Showing papers on "Fibrinoid necrosis published in 1998"

The prognostic significance of specific arterial lesions in acute renal allograft rejection.

Abstract: Diagnosis of albognaft dysfunction relies on the as- sessment of arterial lesions. This study was designed to eval- uate the prognostic significance of common specific vascular lesions in acute albograft rejection. Renal albognaft biopsies (it = 1 1 1) with acute cellular rejection were scored for endan- tenitis, mononuclear cell adherence to endothelial cells, endo- thebial activation, fibrinoid necrosis, foam cells, and intimal fibrosis. These vascular lesions and other classic histologic features were correlated with outcome. Rejection with endar- tenitis (found in 54% of biopsies) was less responsive to steroid treatment than rejection without endartenitis, as judged by recovery of creatinine in 3 wk (P = 0.03). Larger numbers of sampled arteries improved the predictive accuracy. Sticking of mononuclear cells to endothelial cells also correlated with steroid resistance (P < 0.05). Rejection with or without end- artenitis responded to OKT3/antithymocyte globulin treatment equably well (61% versus 65%, respectively). Rejection with fibrinoid arterial necrosis (4% of biopsies) did not respond to either steroids on antibodies (0%). One-year graft failure was 21 % without endarteritis, 28% with endarteritis, and 100% with fibninoid necrosis. Activated endotheliab cells and inter- stitiab hemorrhage were associated with endartenitis and graft failure (all P < 0.05). None of the other scored features had any statistically significant correlation with outcome. Thus, specific arterial lesions (endartenitis, fibninoid necrosis, acti- vated endothebiab cells, mononuclear cell mangination) and interstitial hemorrhage, but not the extent of the interstitial infiltrate or tububitis, are correlated with response to antirejec- tion therapy and/or 1-yr clinical outcome. Grading systems for therapeutic trials and clinical management should emphasize

Secondary microvascular degeneration in amyloid angiopathy of patients with hereditary cerebral hemorrhage with amyloidosis, Dutch type (HCHWA-D)

Abstract: Various secondary microvascular degenerative and inflammatory alterations may complicate cerebral amyloid angiopathy (CAA) and contribute to the morbidity of CAA-associated stroke. We have investigated the severity of CAA-associated microangiopathy in a genetically determined Dutch form of CAA (HCHWA-D) that has major similarities to the type of CAA that more commonly occurs with aging or Alzheimer's disease (AD). The presence and extent of the following vascular abnormalities was assessed: (1) hyalinization/fibrosis, (2) microaneurysm formation, (3) chronic (especially lymphocytic) inflammation, (4) perivascular multinucleated giant cells/granulomatous angiitis, (5) macrophages/histiocytes within the vessel wall, (6) vessel wall calcification, (7) fibrinoid necrosis, and (8) mural or occlusive thrombi. (Of these, calcification of CAA-affected vessel walls has, to our knowledge, been described in only a single patient with CAA-associated cerebral hemorrhage.) Some of the changes, such as histiocytes in blood vessel walls and the relationship of vascular hyalinosis to amyloid beta/A4 protein deposition, were highlighted by immunohistochemistry. By assessing the numbers of sections in which the changes were present for each case, a 'score' reflective of CAA-associated angiopathy could be obtained. This 'score' was reproducible among several observers. We suggest that it might also be applicable to quantifying severe CAA and related microvascular degenerative changes in patients with AD. beta/A4 immunoreactivity was often sparse and adventitial (or almost absent) in severely hyalinized arterioles and microaneurysms. However, macrophages were prominent in the walls of such vessels and may play a role in the pathogenesis and progression of CAA-related microvasculopathy.

Pathogenesis of the vascular and glomerular damage in ANCA-positive vasculitis.

