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A 73-year-old man with an urothelial carcinoma treated with gemcitabine and carboplatinium and an 84-year-old man with a mesothelioma treated with gemcitabine alone developed digital ischemia. In the first patient, the ischemia involved all fingers except the thumbs during the second cycle of treatment. The ischemia developed during the first cycle in the second patient and involved the right major and ring fingers. In the literature, gemcitabine vascular toxicity is probably potentialized by platinium salts. Several nosological entities occur simultaneously. The most widely described involve isolated digital ischemia for doses to the order of 3000mg, and a hemolytic and uremic thrombotic microangiopathy for gemcitabine doses above 10,000mg. The vascular toxicity of platinium salts is not dose-dependent. In these two patients, the clinical course was favorable with interruption of the chemotherapy, treatment by iloprost and aspirin.

Points essentiels L’arteriopathie des membres inferieurs presente des particularites lorsqu’elle survient avant 50 ans. Il ya une grande diversite des causes, puisque, outre l’atherome qui represente les 2/3 des cas et la maladie de Leo Buerger qui en represente 1/4, d’autres causes peuvent etre mises en evidence : cardiopathies emboligenes, syndromes myeloproliferatifs, causes genetiques, compressives, arteriopathies inflammatoires, syndrome des antiphospholipides. Un bilan etiologique doit etre realise en tenant compte de l’orientation a l’interrogatoire et comprenant d’abord une echographie-Doppler, un electrocardiogramme (ECG) et des examens biologiques simples. Dans un deuxieme temps, une echographie cardiaque, d’autres examens d’imagerie et un bilan biologique plus complet peuvent etre realises . Les resultats d’une etude multicentrique qui vient de se terminer devraient nous donner de nouvelles cles dans la comprehension de ces arteriopathies particulieres.

Resume Propos Il s’agit de revoir les donnees de la litterature concernant les consequences therapeutiques d’un bilan de thrombophilie et d’en deduire les indications de ce bilan. Actualites et points forts La recherche de thrombophilies constitutionnelles a fait l’objet d’une extension de ses indications depuis la decouverte d’anomalies fortement prevalentes, comme la mutation Leiden du facteur V ou la mutation G20210A du gene de la prothrombine. Neanmoins, la presence d’une thrombophilie ne parait pas globalement influer sur le risque de recidive, en tous cas beaucoup moins que le caractere spontane de la maladie veineuse thromboembolique. Lorsque l’on regarde l’impact des differentes thrombophilies, la mutation Leiden du facteur V confere un sur-risque modere de recidive, la mutation G20210A du gene de la prothrombine un sur-risque au plus tres faible. Pour les autres anomalies, il n’y a pas de conclusion possible, mais il est probable que le deficit en antithrombine donne un risque accru de recidive. Perspectives et projets Finalement, la recherche d’une thrombophilie constitutionnelle ne change la plupart du temps pas grand chose aux decisions de duree de traitement, mais certaines anomalies (deficit en antithrombine, mutations homozygotes du gene du facteur II ou du facteur V, associations de thrombophilies) ont des consequences sur la strategie therapeutique. Il ne faut pas perdre de vue que la recherche d’un syndrome des antiphospholipides, dont l’impact n’est pas conteste, doit toujours etre associee a la recherche d’une thrombophilie constitutionnelle. Enfin, l’impact du bilan est generalement nul apres un evenement de type thrombose veineuse profonde distale (a l’exception des antiphospholipides) ou thrombose veineuse superficielle.

Endothelial dysfunction is a key event in cardiovascular disease. Measurement of endothelial dysfunction in vivo presents a major challenge, but has important implications since it may identify the clinical need for therapeutic intervention, specifically in primary prevention. Several biological markers have been used as indicators of endothelial dysfunction. The soluble adhesion molecules sICAM-1 and sVCAM-1 lack specificity and are increased in inflammatory processes. Both markers are increased in coronary artery disease. sICAM-1 level predicts the risk for cardiovascular disease or diabetes mellitus in healthy individuals. sE-selectin is specific for the endothelium and is increased in coronary artery disease and diabetes mellitus. sE-selectin is also associated with diabetic risk. The endothelium-specific marker, soluble thrombomodulin, is associated with severity of coronary artery disease, stroke or peripheral occlusive arterial disease and is not increased in healthy or asymptomatic subjects. Interestingly, thrombomodulin decreases during treatment of hypercholesterolemia or hyperhomocysteinemia. In contrast, von Willebrand factor is the best endothelial biomarker and predicts risk for ischemic heart disease or stroke.

