Showing papers on "Fibrinoid necrosis published in 1981"

Renal localization of the membrane attack complex in systemic lupus erythematosus nephritis.

Abstract: The membrane attack complex (MAC) of the complement system was localized in both glomeruli and peritubular regions of 22 kidneys manifesting systemic lupus erythematosus (SLE) nephritis. A similar distribution was observed for immune complex markers (IgG, Clq, and C3) and MAC in glomeruli, although the deposits of MAC were more discrete and showed lesser immunofluorescence staining intensity compared with immunoglobulins and complement components. In contrast, peritubular immune complexes were present in only 7 out of 22 kidneys, involved comparatively small clusters of tubules, exhibited weaker immunofluorescence staining than MAC, and failed to correlate with interstitial foci of inflammation. Granular or irregular, linear aggregates of the MAC were observed at the periphery of larger groups of tubules contiguous to areas of interstitial inflammation. Comparable amounts of IgG, Clq, C3, and MAC were present in blood vessel walls in areas of fibrinoid necrosis. These data suggest that the MAC is a direct mediator of tissue injury occurring in renal glomeruli, tubules, and blood vessels. The discordance between immune complexes and MAC localized in the peritubular region, but not in glomeruli or blood vessels, raises the possibility that both immune complexes and nonimmune agents, such as bacterial antigens, may activate the classical or alternative complement pathways and thereby play a role in the pathogenesis of tubulointerstitial lesions of SLE nephritis.

Vascular changes underlying cerebral lesions in stroke-prone spontaneously hypertensive rats. A serial section study.

Abstract: The relationship of the vascular changes to the cerebral lesions has been studied using serial sections of the brains from five cases of the strokeprone spontaneously hypertensive rats. Infraction was observed in a form of microinfarct related to single or plural occluded arterioles in the brain and subarachnoid space. Though most arterioles with fibrinoid necrosis of the wall were occluded with thrombus, infarct, which was obviously related to the occluded arterioles, was verified only in a few occasions. It was proved that infarction did not develop in all the areas irrigated by the occluded arterioles, and the regional circulation was assumed to have been maintained by the collateral circulation. There was rarefaction of the neuropil with preservation of the neurons in the cortex around the vascular changes, such as fibrinoid necrosis of the wall. Widespread rarefaction and cyst formation were observed in the subjacent white matter, which were more marked in the vicinity of the vascular changes in the cortex. These histological changes were interpreted to be the tissue degeneration secondary to edema.

Plexogenic pulmonary arteriopathy: significance of medial thickness with respect to advanced pulmonary vascular lesions.

Abstract: Plexogenic pulmonary arteriopathy runs a more progressive course in transposition of the great arteries with pulmonary hypertension (TGA) and in primary pulmonary hypertension (PPH) than, for instance, in isolated ventricular septal defect (VSD). Fibrinoid necrosis and plexiform lesions occur more often and at a younger age in TGA and PPH than in VSD. A morphometric study in 18 patients with VSD, 14 patients with TGA, 38 patients with PPH, and 21 controls showed that the media of muscular pulmonary arteries is significantly thicker in VSD than in TGA or PPH, with the sole exception of very young children with PPH. This difference in medial thickness is apparent at any level of pulmonary arterial pressure. Conversely, the more advanced pulmonary vascular lesions were particularly prominent in TGA and PPH. It is likely that medial hypertrophy, at least to a certain extent, protects the pulmonary arteries from the development of more ominous vascular alterations.

Eosinophilic cellulitis. (Well's syndrome) in a child.

Abstract: • Granulomatous dermatitis with eosinophilia (Wells' syndrome) occurred in an 11-year-old boy. To our knowledge, eosinophilic cellulitis in a child in whom atrophic alopecia of the affected scalp later develops during the regression phase has not previously been reported. No notable effect of steroid therapy was observed. The cause of eosinophilic cellulitis is still unknown, but the presence of disseminated fibrinoid necrosis, vasculitis, eosinophilia, and a positive antinuclear factor test result might indicate an autoimmune or allergic disease. ( Arch Dermatol 1981;117:427-429)

The histological course of reactions in borderline leprosy and their outcome.

