Showing papers on "Fibrinoid necrosis published in 1978"

Pathology of the heart in Kawasaki disease.

Abstract: Pathologic studies were done on 20 hearts of patients who had typical clinical signs and symptoms of Kawasaki disease. The cardiac lesions were classified according to the duration of illness at the time of death. Stage I (zero to nine days) was characterized by acute perivasculitis and vasculitis of the microvessels (arterioles, capillaries, and venules) and small arteries, and acute perivasculitis and endarteritis of the three major coronary arteries (MCAs). Pericarditis, myocarditis, inflammation of the atrioventricular conduction system, and endocarditis with valvulitis were also present. Stage II (12 to 25 days) was characterized by panvasculitis of the MCAs and aneurysm with thrombus in the stems. Myocarditis, coagulation necrosis, lesion of the conduction system, pericarditis, and endocarditis with valvulitis were also present. In stage III (28 to 31 days), granulation of the MCAs and disappearance of inflammation in the microvessels were noted. Patients in stage IV (40 days to 4 years) had scarring with severe stenosis in the MCAs. Fibrosis of the myocardium, coagulation necrosis, lesions of the conduction system, and endocardial fibroelastosis were also present. The features observed revealed Kawasaki disease to be acute and inflammatory. The angiitis begins in the microvessels and fibrinoid necrosis of the media is rare. The disease is one with a pathologic pattern previously unknown.

Hypertensive encephalopathy: a clinicopathologic study of 20 cases.

Abstract: The clinical and pathologic findings in 20 patients with hypertensive encephalopathy were reviewed. The dominant central nervous system (CNS) symptoms were altered state of consciousness and severe headache. Nausea, vomiting, and visual disturbances were less common. Seizures and focal signs were infrequent. The changes seen were invariably accompanied both by the characteristic ophthalmoscopic alterations of malignant hypertension and by uremia. The neuropathologic changes consisted of severe vascular alterations (fibrinoid necrosis of arterioles, thrombosis of arterioles and capillaries), and of parenchymal lesions (microinfarcts, petechial hemorrhages) secondary to the vascular lesions. The vascular changes were not confined to the brain but were diffuse, affecting the eyes, kidneys, and other organs. In the CNS the brainstem was most severely affected. Cerebral edema was not observed, even in those patients who had increased cerebrospinal fluid pressure and papilledema.

Disseminated visceral giant cell arteritis: histopathologic description and differentiation from other granulomatous vasculitides.

Abstract: Disseminated visceral giant cell arteristic, a previously unknown entity, was observed in four autopsied patients, all men, aged 33, 67, 59 and 45 years. None of the patients had temporal arteritis, collagen disease, sarcoidosis, hepatitis or other infections, and vasculitis was diagnosed only after death. All had giant cell arteritis of extracranial arteries and arterioles in at least three of the following organs: the heart, lungs, kidneys, liver, pancreas, and stomach in various combinations. Despite some histopathologic similarities, disseminated visceral giant cell arteritis can be distinguished from other necrotizing and granulomatous vasculitides by the type of vessels principally affected and the presence or absence of giant cells, vascular fibrinoid necrosis and eosinophilic infiltrates. The observations suggest that it is a distinctive type of systemic vasculitis.

Adult Hemolytic Uremic Syndrome with Renal Arteriolar Deposition of IgM and C3

Abstract: Two cases of idiopathic adult hemolytic uremic syndrome in which deposits of IgM and C3 were identified in renal arterioles showing fibrinoid necrosis are reported. Fibrin was also identified in the lumina of the involved vessels, but there was no laboratory evidence of disseminated intravascular coagulation. In both cases, serum C3 was decreased and C4 was normal, suggesting involvement of the alternate pathway of complement activation. These two cases suggest that in some instances the adult hemolytic uremic syndrome may be immunologically mediated, and that renal vascular thrombosis is a secondary phenomenon.

Observations on the pathology of canine microsporidiosis

Abstract: The available literature on canine microsporidiosis indicates that this disease, primarily of young dogs, is a distinct clinicopathological entity. It has been confused with canine distemper and rabies, and must be differentiated from toxoplasmosis. Information available on the spectrum of pathological change associated with this disease is incomplete but a distinct pattern emerges from a study of the reports. The aetiological agent appears to have a predilection for the central nervous system and kidneys, but other tissues and organs, and especially the liver, may also be infected. Vasculitis and perivasculitis, which may include fibrinoid necrosis, seem to be a basic lesion. Cellular inflammation ranges from polymorphonuclear leukocyte infiltration in areas of necrosis to focal granulomas. There may be no cellular reaction to compact groups of organisms. Histopathological and ultrastructural studies of this case augment our knowledge of the pathological changes seen with canine microsporidiosis.