Resume Introduction. – Le syndrome des ecchymoses douloureuses decrit par Gardner et Diamond en 1955 est caracterise par l'apparition spontanee d'ecchymoses douloureuses, sans anomalies biologiques associees, chez des jeunes femmes au profil psychologique pathologique. Exegese. – Nous rapportons trois observations de jeunes filles presentant un syndrome des ecchymoses douloureuses. Dans un cas, la mise en place d'une psychotherapie a entraine une nette amelioration des manifestations cutanees et articulaires et dans un autre cas, la placebotherapie a permis la disparition de la symptomatologie de facon prolongee. Conclusion. – Plusieurs hypotheses physiopathologiques sont proposees dans le syndrome de Gardner et Diamond. Cependant, les observations rapportees dans la litterature plaident en faveur d'une origine psychogene. C'est une prise en charge globale, a la fois psychologique et somatique, qui doit etre proposee a ces malades.

A.D. Blann*, J. Constans, P. Carpentier, M. Renard, B. Satger, V. Guerin, M.R. Boisseau, N. Neau-Cransac, C. Conri Haemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Dudley Road, Birmingham, B18 7QH, UK Service de Medecine Interne et Pathologie Vasculaire, Hopital St Andre, 1 rue Jean Burguet, 33075 Bordeaux, France Service de Medecine Interne et Vasculaire, Hopital de la Tronche, BP217, 38043 Grenoble, France Laboratoire d’Hematologie, Universite Victor Segalen-Bordeaux II, 33076 Bordeaux, France Laboratoire d’Immunologie, Hopital Pellegrin, 33076 Bordeaux, France

Resume Introduction. – La distensibilite est la capacite des grosses arteres elastiques a faire varier leur diametre de la diastole a la systole. Lˈune des methodes les plus validees pour la mesurer est la velocite de lˈonde de pouls (VOP), qui peut etre mesuree par divers procedes dont le QKd. Exegese. – Le QKd est lˈintervalle de temps compris entre lˈonde Q de lˈelectrocardiogramme et lˈenregistrement du deuxieme bruit de Korotkoff au niveau de lˈartere humerale, correspondant a la tension arterielle diastolique. Il est mesure par un holter tensionnel et electrocardiographique specifique (normale superieure a 200 ms). La distensibilite arterielle semble interessante pour predire les evenements cardiovasculaires. Il a ete montre que les hypertendus âges avec QKd altere font plus dˈevenements cardiovasculaires que les autres. Le QKd est a lˈetude comme predicteur de la progression des sclerodermies (etude ERAMS). Conclusion. – Le QKd est une methode non invasive et ambulatoire qui couple les mesures de distensibilite et de tension arterielle.

Increased vascular endothelial cell growth factor (VEGF) may be important in cardiovascular pathophysiology (perhaps relating to angiogenesis and collateral vessel development) and binds target endothelium via receptors such as Flt-1. We hypothesized that there would be increased levels of plasma VEGF and Flt-1 in patients with atherosclerosis and others with hyperlipidemia compared with controls, and a reduction in these factors with 3 months of lipid-lowering therapy. Twenty patients with uncomplicated hyperlipidemia but no atherosclerosis, 20 patients with hyperlipidemia plus clear atherosclerosis, and 40 matched controls were studied. Plasma VEGF was higher in patient groups than in healthy controls (p

SummaryWe evaluated two clinical scores for the prediction of deep venous thrombosis (DVT) in hospitalized patients (Wells’ and Kahn’s). We included 273 patients referred to the vascular exploration unit for the suspicion of DVT. A clinical questionnaire was filled in by the practitioner and the scores were calculated from this form. 66 of the 273 patients had a DVT. When Wells’ score was 3, a DVT was found by duplex echography in 51% patients ; when the score was 0, a DVT was found in 9%. Kahn’s score was not adapted to this population. We then developed a new simple score (cancer, palsy or plaster immobilization, warmth, superficial venous dilation, unilateral pitting edema, other diagnosis). A DVT was found in 76% patients with a score of 3 and in 11% in those with a score of 0. We therefore propose a 6-item score whose main advantages are simplicity and usefulness in routine practice.