Abstract: Antineutrophil cytoplasmic autoantibodies (ANCA) Subsequently, there have been many publications that are specific for antigens in the cytoplasm of neutrophils have addressed the correlation between ANCA titer and monocytes. Approximately 90% of ANCA in and the clinical course of the disease [2]. Although patients with vasculitis or glomerulonephritis have there is controversy over whether or not the correlation specificity for either myeloperoxidase (MPO) or pro- is close enough to be used for making therapeutic teinase 3 (PR3), which are located in the primary decisions, there is general agreement that there is at granules of neutrophils and the peroxidase-positive least a rough positive correlation between ANCAlysosomes of monocytes. positivity and disease activity. This is consistent with Beginning with the initial publication about ANCA a cause and eVect relationship, but would also occur [1], they have been strongly associated with a spectrum with an epiphenomenon that was secondary to active of necrotizing small vessel vasculitides that includes Wegener’s granulomatosis, microscopic polyangiitis, and Churg-Strauss syndrome [2,3]. These vasculitides often have necrotizing and crescentic glomerulo- Table 1. Clinical, pathological and experimental evidence of nephritis as a component of the systemic vascular pathogenesis of vasculitis by ANCA injury. A pathologically identical glomerulonephritis also occurs as a renal-limited disease. There is mount- Clinical and pathologic evidence: ing clinical, pathological, and experimental evidence ANCA are very frequent in patients with necrotizing that ANCA are pathogenic ( Table 1). glomerulonephritis and vasculitis ANCA-disease responds to immunosuppressive treatment The vasculitis and glomerulonephritis that are asso- ANCA titers correlate with disease activity ciated with ANCA are characterized, in the acute There is no evidence for anti-GBM or immune complex phase, by segmental fibrinoid necrosis of vessel walls, mediation of pauci-immune ANCA-vasculitis neutrophil and monocyte infiltration with leukocyto- Drug-induced ANCA are associated with pauci-immune necrotizing vasculitis that disappears with discontinuation of

Pathological Changes in Surgically Resected Angiographically Occult Vascular Malformations after Radiation

Abstract: OBJECTIVE: The goal of this study was to evaluate the pathological changes associated with radiation treatment (stereotactic radiosurgery or conventional irradiation) of angiographically occult vascular malformations (AOVMs) METHODS: Eleven patients underwent surgical resection of an AOVM in the mesial temporal lobe, brain stem, thalamus, or basal ganglia after previous radiation treatment The indications for surgery were recurrent symptomatic bleeding from the lesion in 10 patients and recurrent intractable seizures in 1 patient Radiation was used as the initial therapy because the risk of surgical resection was deemed too high Three patients received conventional radiation therapy of 3000 to 5400 rads at an outside institution One patient received radiosurgery with the gamma knife at another institution using a dose of 15 Gy to the margin The remaining 7 patients received stereotactic radiosurgery with a helium-ion particle beam The dose range was from 18 to 26 Gy equivalents The interval from radiation to surgical resection ranged from 1 to 10 years, with a mean of 35 years These lesions were compared with 10 nonirradiated cavernous malformations RESULTS: One irradiated lesion was identified pathologically as a true arteriovenous malformation despite being angiographically occult This lesion did not demonstrate significant changes in the vasculature but did have radiation necrosis of the surrounding brain 5 years after 25 Gy equivalents of helium-ion radiosurgery Two other specimens were too small to identify the type of vascular malformation adequately Of the remaining eight malformations identified as cavernous malformations, six showed a combination of marked fibrosis of the vascular channels, fibrinoid necrosis, and ferrugination However, the fibrinoid necrosis was the only finding unique to the irradiated lesions compared with nonirradiated controls All the irradiated lesions still had patent vascular channels; none were completely thrombosed CONCLUSION: Radiosurgery or conventional radiation therapy did not cause histologic vascular obliteration in intracranial AOVMs evaluated 1 to 10 years (mean 35 yr) after radiation delivery It should be recognized that these patients are irradiation failures who may not be representative of all irradiated patients However, recurrent bleeding from AOVMs may relate to poor radiation response in some patients

Inhibition of tissue angiotensin converting enzyme activity prevents malignant hypertension in TGR(mREN2)27

Abstract: BackgroundActivation of the renin–angiotensin system has been implicated strongly in the transition from benign to malignant hypertension. However, the concomitant rise in blood pressure might also have a direct effect on the vascular wall by initiating fibrinoid necrosis and myointimal proliferatio

Microvasculopathy Is Associated With the Number of Cerebrovascular Lesions in Hereditary Cerebral Hemorrhage With Amyloidosis, Dutch Type