The electron microscopy of "fibrinoid necrosis" in pulmonary arteries.

Abstract: Fibrinoid necrosis was induced in the pulmonary arteries of five male Wistar albino rats by feeding them on a diet adulterated by the addition of 0.07% ground Crotalaria spectabilis seeds by weight. Electron microscopy of the arteries affected by the process showed fibrin in the thrombus occluding their lumens and in the arterial intima, held up from further penetration of the media by the inner elastic lamina. Naturally occurring gaps in this lamina were found, and it is postulated that they determine the characteristic histological configuration of fibrinous vasculosis. The smooth muscle cells of the media of the pulmonary veins showed clear evaginations, devoid of myofilaments and organells, indicative of sustained constriction compatible with viability of the cells. In contrast, the smooth muscle cells of the media of the pulmonary arteries showed loss of myofilaments leading to frank necrosis. Other cells seen in the media include fibrocytes and "vasoformative reserve cells." The authors consider that the latter have considerable and varied potential. Once liberated during the process of fibrinoid necrosis in the arterial media they may play an important part in pulmonary vascular pathology as, for example, in the formation of the plexiform lesion.

Allergic granulomatous angiitis.

Abstract: A 15-year-old boy died after a 3 years' illness; asthmatic bronchitis, recurrent heart failure and eosinophilia were the essential manifestations. The autopsy elicited a diagnosis of allergic granulomatous angiitis, because of angiitis with fibrinoid necrosis and granulomatous lesions in vascular and extravascular regions. The most important differential diagnostic aspects of this disease are discussed, especially the resemblances to Wegener's granulomatosis, hypersensitivity angiitis and polyarteritis nodosa.

Radiation nephritis and intravascular coagulation.

Abstract: A 23 year old male with embryonal cell carcinoma of the testicle was treated with radiation, receiving 2250 Rads to his abdomen twice, only once with kidney shielding. He developed acute renal failure approximately eleven months later. Associated with the renal failure were hemolytic anemia, thrombocytopenia, hypofibrinogenemia, and other evidence for intravascular coagulation. The kidney biopsy showed fibrinoid necrosis of arteries and arterioles. By electron microscopy, there was extensive endothelial cell damage and subendothelial electron lucent material compatible with radiation nephritis. The renal pathologic abnormalities suggest that the local renal vascular injury induced by radiation could have been responsible for intravascular coagulation in the kidneys and the systemic hematologic abnormalities. Prednisone appeared to accelerate the renal and hematologic dysfunction and heparin is proposed as a more promising therapy.

Thiamine deficiency encephalopathy in a specific-pathogen-free cat colony.

Abstract: Thiamine deficiency encephalopathy occurred in a specific-pathogen-free cat colony where the diet consisted exclusively of commercially canned diet. This product was described by the manufacturer as a complete diet for cats. The clinical diagnosis was confirmed by the demonstration of bilaterally symmetrical hemorrhage and microvascular fibrinoid necrosis in the brain and low erythrocyte transketolase levels. Treatment of clinically ill cats with vitamin B complex was followed by recovery within 24 hours.

Arteriolar Nephrosclerosis in the Syrian Hamster

Abstract: Syrian hamsters developed spontaneous renal lesions that resembled those of arteriolar nephrosclerosis in man, and differed from other spontaneously occurring or virus-induced renal diseases in other rodent species. Morphologic changes were mainly degenerative with little cellular exudation and were associated with histologic changes in the intrarenal vasculature. The renal lesions were progressive, often fatal and sometimes were complicated by glomerular amyloidosis with the nephrotic syndrome and uremia. Endstage kidneys often had fibrinoid necrosis of intrarenal arterioles and thus resembled lesions characteristic of the malignant phase of human essential hypertension. Fibrinoid necrosis of small arterioles was common in the uterus, ovaries or testes of affected animals; it was less frequent in mesenteric or coronary vessels. Cardiac thrombosis, often involving the left atrium or left atrioventricular valves, also was common. Changes occurred earlier and often were more severe in females than in males. This disease was a major cause of morbidity and mortality and hampered life-span studies.

Hypersensitivity reaction to allopurinol

Abstract: Major hypersensitivity reactions to allopurinol are rare. They are characterized by systemic vasculitis associated with a grave clinical picture. 20 days after beginning treatment with allopurinol, a 70-year-old patient presented with a maculo-papular, erythemato-squamous eruption which developed into erythroderma with fever, edema, polyadenopathy, marked eosinophilia, cholostatic jaudice, and aggravation of preexisting renal insufficiency. Skin biopsy showed vasculitis with fibrinoid necrosis and a chiefly lymphocytic infiltrate suggestive of a malignant lymphoma-type process. As soon as allopurinol was discontinued, and without steroid treatment, the patient spontaneously recovered. A lymphocyte transformation test was positive for this drug. The poorly know mechanism is immunological, with formation of immune complex deposits on the endothelial cells and at the dermo-epidermal junction, fibrinoid necrosis of small vessels and cellular reaction which is lymphocytic. It is not a toxic reaction related to the dose administered, though most authors have emphasized that preexisting renal insufficiency could favor hypersensitivity to allopurinol.