The purpose of this paper was to revisit the old concept of cannabis arteritis first described in the 1960s and report 10 new cases. Ten male patients, with a median age of 23.7 years developed subacute distal ischemia of lower or upper limbs, leading to necrosis in the toes and/or fingers and sometimes to distal limb gangrene. Two of the patients also presented with venous thrombosis and three patients were suffering from a recent Raynaud's phenomenon. Biological test results did not show evidence of the classical vascular risk factors for throm bosis. Arteriographic evaluation in all cases revealed distal abnormalities in the arteries of feet, legs, forearms, and hands resembling those of Buerger's disease. A collateral circulation sometimes with opacification of the vasa nervorum was noted. In some cases, arterial proximal atherosclerotic lesions and venous thrombosis were observed. All patients were moderate tobacco smokers and regular cannabis users. Despite treatment with ilomedine and heparin in all cases, five amputations were necessary in four patients. The vasoconstrictor effect of cannabis on the vascular system has been known for a long time. It has been shown that delta-8- and delta-9-tetrahydrocanabinols may induce peripheral vasoconstrictor activity. Cannabis arteritis resembles Buerger's disease, but patients were moderate tobacco smokers and regular cannabis users. These cases show that prolonged use of cannabis could be an additive risk factor for juvenile and young adult arteritis. Cannabis arteritis is a forgotten and severe occlusive vascular disease occurring in young adults. Search for cannabis use may be an important tool for a better knowledge of arteritis in young smokers.

Resume Propos. — Les fistules aortoduodenales sont les plus frequentes des fistules aortodigestives. Elles peuvent etre primitives (survenant sur un anevrisme de l'aorte native) ou secondaires (survenant sur une prothese aortique). Les fistules aortoduodenales sont une complication rare des protheses aortiques. Elles peuvent provenir d'une infection prothetique ou d'une erosion mecanique due au port d'une prothese parfois mal adaptee. Methodes. — Nous rapportons sept cas de fistules aortoduodenales secondaires qui illustrent les problemes poses sur le plan du diagnostic et de la therapeutique. Resultats. — Le delai de survenue est variable, en moyenne 3 ans, comme le montre la litterature. Le tableau clinique comprend surtout des hemorragies digestives hautes, parfois de la fievre, des douleurs ou un syndrome douloureux abdominal. Le diagnostic est difficile, parfois suggere par la fibroscopie gastrique ou la tomodensitometrie. Les autres examens complementaires n'ont guere d'utilite et ne doivent pas etre multiplies. C'est surtout l'intervention chirurgicale qui en assure le diagnostic de certitude et le traitement, ce dernier etant constitue de la suture du duodenum et du geste sur la prothese vasculaire. Nos observations, dont la duree de suivi est prolongee, ainsi que les donnees de la litterature plaident pour le pontage extra-anatomique axillobifemoral qui constitue la technique de reference pour la plupart des auteurs. Conclusion. — La mortalite liee a l'existence d'une fistule aortoduodenale (cinq de nos sept patients) justifie tous les efforts de prevention (technique chirurgicale parfaite, traitement antibiotique de tout episode d'infection bacterienne). Le diagnostic doit etre evoque devant tout saignement digestif ou toute fievre inexpliquee chez un patient porteur d'une prothese aortique.

Membrane thrombomodulin (TM) is a very efficient natural anti-thrombin glycoprotein with anticoagulant properties expressed on endothelial cell surface. Circulating plasmatic thrombomodulin (TMp) detected by enzyme immunoassay in plasma is considered as a cell marker of endothelial injury. The TMp levels are increased in many conditions (diabetes mellitus, atheromatous disease...). In cases of collagen vascular diseases, where vascular endothelium damage is suspected, TMp is increased particularly in systemic lupus erythematosus (SLE) and systemic sclerosis (SSc). It is noteworthy that the TMp level is correlated with disease activity. Since TMp is a non specific marker of endothelial damage, it may be of interest as a useful marker for the supervision of these diseases. Further studies are needed on larger series. TMp level change during spontaneous evolution or under treatment will help determine wether TMp is a predictor and prognostic marker of these systemic diseases.