Abstract: Background and Purpose—Microvascular changes such as microaneurysms and fibrinoid necrosis have been found in the presence of cerebral amyloid angiopathy (CAA). These CAA-associated microvasculopathies (CAA-AM) may contribute to the development of CAA-associated hemorrhages and/or infarcts, hereafter referred to as “cerebrovascular lesions.” Hereditary cerebral hemorrhage with amyloidosis, Dutch type (HCHWA-D) is an autosomal dominant form of CAA, in which the amyloid angiopathy is pathologically and biochemically similar to sporadic CAA associated with aging and Alzheimer disease. To determine the significance of CAA-AM for CAA-associated cerebrovascular complications, we investigated the association between CAA-AM and cerebrovascular lesions in HCHWA-D patients. Methods—In a previous autopsy study we semiquantitatively scored CAA-AM in 29 HCHWA-D patients. In the present study we reviewed clinical charts and autopsy protocols of these same patients. We investigated whether CAA-AM was associated with age...

The diagnostic value of perivascular infiltrates in muscle biopsy specimens for the assessment of rheumatoid vasculitis

Abstract: OBJECTIVE To determine the diagnostic value of perivascular infiltrates (PVI) in randomly obtained muscle biopsy specimens for the assessment of rheumatoid vasculitis (RV). METHODS The number and size of PVIs, defined as the presence of mononuclear or polymorphonuclear cells around ⩾ 50% of the circumference of a vessel wall, as well as the presence of fibrinoid necrosis were determined in frozen sections of muscle samples of RV patients with histologically confirmed vasculitis in fixed muscle tissue (n=12). The findings were compared with those observed in frozen sections of muscle biopsy specimens of rheumatoid arthritis (RA) patients not suspected of vasculitis (n=14) and patients with osteoarthritis (OA) (n=11). The presence of PVIs and of fibrinoid necrosis were sought in four frozen sections of the muscle biopsy specimen. RESULTS PVIs were observed in 75% of the RV patients, which was significantly (p CONCLUSIONS The assessment of PVIs with ⩾ three cell layers in a muscle biopsy specimen is a specific and reliable test in discriminating RV from RA without vasculitis. The demonstration in muscle of PVIs with ⩾ three cell layers is more sensitive than that of fibrinoid necrosis in the diagnosis of RV.

Atypical decubital fibroplasia: a series of three cases

Abstract: We report three cases of atypical decubital fibroplasia (ADF), a benign, reactive pathologic process that develops in the skin and subcutaneous tissue of immobilized or debilitated patients. Two patients were immobilized, one wheelchair bound, and one bedridden. The third patient frequently lay over the affected area. Two were male, one female, ages 49, 66, and 89 (mean 68 years old). Each patient presented with a subcutaneous mass, one with focal surface ulceration, present for 5 months, 6 months, and 12 months (mean 7.7 months). The locations included back, lateral thigh (over greater trochanter), and lateral chest wall. No other lesions were present, and none had recurrences. Histologically, atypical decubital fibroplasia is characterized principally by dermal and subcutaneous tissue involvement with fibrinoid necrosis, reactive fibrosis, and focal myxoid change with surrounding more cellular zones of prominent reactive neovascularization including granulation tissue and ectatic vessels with reactive atypical fibroblasts and fat necrosis. Other findings include hyalinization of vessel walls, fibrin thrombi, red blood cell extravasation, hemosiderin deposition, and acute and chronic inflammation. Although the changes are predominantly deep, involving the dermis, subcutaneous tissue and skeletal muscle, the overlying epidermis may ulcerate. Recognition of atypical decubital fibroplasia is of paramount importance, for it may be misinterpreted as a sarcoma, both clinically and histologically.

Multiple scalp aneurysms caused by atypical temporal arteritis--case report.

Abstract: A 55-year-old male suffered sudden onset of dysarthria and mild left hemiparesis due to a right intracerebral small hemorrhage. On admission, six subcutaneous elastic hard lumps were found on the scalp with painless and regular pulsation. The lumps were located along the course of the bilateral superficial temporal arteries (5 locations) and the occipital artery. The patient did not have symptoms of headache or blurred vision associated with temporal arteritis. The largest lump was removed for cosmetic reasons and definitive diagnosis. Histological examination demonstrated many infiltrating inflammatory cells along the entire vascular wall but without giant or fibrinoid necrosis. These multiple scalp aneurysms were probably caused by atypical temporal arteritis.

