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Serum vanadium levels have been measured by neutron activation analysis. They are higher (3.10 +/- 1.38 ng/mL) in patients suffering depressive illness than in normal subjects (0.67 +/- 0.32 ng/mL).

Resume Introduction Les effets indesirables (EI) psychiatriques des fluoroquinolones sont connus depuis longtemps, mais peuvent etre non diagnostiques. Ce travail analyse les cas notifies aux centres regionaux de pharmacovigilance. Methodes Les cas d'EI psychiatriques dus aux fluoroquinolones notifies entre janvier 1985 et juin 2002 ont ete extraits de la base de donnees nationale. Une analyse descriptive a ete faite, incluant : âge, sexe, nature de l'EI, fluoroquinolones en cause, gravite, evolution. Resultats En 17 ans, 590 cas ont ete notifies, concernant 273 hommes et 316 femmes (non precise dans un cas) ; l'âge moyen etait de 66 ans (mediane : 70 ans, extremes : 12–102 ans). Les principaux EI psychiatriques etaient : confusion (51 %), hallucinations (27 %), agitation (13 %), delire (12 %), insomnie (8 %), somnolence (4 %) (plusieurs EI pouvaient etre notifies pour chaque patient). Les molecules en cause etaient : ofloxacine (28 %), pefloxacine (27,5 %), ciprofloxacine (24,6 %), norfloxacine (18,5 %), levofloxacine (1,2 %), sparfloxacine (0,8 %), enoxacine (0,7 %), lomefloxacine (0,7 %) (total superieur a 100 % en raison de la presence de plusieurs fluoroquinolones dans certains cas). Les cas graves representaient 21,7 % des dossiers, essentiellement representes par des hospitalisations ou des prolongations d'hospitalisation. Dans 88,5 % des cas, il y a eu regression complete de l'effet (dans 9,5 % des cas, l'evolution etait en cours ou inconnue). Conclusion Le nombre de cas est relativement faible, mais la sous-notification est probablement importante. La possibilite de survenue de ce type d'EI doit donc etre presente a l'esprit, particulierement chez les sujets âges, ou la posologie des fluoroquinolones doit etre adaptee a la fonction renale.

To investigate the effects of selenium or beta-carotene supplementation in human immunodeficiency virus (HIV)-infected patients, who are known to have deficiencies of selenium and vitamin A, we evaluated the blood enzymatic antioxidant system, including superoxide dismutase (SOD), selenodependent glutathione peroxidase (GPX), and catalase (Cat); glutathione (GSH) status; and plasma selenium concentration. The placebo group consisted of 18 HIV-infected patients with no supplementation, the selenium group was composed of 14 patients receiving oral selenium treatment, and the beta-carotene group comprised 13 patients receiving oral beta-carotene supplementation. All groups were studied for 1 y. At the beginning of the study, a significantly higher SOD activity (P < 0.001) was observed in all HIV-infected patients compared with uninfected control subjects, and GPX activity at baseline was higher in the placebo (P < 0.004) and selenium (P < 0.014) groups than in the control subjects. These higher enzyme activities could be related to an increased synthesis of these enzymes in erythrocyte precursors under oxidative stress. Moreover, we observed significantly lower GSH values in all HIV-infected patients than in control subjects at the beginning of the study (P < 0.001). After selenium or beta-carotene supplementation, no significant difference was observed for SOD activity compared with baseline. On the contrary, GPX activity increased significantly after selenium treatment (P < 0.04 between 3 and 6 mo), whereas a slight increase was found after beta-carotene treatment. Similarly, a significant increase in GSH values was observed at 12 mo compared with baseline both after selenium supplementation (P < 0.001) and beta-carotene supplementation (P < 0.01). Because GPX and GSH play an important role in the natural enzymatic defense system in detoxifying hydrogen peroxide in water, selenium supplementation could be of great interest in protecting cells against oxidative stress. The lower efficiency of beta-carotene could be attributed to the seriousness of the pathology at the time of recruitment into the beta-carotene group.