A 51-year-old woman had no known cardiovascular risk factor. She presented with bilateral calf intermittent claudication from February. She was hospitalized in August for acute right leg ischemia without loss of sensorymotor functions, following angiography by one week. She had an occlusion of both superficial femoral arteries and abdominal aorta thrombus, plausible source for embolism. Her condition quickly improved with heparin and iloprost infusion. Since the aortic thrombus was removed on ultrasound, aortic surgery was not performed at this time. Investigations showed hyperhomocysteinemia (25 microg/L after overnight fasting and 115 after methionin load) and decrease in folic acid. This report highlights the occurrence of severe arterial disease in young women with high serum homocysteine levels.

Resume Nous rapportons le troisieme cas de thrombose de l'artere mesenterique superieure au cours d'un syndrome de Behcet repondant aux criteres de la classification de Mason et Barnes. Les manifestations cliniques fonctionnelles de la patiente se resument a un angor intestinal severe associe a une alteration de l'etat general. Une revue de la litterature des atteintes vasculaires, notamment thrombotiques, de la maladie de Behcet est colligee. L'interet des techniques d'exploration arterielles digestives non invasives est discute.

International audience; BACKGROUND: This study aimed to determine the prevalence of genetic and environmental vascular risk factors in non diabetic patients with premature peripheral arterial disease, either peripheral arterial occlusive disease or thromboangiitis obliterans, the two main entities of peripheral arterial disease, and to established whether some of them are specifically associated with one or another of the premature peripheral arterial disease subgroups. METHODS AND RESULTS: This study included 113 non diabetic patients with premature peripheral arterial disease (diagnosis

Resume Nous rapportons huit cas de pneumopathie a l'amiodarone. La presentation clinique est dominee par une dyspnee aigue, subaigue ou progressive. La responsabilite de l'amiodarone est suspectee sur un faisceau d'arguments: des signes cliniques rarement au complet (dyspnee, fievre, toux), des signes radiologiques (TDM haute resolution qui montrent des images interstitielles ou alveolointestitielles asymetriques, souvent bilaterales, de forte densite scanographique), une hypoxemie, des anomalies de la cellularite au cours des lavages bronchoalveolaires (rarement specifiques) voire des arguments histologiques par biopsie pulmonaire. Il est surtout important d'eliminer toutes les autres causes possibles de pneumopathies subaigues ou chroniques en particulier neoplasiques, infectieuses ou liees a une insuffisance cardiaque. La dose cumulee d'amiodarone n'est pas determinante car certains cas surviennent precocement (1 a 2 mois) avec un tableau de dyspnee aigue febrile, parfois grave evoquant un mecanisme immunoallergique. La preuve de la responsabilite de l'amiodarone ne peut etre obtenue qu'avec l'arret du medicament; la disparition des symptomes cliniques et radiologiques est parfois retardee de 2 a 6 mois.

Objectives Altered angiogenesis is a characteristic feature in SSc and remains ill-understood. VEGF is believed to play a central role. Serum VEGF is elevated in SSc patients but questions remain concerning the source of circulating VEGF. Here we investigated platelet activation and the role of platelets as a source of VEGF and other angiogenic mediators in this disease. Methods A cohort of 40 patients with SSc was included. Age- and sex-matched healthy subjects and subjects presenting a primary RP were included as controls. Platelets were isolated, activated with thrombin and the secretion of VEGF, platelet derived growth factor, homodimeric form BB (PDGF-BB), TGF-beta1 and angiopoietins-1 and -2 measured. Plasma concentrations of these mediators and the functionality of platelet-derived VEGF were also studied. Platelet activation was assayed by measuring plasma beta-thromboglobulin and expression of P-selectin on platelets. The effect of iloprost on VEGF secretion by platelets was studied. Results Platelets from SSc patients, in contrast to controls, secreted large amounts of VEGF when activated, but not PDGF-BB, TGF-beta1 or angiopoietins. Increased expression of membrane P-selectin confirmed platelet activation in the patients. Iloprost inhibited VEGF secretion by platelets both in vivo and in vitro, through inhibition of platelet activation. Conclusions Platelets transport high levels of VEGF in SSc. They may contribute to circulating VEGF because of ongoing activation in the course of the disease. If activated at the contact of injured endothelium, platelets may be important in the altered angiogenesis associated with the disease through the secretion of high levels of VEGF.