Coronary artery inflammation and thrombosis in Wegener's granulomatosis-polyarteritis nodosa overlap syndrome.

Abstract: Coronary arteries are frequently involved in systemic arteritis. The inflammatory infiltrate damages the intima and may trigger the occurrence of coronary thrombosis. We report an extreme example of how intimal inflammation in multiple sites of a coronary tree with and without atherosclerosis may trigger coronary thrombosis, in an elderly female patient who died of a clinically unrecognized systemic autoimmune-inflammatory disorder with necrotizing arteritis. The clinical picture was dominated by abdominal symptoms (peritonitis and possible chronic hepatic disease), renal failure and pulmonary X-ray opacities. A precise clinical diagnosis was not formulated, and the patient died of cardiac arrest 15 days after admission. Autopsy showed findings typical of Wegener's granulomatosis and of systemic arteritis with fibrinoid necrosis and multiorgan infarctions. Wegener's granulomatosis-polyarteritis nodosa overlap syndrome was pathologically diagnosed. Although there were no clinical signs of heart involvement, the coronary tree showed inflammation associated with multiple mural and occlusive thrombi. The atypical severe clinical presentation, the short course of the disease and the age of the patient probably contributed to the non proper clinical diagnosis. Old age does not preclude the occurrence of autoimmune disorders, whose course may be dramatically fatal. The abrupt occurrence of a systemic disease with renal failure, hepatomegaly, lung opacities and serositis should prompt analysis to consider these disorders. If properly diagnosed, cardiac involvement should be suspected in autoimmune disorders, even when clinically silent or masked by the systemic clinical picture. In our patient, the role that heart involvement played in the outcome, if any, remains unknown, even though the postmortem pathological identification of coronary mural and occlusive thrombi is generally sufficient to attribute the final cause of death to coronary thrombosis itself.

A case of MPO-ANCA-related vasculitis that recurred as gastrointestinal bleeding and presented difficulty in treatment

Abstract: A 54-year-old man, who had been diagnosed as having MPO-ANCA-related glomerulonephritis in 1993, developed severe anemia and was admitted to our hospital on October, 1997 Endoscopic examination of the upper gastrointestinal tract revealed melena due to duodenal ulcer (Dieulafoy type) The level of ANCA titer was elevated considerably (640 EU), but otherwise there was no evidence of systemic vasculitis activation such as fever, arthralgia, skin eruption, renal insufficiency, and rise in C reactive protein A renal biopsy showed neither crescentic formation nor necrosis of glomerulus Subsequently he developed hematochezia and renal dysfunction rapidly progressed thereafter Angiographical examination of superior mesenteric artery revealed that the bleeding was responsible for the lesion of the small intestine, probably the ileum In spite of TAE (transarterial embolization) he had recurrence of severe hematochezia three days later Partial ileotomy was performed and progression of the anemia was stopped Multiple ulcer was found in the resected ileum The small arteries in the submucosa at the ulceration showed fibrinoid necrosis of the vessel walls These findings suggested that ANCA-related vasculitis had relapsed The patient received methylprednisolone pulse therapy, followed by oral administration of prednisolone after the operation Both serum levels of creatinine and MPO-ANCA gradually decreased after the initiation of treatment However, 24 days later, he suddenly manifested severe abdominal pain, and was diagnosed as having perforation of the stomach or duodenum Due to supportive therapy and reduction of the steroid dose, peritonitis subsided, but symptoms caused by systemic vasculitis developed Later raised the dose of steroid suppressed the activity of systemic vasculitis In this case, elevation of the ANCA titer demonstrated recurrence of MPO-ANCA-related vasculitis as gastrointestinal bleeding

Incidence of acute atherosis in complete molar pregnancy.

Abstract: A clinicohistological study of acute atherosis in molar pregnancy was undertaken. Maternal decidual vessels in currettage samples of 38 histologically confirmed complete hydatidiform moles were examined histologically for acute atherosis, recognised as fibrinoid necrosis of the smooth muscle wall with a perivascular mononuclear cell infiltrate, with or without lipophages. Acute atherosis was detected in eight of 38 cases, an incidence of 18.4%. All the patients were normotensive. The significance of acute atherosis in molar pregnancy remains to be clarified.