Abstract: The histological course and the outcome of reactions was followed in 12 patients who were all in the borderline (BT-BL) zone of the spectrum at some time during the reaction. In eight patients the reaction proved to be of the upgrading or reversal type with a shift in classification toward the tuberculoid pole. In two patients the reaction was of the opposite downgrading type, and in two there was no significant change in classification as a result of the reaction. Early reactions were characterized by edema and an increase in the number of lymphocytes which was more marked in upgrading than downgrading reactions, but at this stage the outcome could not be reliably predicted. In the acute stage necrosis was apparent in severe cases and was followed by giant cell formation and the evolution of the granuloma cells depending on the direction of the shift: organized clusters of mature epithelioid cells in upgrading, macrophages in downgrading. At all stages the collagen of the dermis might be involved in varying degree, which in extreme cases included fibrinoid necrosis and scarring in the late stage. The histology is compared to that of tuberculin reactions. All cases were bacteriologically positive at the onset of the reaction. The results were consistent with the view that these reactions are delayed type hypersensitivity phenomena associated with the unmasking of bacterial antigen in nerve or other protected sites, or with an increase of hypersensitivity as a result of treatment. They demonstrate the evolution of a granuloma in mycobacterial disease.

Focal Prostatic Granulomas: A Sequel to Transurethral Resection

Abstract: Clinical and histologic findings in 6 cases of prostatic granuloma following transurethral prostatic resection are described. The repeat operations were performed 1 week to 14 months after the initial resection because of severe micturition urgency, voiding difficulty or persistent haematuria. Bacteriuria did not seem to be of aetiologic importance for the granulomas. In all cases the granulomas contained areas of fibrinoid necrosis, and in three cases the granulomas were surrounded by eosinophilic infiltrates. The condition is not widely reconized by pathologists, which was illustrated by the initial diagnosis of specific inflammation consistent with tuberculosis in three patients. Though the disorder seems to be self-limiting, its association with persistent haematuria after transurethral prostatic resection is noteworthy.

Radiologic recognition of extrahepatic manifestations of hepatitis B antigenemia.

Abstract: Extrahepatic manifestations due to an immunologic response to a surface antigen of hepatitis B virus have been identified. These include a serum sicknesslike syndrome and a necrotizing vasculitis. The latter is far more important and in indistinguishable histologically from nonhepatitis related polyarteritis. At least 90 cases have been reported in the decade since 1970, and five are added here. The necrotizing vasculitis syndrome results from fibrinoid necrosis and inflammation of small and medium-sized arterial walls recognizable angiographically by arterial microaneurysms and often by visceral infarction and hemorrhage. Renal failure is common and often associated with pulmonary edema. Gastrointestinal symptoms are a prominent feature due to bowel ischemia. Infarction and perforation are significant causes of morbidity and mortality. Necrotizing vasculitis is also one cause of pancreatitis and of cholecystitis. Plain films, contrast studies, computed tomography, and sonography have been shown to be use...

Giant cell arteritis detected by bone marrow biopsy.

Abstract: A case of giant cell arteritis is reported that was detected by bone marrow biopsy. The histopathologic features of the bone marrow lesion included an enlarged artery, whose wall showed intimal thickening, fibrinoid necrosis, destruction of the internal elastic lamina, and multinucleated giant cells. The demonstration of involvement of bone marrow vessels by giant cell arteritis reaffirms the systemic nature of the disease. Bone marrow biopsy is not the method of choice for establishment of the diagnosis of giant cell arteritis, but it may lead to the diagnosis in rare instances.

Ultrastructural study of lichen planus: an evaluation of the colloid bodies.

Abstract: Colloid bodies, which are eosinophilic, dyskeratotic, damaged epidermal cells that show signs of fibrinoid necrosis and premature keratinization, may play a rote in the pathogenesis of lichen planus. An ultrastructural study of two patients with lichen planus focusing on the colloid bodies suggests the possibility of these bodies initiating the lichenoid dermal reaction.

The pathogenesis of small arterial lesions in nephrectomized rats by the administration of renin.

Abstract: Intraperitoneal injection of purified hog renal renin produced a marked and sustained elevation of arterial pressure and lesions of the "fibrinoid necrosis" type in the small arteries and arterioles of the pancreas, heart and mesentery, but not of the brain, in bilaterally nephrectomized rats. Both the elevation of arterial pressure and the production of arterial lesions were completely prevented by pretreatment with oral SQ14225. Plasma renin clearance in bilaterally nephrectomized rats was markedly slower than that in sham-nephrectomized rats. Pre-treatment with oral SQ14225 did not affect renin clearance. It is suggested that sustained high blood pressure due to the sustained high plasma renin concentration in bilaterally nephrectomized rat was responsible for the production by renin of lesions of the fibrinoid necrosis type in the arteries.

