Obliterative Endarteritis, and the Inflammatory Changes in the Coats of the Small Vessels.
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Diagnosis of allograft dysfunction relies on the assessment of arterial lesions. This study was designed to evaluate the prognostic significance of common specific vascular lesions in acute allograft rejection. Renal allograft biopsies (n = 111) with acute cellular rejection were scored for endarteritis, mononuclear cell adherence to endothelial cells, endothelial activation, fibrinoid necrosis, foam cells, and intimal fibrosis. These vascular lesions and other classic histologic features were correlated with outcome. Rejection with endarteritis (found in 54% of biopsies) was less responsive to steroid treatment than rejection without endarteritis, 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 endarteritis responded to OKT3/antithymocyte globulin treatment equally well (61% versus 65%, respectively). Rejection with fibrinoid arterial necrosis (4% of biopsies) did not respond to either steroids or antibodies (0%). One-year graft failure was 21% without endarteritis, 28% with endarteritis, and 100% with fibrinoid necrosis. Activated endothelial cells and interstitial hemorrhage were associated with endarteritis and graft failure (all P < 0.05). None of the other scored features had any statistically significant correlation with outcome. Thus, specific arterial lesions (endarteritis, fibrinoid necrosis, activated endothelial cells, mononuclear cell margination) and interstitial hemorrhage, but not the extent of the interstitial infiltrate or tubulitis, are correlated with response to antirejection therapy and/or 1-yr clinical outcome. Grading systems for therapeutic trials and clinical management should emphasize scoring of specific vascular lesions.
BACKGROUND: We observed two cases of juvenile endarteritis which might suggest a possible link between Winiwarter-Buerger disease and cannabis-induced endarteritis. CASE REPORTS: Our two patients were young men aged 18 and 20 years. Both developed acute distal ischemia of the lower or upper limbs with arteriographic evidence suggestive of Winiwarter-Buerger disease. Both smoked regularly but not excessively and both used cannabis regularly. In one case, the therapeutic response to withdrawal of cannabis was good. In the second, use of cannabis continued and arterial disease persisted. DISCUSSION: The cause of Winiwarter-Buerger disease remains elusive although smoking is undoubtedly involved in the pathogenic mechanism. Our two cases recall the cannabis-induced endarteritis described in the sixties in Kif smokers in North Africa. The main clinical and radiographical features in this condition are the same as in Winiwarter-Buerger disease. CONCLUSION: Winiwarter-Buerger disease and cannabis-induced endarteritis are 2 very similar conditions. The probably rare finding of juvenile endarteritis mimicking thromboangeitis obliterans should, in our opinion, be considered as a secondary and possibly toxic effect of cannabis.
Thirteen patients with clinical suspicion of patent ductus arteriosus were evaluated by transthoracic and transesophageal echocardiographic studies. Findings were corroborated during corrective surgery in 8 patients and by cardiac catheterization in 5. Transthoracic echocardiography confirmed the diagnosis in 7 patients; in 2 of the patients endarteritis of the pulmonary artery was demonstrated, and in one infective vegetations in aortic and mitral valves. With transesophageal echocardiography, patent ductus arteriosus was established in all 8 patients and endarteritis of the pulmonary artery was shown in 3, including 1 not discovered by transthoracic technique. In 1 of these patients, vegetations were also found on the pulmonic valve. Both techniques demonstrated significant pulmonary hypertension in 5 cases; contrast studies showed the venoarterial shunt between the pulmonary artery and the aorta with particular clarity in transesophageal images. On the basis of these findings it may be concluded that transesophageal echocardiography complements the information provided by transthoracic recordings in adult patients with patent ductus arteriosus, especially when it is associated with pulmonary hypertension or pulmonary endarteritis.