Isolated Fibrinoid Vasculitis in Renal Angiomyolipoma

Abstract: Renal angiomyolipoma is a tumor composed of a mixture of thick-walled blood vessels, smooth muscle, and mature adipose tissue. It may present as a single unilateral lesion or as a multifocal uni- or bilateral neoplasm. The histologic spectrum of angiomyolipoma is wide but as far as we know intratumoral fibrinoid vasculitis has not been described in the tumor. This is the first report of isolated intratumoral fibrinoid vasculitis observed in two nodules of a unilateral multifocal renal angiomyolipoma. The vasculitis arose in a hypertensive 62-year-old woman who presented with a history of dull right flank and low back pain of 3 months' duration. There were no signs of generalized disease. Immunophenotyping of the vascular cellular infiltrate disclosed abundant T lymphocytes, significant numbers of histiocytes, and absence of B lymphocytes. The diagnosis of isolated intratumoral arteritis depends on the exclusion of systemic disease. It is important to distinguish cases like this one to avoid misdiagnosis and to prevent unnecessary treatment.

Bullous pemphigoid associated with cutaneous leukocytoclastic vasculitis

Abstract: UK A 79-year-old man presented with palpable purpura and poorly defined erythematous plaques on his limbs (Fig 1) History, examination, and clinical investigations (which included a full blood count, urea, electrolyte, and liver function tests, negative antinuclear and DNA antibodies, antineutrophil cytoplasmic antibody (ANCA), and cold agglutinins) showed no systemic involvement or triggering factors He had not lost weight and took no medication A diagnosis of cutaneous vasculitis was made and the patient's eruption improved with bed rest He returned 2 months later with widespread tense blisters (Fig 2) and an erythrocyte sedimentation rate (ESR) of 90 The blisters were symmetrically distributed and sited predominantly on the flexural aspects of the upper limbs and trunk Additional investigations were performed, with negative blood cultures, chest X-ray, sputum cytology, sigmoidoscopy, fecal occult bloods, mid-stream urine, abdominal ultrasound, and echocardiogram He responded well to oral corticosteroids, with a rapid reduction in ESR Twelve months later his condition remains well controlled on 75 mg of prednisolone daily Figure 1 Painful palpable purpura on the left thigh Figure 2 Tense blisters on the patient's left arm 2 months later Histopathology of the skin from an area of palpable purpura on the upper aspect of the thigh showed an intense leukocytoclastic vasculitis (Fig 3) The upper portion of the dermis showed foci of fibrinoid necrosis of small vessels associated with vessel wall permeation by neutrophil polymorphs and mononuclear inflammatory cells Surrounding the vessels and throughout the dermis there was conspicuous leukocytoclasia No epidermal separation or blister formation were present, but eosinophils were noted to be abundant in the infiltrate Skin biopsy from an erythematous plaque on the upper limb showed similar features, with prominent leukocytoclasia, endothelial swelling, and edema Direct immunofluorescence of perilesional skin showed strong linear deposition of immunoglobulin G (IgG) at the dermo-epidermal junction Figure 3 Photomicrograph demonstrating fibrinoid capillary necrosis in the dermis due to leukocytoclastic vasculitis Note the prominent eosinophils in the infiltrate (hematoxylin and eosin stain; original magnification, ×400) Histopathology from a subsequent bullous lesion demonstrated a subepidermal blister containing serum exudate, fibrin, and many eosinophils (Fig 4) In the underlying dermis there was a perivascular and diffuse mononuclear infiltrate with prominent eosinophils No leukocytoclastic vasculitis was evident The roof of the blister was composed of normal epidermis The appearance was entirely consistent with bullous pemphigoid Figure 4 Bullous pemphigoid A subepidermal blister containing an exudate rich in eosinophils (hematoxylin and eosin stain; original magnification, ×400) Discussion Cutaneous bullous pemphigoid has a worldwide distribution and is the most common autoimmune blistering dermatosis1It is characterized by a widespread eruption of tense bulla on normal or erythematous skin Histologically, the finding of a subepidermal blister associated with an infiltrate of eosinophils in the blister and underlying skin is suggestive of the diagnosis This is supported by the finding of linear immunoglobulin G (IgG) and/or C3 at the dermo-epidermal junction, which occurs in the vast majority of patients Up to 80% of patients show anti-basement membrane antibodies in the serum2Before blistering occurs, a variety of prodromal skin eruptions may be seen3,4These may be erythematous, urticarial, or occasionally eczematous Histologically, a prodromal biopsy may show only nonspecific dermal edema with a perivascular and interstitial mononuclear infiltrate with eosinophils Eosinophilic spongiosis is also frequently seen5Direct immunofluorescence may be positive on skin biopsies taken before the blisters are manifest3,4 Cutaneous leukocytoclastic vasculitis has many associations, including bacterial or viral infections, reactions to drugs or toxins, systemic lupus erythematosus (SLE), and various malignancies6It results from immune complex deposition in vessels leading to complement activation Histologic examination shows fibrinoid necrosis of capillaries and post-capillary venules with endothelial swelling Vessel walls show infiltration by neutrophil polymorphs and mononuclear cells and there is surrounding leukocytoclasia Classically, direct immunofluorescence shows patchy perivascular immunoglobulin and complement deposition in early lesions7 To the best of our knowledge, leukocytoclastic vasculitis has never been described in association with established or prodromal bullous pemphigoid Indeed, an authoritative text of dermatopathology8states that leukocytoclasia or a vasculitis are never seen