Resume Le virus de l'immunodeficience humaine VIH peut etre responsable de vascularite de type variable: leucocytoclasique, angeite granulomateuse, angeite associee a des syndromes lymphoproliferatifs, vascularite necrosante dont d'authentiques periarterites noueuses (PAN). Nous rapportons un cas de PAN chez une patiente de 62 ans, VIH positive. La patiente n'a pas de co-infection par le virus de l'hepatite B, et n'a pas d'anticorps anti-nucleaires. Elle s'est representee sous un tableau associant un syndrome sec, un purpura necrotique, des myalgies et une polyneuropathie. Les biopsies (peau, muscles, nerfs) montrent des signes de vascularite necrosante. Il existe sur les branches de l'aorte abdominale de multiples micro-anevrysmes typiques d'une PAN. Les symptomes lies a la vascularite se sont ameliores apres traitement associant corticosteroides (bolus) et echanges plasmatiques. La patiente n'a pas recu d'AZT du fait d'une intolerance. Une revue des cas publies de vascularite associee a l'infection VIH est realisee.

Lower limb arterial disease has unusual features when occurring before 50 years old. The most important one is the number of causes: atherosclerosis in 2/3 cases, Leo Buerger's disease in 1/4, but also sometimes embolic cardiopathies, antiphospholipid syndrome, myeloproliferative disorders, genetic or compressive diseases, inflammatory arterial disease. When peripheral arterial disease occurs before 50, explorations have to be performed according to anamnesis: duplex echography, EKG, blood sample. Afterwards other explorations may be performed such as other vascular imaging techniques, echocardiography or more complete biological investigation. Results from an ongoing multicenter study should be soon available and give more knowledge about these special peripheral arterial diseases.

SummaryIt was the objective of this study to design a clinical prediction score for the diagnosis of upper extremity deep venous thrombosis (UEDVT).A score was built by multivariate logistic regression in a sample of patients hospitalized for suspicion of UEDVT (derivation sample). It was validated in a second sample in the same university hospital, then in a sample from the multicenter OPTIMEV study that included both outpatients and inpatients. In these three samples, UEDVT diagnosis was objectively confirmed by ultrasound. The derivation sample included 140 patients among whom 50 had confirmed UEDVT, the validation sample included 103 patients among whom 46 had UEDVT, and the OPTIMEV sample included 214 patients among whom 65 had UEDVT. The clinical score identified a combination of four items (venous material, localized pain, unilateral pitting edema and other diagnosis as plausible). One point was attributed to each item (positive for the first 3 and negative for the other diagnosis). A score of –1 or 0 characterized low probability patients, a score of 1 identified intermediate probability patients, and a score of 2 or 3 identified patients with high probability. Low probability score identified a prevalence of UEDVT of 12, 9 and 13%, respectively, in the derivation, validation and OPTIMEV samples. High probability score identified a prevalence of UEDVT of 70, 64 and 69% respectively. In conclusion we propose a simple score to calculate clinical probability of UEDVT. This score might be a useful test in clinical trials as well as in clinical practice.

Objective The ERAMS study addressed the value of arterial stiffness in predicting the severity of systemic sclerosis. Methods ERAMS was a prospective multicentre cohort study including patients with definite systemic sclerosis. Arterial stiffness was measured by the standardized non-invasive QKd 100-60 method. Clinical evaluation, biological measurements, functional respiratory tests and cardiac Doppler echography were performed at inclusion then each year until 3 years' follow-up was completed. Progression was defined as mild (articulations, muscle, oesophagus or skin involvement) or severe (lung, heart or kidney involvement) by a critical event committee. The prediction of severe progression was studied for QKd 100-60 as well as clinical and biological data at baseline by univariate and multivariate analysis. Results Ninety-nine patients were included (81 women, 18 men, mean age 57 years, standard deviation 12.5). Although their blood pressure profile was normal, half the patients had increased arterial stiffness (QKd 100-60 < 200ms). There was a significant relationship between age-adjusted arterial stiffness and decrease in carbon dioxide diffusion (P

Resume Introduction. — Les formes familiales d'hepatites auto-immunes sont exceptionnelles. Nous en rapportons une observation associee a un deficit en fraction C4 du complement. Exegese. — Il s'agissait d'une hepatite auto-immune de type I decouverte chez une patiente âgee de 38 ans qui presentait un tableau de lupus erythemateux dissemine. Sa fille avait du subir a l'âge de 9 ans une splenectomie pour purpura thrombopenique immunologique, puis avait presente a l'âge de 13 ans une hepatite auto-immune de type I. Toutes deux ont eu durant le suivi (respectivement 4 et 8 ans) un abaissement modere mais constant du C4. Conclusions. — Le deficit en C4 est plus frequent dans les familles des patients atteints d'hepatite auto-immune. Il est egalement frequent dans les observations de lupus familiaux et pourrait avoir eu un role pathogenique central chez les deux patientes.