During a twin pregnancy of a 41-year old woman, a selective sectio parva was performed, without removing the placenta, in the 23rd week of gestation. An amniotic fluid examination after routine amniocentesis showed a free trisomy 21 in only one of the twins. The twin with normal caryotype was delivered in the 28th week. His placenta was well developed, whereas the placenta of the other child showed severe obliterations of the stem arteries with partial avascularity of the villi. The histological aspect was that of a so-called "endarteritis obliterans". Since the twin delivered via sectio parva showed no signs of dystrophy, we presume that at the time of delivery his placenta had developed regularly. The changes of the placenta, demonstrated by histological examinations, seemed to be caused by the stopping of the foetal blood circulation. We suggest that the intrauterine death is not caused by "endarteritis obliterans" only as often described previously. Obviously, the morphological picture of endarteritis obliterans can be the result of cessation of foetal blood circulation. Obliteration of stem arteries might be the main reason for the stillbirth with significant signs of dystrophy. The similar histological picture in placentae of normally developed stillbirths is obviously caused by discontinuation of foetal blood circulation.
During a ten-year period, we observed three patients with complicated rheumatoid arthritis (RA) and bowel infarction in which the distal mesenteric vessels were occluded by proliferative endarteritis characterized by intimal proliferation, without vessel wall necrosis or inflammation. Proliferative endarteritis was originally described in patients with RA and digital infarcts and has only rarely been noted in patients with visceral infarcts. Our three patients' pathologic features suggested that these vascular lesions were progressive and rendered patients vulnerable to bowel infarction during periods of decreased cardiac output. Two of the three patients had intestinal infarction without clinical or pathologic evidence of systemic vasculitis. Proliferative endarteritis of visceral arteries rarely causes morbidity and mortality in patients with RA.
BACKGROUND: Platelet-derived growth factor (PDGF) has an important role in cellular function, proliferation, and angiogenesis. It is also associated with tissue injury and repair, and its involvement in atherosclerosis has been studied extensively. Tissue injury is also found in pre-eclampsia (PRE). The morphological and physiological changes that are taking place in the PRE placenta may be associated with this growth factor. The objective of this study was to determine if PDGF-AA and its alpha receptor are present in the cells and vessels of normotensive (NORM) and PRE placentas at term. METHODS: Placental tissue was obtained from 6 preeclamptic and 8 normotensive women. Gestational age ranged from 38-42 weeks. Deliveries were either vaginal (vag, n = 10) or c-section (c-sec, n = 4). Tissue samples were analyzed for PDGF-AA by immunocytochemistry. RESULTS: PDGF-AA and the alpha receptor were present in both NORM and PRE placentas. Immunoreactive staining revealed PDGF-AA and its receptor in the intimal/endothelial layer of fetal vessels and the trophoblastic layer. Staining intensity was greater in preeclamptic tissue when obliterative endarteritis was present. CONCLUSIONS: In pre-eclampsia, PDGF-AA may play a role in the restructuring of the fetoplacental vasculature, in particular when there is inflammation of the vascular intimal layer, as found in obliterative endarteritis. Increased staining in the trophoblast layer in patients with obliterative endarteritis also may be indicative of more widespread damage throughout the placenta itself, and PDGF-AA may play a significant role in the repair of this damage.
Three cases of polyarteritis nodosa (P.A.N.) studied by abdominal arteriography with a follow-up examination between the 6th and 9th month are reported. In the first case, the initial arteriogram showed only the appearances of endarteritis. The second arteriogram, 9 months later, following a worsening of general condition, revealed diffuse aneurysms in the abdomen. In the second patient, who had multiple aneurysms at the time of the initial examination, arteriography agter 6 months following a new episode of the disease with an acute abdominal syndrome and collapse revealed, alongside the multiplication of the aneurysms with rupture of one of them, the disappearance of some ectasias with the obliteration of certain arteries. In the third patient, the follow-up arteriogram after treatment showed disappearance of the renal arteriograms which the first study had revealed 7 months before. These three cases give an idea of the different radiological appearances of P.A.N. The appearance of endarteritis with no specific characteristics indicates and inflammatory localisation of the disease. This is an initial stage leading to ectasia. Aneurysms may progress to rupture or may multiply. Endarteritis and ectasia may also progress towards scarring and disappear. A method of early diagnosis, arteriography makes it possible to institute treatment before the lesions reach a stage at which they must inevitably develop either into aneurysms or lead to obstruction with distal ischaemia.