Nerve biopsy in patients with AIDS.

Abstract: Patients with AIDS can present clinical involvement of the peripheral nervous system due to different causes In the present work, it was studied the histopathological changes in sural nerve biopsy of fifteen patients with AIDS with this clinical involvement It was observed the presence of a polyarteritis nodosa-like vasculitis of small arteries with fibrinoid necrosis in the sural nerve of 3 patients, one of them associated to polyradiculitis due to cytomegalovirus infection (CMV) Six patients presented mild axonal loss by light microscopy Three other patients had a more important axonal neuropathy with myelin ovoids by teasing By the electron microscopy in these patients were observed some fibers with axonal damage The other three patients had normal sural nerves We concluded that sural nerve biopsy may be important in peripheral neuropathies or myelo-radiculo-polyneuropathies in AIDS especially to search for nerve vasculitis, because it can change the therapeutic approach

The Hemolytic Uremic Syndrome as a Complication of Adriamycin Nephropathy

Abstract: Rats treated with two injections of adriamycin (week 0 and week 12) developed glomerusclerosis and severe tubulointerstitial lesions as described in the literature. In addition, a number of glomerular alterations were present. These included capillary loop dilation, insudation of eosinophilic material, necrosis, duplication of the glomerular basement membrane, severe mesangiolysis with disruption of the mesangial matrix and segmental double-contours. The renal arterioles and interlobular arteries showed endothelial cell swelling. The subendothelial space was infiltrated by fibrinoid material and there was intensive fibrinoid necrosis of the wall of both arteries and arterioles extending into the glomerular tuft. These alterations were very similar to those observed in the hemolytic uremic syndrome. This observation suggests that the two injections of adriamycin, with a long interval in between them, might induce renal lesions similar to those observed in the hemolytic uremic syndrome.

A case of polyarteritis nodosa causing small intestinal necrosis which presented acute abdomen

Abstract: A 29-year-old man was urgently admitted to the hospital because of abdominal pain and vomiting. He developed waterly diarrhea on the second day after admission. Moreover, an abdominal computed tomography showed massive ascites, intestinal edema and paralytic ileus on the sixth day.Emergency laparotomy was performed with a diagnosis of acute peritonitis. At operation, 1800ml of serous ascites and severe inflammation of the small intestine were noted. Ninety centimeter of the necrotic small intestine was resected, followed by establishment of jejunostomy and ileostomy. Histological examination of the resected material revealed fibrinoid necrosis with neutrophil infiltration at submucosal small artery and the diagnosis of polyarteritis nodosa was made. The patient suffered from renal failure after the operation, but he recovered with hemodialysis. Steroid therapy was conducted as a treatment of primary disease. Polyarteritis nodosa with necrosis of the small intestine is relatively rare. All the cases reported in Japan are accumulated and some bibliographical notes are also presented.