Pathology of malignant nephrosclerosis with special reference to the difference between histologic manifestations of pure and exacerbated forms.

Abstract: Fourteen autopsied cases of malignant nephrosclerosis were classified into 6 of pure form in which syndrome of malignant hypertension developed from the beginning of the disease, and 8 of exacerbated form with appearance of the syndrome in the course of essential hypertension. Pathohistological study of these cases elucidated the differences in histologic manifestations between pure and exacerbated forms of malignant nephrosclerosis as to which little had been known as yet. In the pure form arterioles and small arteries characteristically demonstrated acute or recent lesions such as fibrinoid necrosis and hemorrhage into intima, and intimal cellular hyperplasia of somewhat longer duration, whereas in the exacerbated form coexistence of vascular lesions of various intensities and durations, acute (fibrinoid necrosis and hemorrhage), intermediate (intimal cellular hyperplasia) to chronic (sclerosis and lamellar elastosis), and superposition of more recent vascular lesions on more advanced or older ones were noted. Superposition of vascular alterations was interpreted to be not necessarily specific for exacerbated form but histologic manifestation of recurrence which is liable to be the case more frequently in exacerbated form than in pure form in the longer course of essential hypertension or of malignant hypertension. Some other related problems were also considered and discussed.

Renal Changes Caused by Vascular Disease

Abstract: Renal vascular changes are strikingly common. Very often they arise secondarily in association with other renal diseases and lead to further parenchymal damage so that very complex findings are generated.

The myocardiopathies of systemic lupus erythematosus

Abstract: Myocardial involvement in lupus erythematosis takes the form of an interstitial myocarditis with cellular infiltration and fibrinoid necrosis The most lesions are perivascular, and involve the arterioles The myocardial fibres are involved secondarily to the vascular lesions, or by grossly, damaging sclerosis The clinical features are variable:--no clinical features, but haemodynamic evidence of abnormal ventricular function, and perhaps sudden death;--arrhythmias and disorders of atrio-ventricular conduction;--cardiac failure, which may be due to a genuine cardiomyopathy (a part may be played by hypertension, pulmonary hypertension, renal failure, constrictive pericarditis or haemodynamically major valve disorders);--abnormalities of the coronary trunk in a certain number of cases If anti-nuclear antibodies are present in a cardiomyopathy, the presence of DLE or of a drug-induced lupus syndrome must be suspected There remain some awkward cases which defy classification, and which systematic use of echocardiography and pericardial and myocardial biopsy may be able to define more accurately

Marked hyperbilirubinemia with Gilbert syndrome and immunohemolytic anemia

Abstract: The etiology of pulmonary hemorrhage in lupus is unclear. Fayemi 7 identified fibrinoid necrosis and vasculitis in pulmonary vessels of autopsied patients. Reports of electron-dense deposits in alveolar basement membranes observed by electron microscopy, low levels of C3, and the occurrence of pulmonary hemorrhage during the acute phases of SLE suggest that pulmonary hemorrhage may result from vascular injury mediated by immune complexes. Hemoptysis in a patient with SLE is more commonly associated with pulmonary infection, pulmonary emboli, and congestive heart failure. To ensure appropriate therapy, each of these possibilities must be investigated in the patient who has SLE with hemoptysis. However, pulmonary hemorrhage per se is a known, but often fatal, complication of SLE and prompt recognition is essential; early diagnosis and prompt treatment with steroids and positive end expiratory pressure, and concomitant therapy of thrombocytopenia with platelet transfusions, permitted the survival of our patient.

An accelerated hypertension with neither malignant nephrosclerosis nor elevation of plasma renin activity.

Abstract: A case of accelerated hypertension, which was unique in a resistance to an angiotensin antagonist, and a lack of the elevation of plasma renin activity (PRA) is reported. Non-elevated PRA was coincided with non-malignant nephrosclerosis in renal histology. The acceleration was attributed to the neurological cause i.e., cerebral hemorrhage in the right hypothalamus which extended to the ventricle and subarachnoid space. The case therefore clinically seemed malignant-like, but it was not malignant hypertension in the sense of Volhard's classical definition. This does not conflict with the usefulness of the determination of PRA in the diagnosis of malignant hypertension with nephrosclerosis.