Introduction Some viral infections are associated with deep venous thrombosis. We report a case of deep venous thrombosis in an adult with varicella. He had neither known predisposing factors for thrombosis nor thrombophilia. Exegesis Transient significant level of antiphospholipid antibodies and lupus circulating anticoagulant were observed. There was no evidence of thrombophilia. Deep venous thrombosis has been mostly associated with varicella in children. A transient protein S deficiency was present in almost all cases, though it was sometimes related to an anti-protein S antibody. This association is exceptional in adults. Some viruses such as herpesvirus and HIV are responsible for endothelium dysfunction, but this is still unclear in the case of varicella-zoster virus. Conclusion In our observation, endothelium activation or antiphospholipid antibodies might be responsible for thrombosis.

SummaryPatients infected with HIV are at increased risk of atherosclerosis, and have evidence of endothelium dysfunction. The hypothesis was tested that HIV-related endothelium dysfunction is related to loss of antioxidants. This was done by the supplementation of the antioxidants selenium and beta-carotene. We supplemented the diet of 10 HIV-sero-positive subjects with 100 μg selenium daily, 11 subjects with 30 mg beta-carotene twice daily while 15 subjects were not supplemented. Plasma was obtained at outset and after a year, and tested by ELISA for endothelial cell, platelet and inflammatory markers.The non-supplemented patients experienced increases in von Wille-brand factor and soluble thrombomodulin (both p < 0.01). There were no changes in any of the indices in the patients taking selenium or beta-carotene.Increased von Willebrand factor and soluble thrombomodulin in the non-supplemented patients imply increased damage to the endothelium over the year of the study. Therefore we interpret the lack of increase in the patients taking antioxidants as evidence of the protection of the endothelium by these agents.

Purpose We compared three scores for the prediction of deep venous thrombosis with a new score designed specifically for outpatients. Methods Patients referred for evaluation because of suspected deep venous thrombosis were examined by ultrasonography. Sensitivity and specificity were calculated for three clinical scores (Wells [nine components], Kahn [four components], and St. Andre [six components]). We developed a new score by multivariate analysis, and then compared this score with the others in a new sample. Results Four hundred and forty-four outpatients were included in the first sample, of whom 126 (28%) had deep venous thrombosis. The Wells score was a better predictor of deep venous thrombosis than the Kahn and St. Andre scores. According to the Wells score, 73 patients had a high probability of deep venous thrombosis (of whom 51 [70%] actually had a thrombosis) and 178 had a low probability of deep venous thrombosis (of whom 19 [11%] had a thrombosis). A new score was developed as follows: male sex (+1), lower limb palsy or immobilization (+1), confinement to bed >3 days (+1), lower limb enlargement (+1), unilateral lower limb pain (+1), and other plausible diagnosis (–1). In a validation sample of 282 outpatients, this score identified 31 patients who had a high probability of deep venous thrombosis (score ≥3), of whom 18 (58%) had a thrombosis, and 70 patients who had a low probability (score ≤0), of whom 3 (4%) had a thrombosis. The Wells score and this ambulatory score had similar test operating characteristics in the validation sample. Conclusion Our new six-component score had similar diagnostic utility as the nine-component Wells score among outpatients being evaluated for deep venous thrombosis.

To determine if anti-endothelial cell antibodies (AECA) and plasma markers of endothelial cell function are related to disease severity in systemic lupus erythematosus (SLE).We measured AECA by human umbilical vein endothelial cell binding, endothelial markers von Willebrand factor, soluble thrombomodulin, and soluble E-selectin by ELISA, and disease severity by SLEDAI and SLICC/ACR in 35 patients with SLE.Despite high levels of IgG AECA (p = 0.001) and von Willebrand factor (p = 0.0007) compared to 21 healthy controls, we found a positive correlation only between IgG AECA and the SLEDAI index (r = 0.393, p = 0.021).IgG AECA seem to be related to disease activity in SLE, possibly in a pathogenic role. Conversely, plasma markers of endothelial cell damage seem to be an epiphenomenon and may simply be related to excess inflammation.

