vasculitis and perivasculitis with images of leucocytoclasia and fibrinoid necrosis Surgery is often necessary, requiring wide intestinal resections and long-term derivation ileostomies because of the high incidence of recurrent ulcers at the site of anastomosis, where fistulae may also develop

Morphological characteristics of hemorrhagic myocardial infarction

Abstract: The main features of hemorrhagic myocardial infarction (HMI) are presented basing on the light and electron microscopic study of 32 cases. HMI is distinguished macroscopically from the ischemic infarction by its dark-red colour due to a diffuse hemorrhagic imbibition and by the clear borders already seen within, the first hours of the disease. Histologically HMI is distinct due to the fibrinoid necrosis of the walls of small arteries, capillaries and, first of all, veins with their thrombosis. This results in the increasing vessel permeability, large hemorrhages into the interstitium with the fibrin deposits and the penetration of erythrocytes and fibrin into cardiomyocytes. Pathogenetic peculiarity of HMI is the blockade of the microcirculatory and venous bed in the background of normal coronary circulation. These events develop probably primarily in natural course of HMI and secondarily when fibrinolytic therapy is used. The thrombi of big arteries found in 9 out of 32 cases seem to arise secondarily in the background of the altered venous circulation. Possible causes of the microcirculatory-venous blockade in HMI may be persistent angiospasm, alteration of the blood coagulation, complications of the fibrinolytic therapy as well as toxicoallergic reactions and microembolism.

Immune Complexes, Vasoactive Mediators, and Fibrinoid Necrosis in Connective Tissue Diseases

Abstract: Although the inflammatory mechanisms operative in the various connective tissue diseases are all different, there are certain features common to many of them. These include tissue deposition of circulating immune complexes, a vasculopathy, and fibrinoid necrosis of the surrounding tissue. Other chapters in this text deal with immune complexes, activation of complement, and recruitment and activation of neutrophils, all of which are important aspects of immunologically mediated inflammation. This chapter focuses on the tissue deposition of immune complexes, the role of vasoactive factors in the inflammatory response, and the interrelationship of these events with coagulation and fibrinolysis to cause fibrinoid necrosis.

Inflammatory Myopathy II

Abstract: Minor inflammatory changes may be found in muscle in connective disease without the full clinical and pathological picture of polymyositis. It seems logical to consider polymyalgia rheumatica with this group, although genuine myositis is most unusual. Inclusion body myositis is also usually included with the inflammatory myopathies, but despite the name, its qualifications are rather slight.