Temporal Arteritis With Scalp Necrosis

Abstract: To the Editor.— In the July 1980Archives(116:749), Quintanilla and colleagues reported an unusual case of temporal arteritis with gangrene of the scalp. 1 We want to elaborate on the histologic aspects of the skin lesions that are not frequently described. 2 Report of a Case.— Recently, we treated a patient with chronic, asymptomatic, lymphocytic leukemia in whom severe headaches and tender, indurated, and pulseless temporal arteries, followed by violet skin changes in both parietal regions, with cutaneous necrosis and crust formation (Fig 1), developed. The biopsy specimen of the temporal artery confirmed a typical pattern of temporal arteritis. Clinically, this patient's scalp lesions were similar to those previously reported in temporal arteritis. 1 We performed a biopsy on one of these as well. Microscopically, there Fig 1.—Ulcerations with eschar formation on parietal region of scalp. Fig 2.—Arteriolar vasculitis in reticular dermis showing fibrinoid necrosis and inflammatory changes with

Hypertension, Vasopressors, and Susceptibility to Vascular Injury: Experimental and Clinical Studies

Abstract: The association of high blood pressure with vascular damage has long been recognized, and so has the fact that control of severe hypertension may lead to reversal of certain vascular changes (1). It is also recognized that hypertension of comparable magnitude and duration in different subjects may cause vascular lesions of different severity, suggesting that the mechanical effect is not sufficient to explain these lesions. Moreover, microvascular lesions similar to those of malignant hypertension (i.e., fibrinoid necrosis and hyalinization) have been observed in the absence of excessive blood pressure elevation (e.g., in progressive systemic sclerosis with renal involvement, Bartter’s syndrome, and familial chloride diarrhea). A number of clinical and experimental studies lend support to the thesis that humoral factors such as blood viscosity, sodium kinetics, and vasoactive hormones may affect vascular pathology.

Placental immunopathology in gestational diabetes.

Abstract: Gestational diabetes and insulin-dependent diabetes are characterized by distinct pathophysiological mechanisms. However, their presence in pregnancy poses similar risks to the fetus. It is possible that factors common to both diseases are responsible for the increased morbidity and mortality in offspring of such pregnancies. Recent studies of placentae from insulin-dependent diabetics revealed evidence of immunopathological change which may support the possible role of immunological factors in the complications of diabetic pregnancy. In the present study, we have similarly examined placentae derived from 30 pregnancies complicated by gestational diabetes and from 10 normal pregnancies. The most striking differences detected by immunofluorescence were increased amounts of clotting factors related to areas of fibrinoid necrosis, and large quantities of complement components C4 and C3 in the intervillous spaces and trophoblast basement membrane respectively. These results are similar to those found in placentae from insulin-dependent diabetics, suggesting that glucose intolerance in pregnancy, even of minor degree, is frequently associated with immunopathological processes that are reflected in the placenta.

Extensive Intestinal Infarction Complicating Systemic Lupus Erythematosus

Abstract: A 42-year-old Japanese housewife with systemic lupus erythematosus (SLE) developed severe abdominal pain. An emergency operation revealed a thrombosis at a major artery of the mesenterium associated with a 70-cm-long necrotic segment of the terminal ileum. There was no evidence of cellular.infiltrates or fibrinoid necrosis within the vascular wall. The recovery was uneventful. Although rare, intestinal infarction must be carefully ruled out in the differential diagnosis of severe abdominal pain in SLE.

Vascular changes underlying cerebral lesions in the stroke-prone spontaneous hypertensive rats

Abstract: The relationship of the vascular changes to the cerebral lesions has been studied using serial sections of the brains from five cases of the strokeprone spontaneously hypertensive rats. Infraction was observed in a form of microinfarct related to single or plural occluded arterioles in the brain and subarachnoid space. Though most arterioles with fibrinoid necrosis of the wall were occluded with thrombus, infarct, which was obviously related to the occluded arterioles, was verified only in a few occasions. It was proved that infarction did not develop in all the areas irrigated by the occluded arterioles, and the regional circulation was assumed to have been maintained by the collateral circulation.