Heart involvement is frequent in systemic sclerosis. Cardiomyopathy is the main localization but its diagnosis is often late. Cardiac echography or radionuclide imaging show early involvement of the myocardium while showing alterations of diastolic function of the left ventricle or perfusion defects. The pathogenesis of this cardiomyopathy is supposed to be related to myocardial ischemia in relation with vasospasm, or with organic lesions of small arteries or coronary microcirculation. Pericarditis rarely is of clinical significance. Pulmonary hypertension concerns patients with proximal and advanced systemic sclerosis or limited forms such as CREST. It can be efficiently diagnosed by doppler echography but its therapy is difficult and its prognosis is poor. Epoprostenol in continuous venous infusion seems to be efficient but the accessibility to this therapy is difficult. While the involvement of middle-sized arteries of the hands is common, systemic sclerosis seems to be associated to an increased frequency of large-sized arteries disease.

We report two observations of significant left heart involvement in patients with the carcinoid syndrome assessed by transthoracic and transoesophageal echocardiography. Echocardiographic lesions of this kind have only been reported twice. In the present cases, there was mitral involvement with mitral regurgitation in one case and a mitro-aortic involvement with mitral and aortic regurgitation in the other. The mechanism of left heart lesions is unclear since in both cases no right-to-left cardiac shunt was present, as attested by colour Doppler and saline contrast transoesophageal echocardiography. The location of the primary tumour was unknown in one case and ileal in the other; no pulmonary metastasis was detected. The use of transoesophageal echocardiography might make it possible to detect left-sided cardiac lesions more frequently since they were found in anatomical series, in 30% of patients with carcinoid syndrome.

Hyperhomocysteinaemia is a risk factor for premature atherosclerosis and venous thromboembolic disease. Supplementation with folic acid and vitamin B6 has been shown to decrease plasma homocysteine but data fail to assess an effect on the progression of vascular disease. We measured plasma homocysteine and two markers of endothelial injury (plasma soluble thrombomodulin and von Willebrand factor) at baseline and after 3 months of treatment with folic acid and vitamin B6. After this treatment there was a significant decrease in fasting soluble thrombomodulin (−15 ng/ml, 95%CI 5–22.2). Von Willebrand factor was significantly raised after methionine load at baseline but did not significantly rise after supplementation.

Malnutrition is frequent in HIV infection. Wasting may be the only AIDS-defining condition in some patients (weight loss greater than 10% body weight), but in many cases wasting occurs in patients with opportunistic infection or chronic diarrhea (Serwadda et al., 1985). Even at an early stage of disease, nutritional abnormalities can be demonstrated by studies of body composition (Kotler et al., 1985), and malabsorption may be present in as many as one third of patients without diarrhea (Laine et al., 1993). Furthermore, a correlation has been demonstrated between lean body mass and the timing of death from AIDS (Kotler et al., 1989). Wasting, together with opportunistic infections, may contribute to depletion in some micronutrients, deficits in several of which have been demonstrated in HIV-positive patients: vitamins, B6, B12, D, and A, folates, zinc, copper, iron, selenium (Forest and Confalonieri, 1987; Baum et al., 1991; Rule et al., 1994; Haug et al., 1994; Smith et al., 1987; Graham et al., 1991). Few studies have been conducted about vitamin E status in HIV infection, but several works have demonstrated a decrease in plasma vitamin A in HIV-positive subjects (Constans et al., 1995b; Beach et al., 1992; Semba et al., 1993a; Karter et al., 1995). Vitamin A plays a positive role in immune functions, and a deficit in vitamin A in children results in a decrease in CD4 cell count (Krishnan et al., 1974). Therefore a negative role of vitamin A depletion on the course of HIV infection has been suggested.

SummaryEndothelial damage is present in HIV infection but our understanding of markers and mechanisms is incomplete. We found increased levels of markers of endothelial cell damage such as von Willebrand factor (vWf), soluble thrombomodulin (sTM) and adhesion molecule E- selectin in 90 subjects seropositive for HIV relative to healthy controls. sTM was strongly raised in those patients with the lowest CD4+ cell count (p