SUMMARY Malondialdehyde (MDA), a peroxidative end-product released during polyunsaturated fatty acid degradation, reacts strongly with lysine residues of cellular proteins. MDA-modified proteins become immunogenic and may elicit specific autoantibody formation. We hypothesized that systemic diseases in which inflammatory events occur, could be an interesting model for studying oxidative stress. A few studies have suggested that MDA-modified proteins may exist in systemic diseases, and that autoantibodies to MDA-modified structures might reflect this oxidative process. Autoantibodies to MDA-modified epitope(s) were therefore assayed in sera of patients with systemic lupus erythematosus (SLE, n = 29), scleroderma (SCL, n = 11), giant cell arteritis (GCA, n = 11), periarteritis nodosa (PAN, n = 10), rheumatoid arthritis (RA, n = 9), and healthy subjects (HS, n = 32). Significantly increased anti-MDA-modified epitope(s) autoantibodies were found in patients with SLE and also in other systemic diseases such as PAN and SCL. Autoantibodies to MDA-modified epitope(s) were predominantly of IgM isotype, with low levels of IgG and no IgA activity. In SLE, anti-MDA-modified epitope(s) autoantibody titres correlated strongly with systemic lupus activity measure (SLAM, r = 0·702, P = 0·0001), anti-nuclear antigen autoantibodies (ANA, r = 0·4, P = 0·029), IgG anti-cardiolipin (r = 0·558, P = 0·03) and the steroid drug regimen (r = 0·52, P = 0·004). Autoantibodies to MDA-modified epitope(s) may reflect oxidative modifications occurring in systemic diseases, and might be useful as clinical markers of SLE activity if further investigated.

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.

The objectives of this article are to review the data about the consequences of thrombophilia testing and to think about its indications.The indications of congenital thrombophilic testing have extended since the discovery of prevalent abnormalities, such as mutations of factor V or II genes. However, thrombophilia does not result in a significant increase in the risk of recurrence unlike the spontaneous occurrence of thrombotic events. The factor V Leiden mutation is associated with a moderate increase in recurrence rate, while the G20210A mutation of factor II is not associated with a significant increase in recurrence. Regarding the decrease in natural anticoagulants is concerned, there is no definite conclusion, although the decrease in antithrombin is suspected of being associated with an increase in recurrence.Finally, identification of a constitutional thrombophilia most often do not influence the therapeutic decisions unless some rare abnormalities are found, such as a decrease in antithrombin, homozygous mutations in factors V or II genes or associations of thrombophilia. One must remember that antiphospholipid antibodies must be searched because their impact on recurrences is well-known. Diagnostic work-up for thrombophilia is not useful after a distal or a superficial venous thrombosis (except for antiphospholipid antibodies in case of distal venous thrombosis).

Psychiatric adverse effects of fluoroquinolones are known for long, but can sometimes be missed. We analyse cases spontaneously reported to the French pharmacovigilance.Cases of psychiatric adverse effects with fluoroquinolones reported to the French pharmacovigilance system were analysed. The studied period was from January 1985 and June 2002. Data analysed included age, sex, adverse effect, fluoroquinolone, seriousness and evolution.Five hundred ninety cases have been reported concerning 273 males and 316 females (sex unknown in 1 case). Mean age was 66 years (median: 70, range: 12-102). The most frequently reported psychiatric adverse effects were confusion (51%), hallucinations (27%), agitation (13%), delusion (12%), insomnia (8%), somnolence (4%) (several adverse effects could be associated in a single patient). Serious cases represented 21.7% (resulting in hospitalisation in most cases). Evolution was favourable in most cases (88.5%), and was unknown in 9.5% of cases.The number of cases reported during this period is moderate, but under-reporting probably interferes. The eventuality of this kind of adverse effect with fluoroquinolones should be kept in mind. Dose should be adjusted to renal function, especially in older patients.

Painful bruising syndrome was described by Gardner and Diamond in 1955. It is marked by spontaneous bruising, without any biological abnormality, affecting young women with pathological mental context.We report three observations with painful bruising syndrome. In a patient, psychotherapy induced improvement in dermatological and articular manifestations. In other case, placebotherapy made clinical symptoms go away for a prolonged period.Some etiological hypotheses have been postulated for Gardner and Diamond syndrome. However, published cases speak in favour of psychogenic hypothesis. Somatic and psychological approach must be offered to these patients.

The association between adult Henoch-Schonlein purpura and prostatic carcinoma is exceptional. We report a new case.The diagnosis of prostatic adenocarcinoma, suspected because of prostatic induration is made after anatomopathological study. The patient has all the clinical (purpura, polyarthralgia), biological (circulating monocmonal IgA), and histological (leukocytoclastic vasculitis, with IgA and C3 deposits) criteria of Henoch-Schonlein purpura too. The simultaneous appearance of vasculitis and neoplasia is known. The association between adult Henoch-Schonlein purpura and malignant neoplasm like lung carcinoma or lymphoma exists too. The initial events leading to the development of these vasculitis could be tumor antigens or abnormal IgA production.The simultaneous appearance of these two disease asks here the question of mechanisms implicated in these association.

Juvenile peripheral obstructive arterial diseases (POAD) have been poorly investigated but account for 1 to 7% of POAD. We analyzed retrospectively a cohort of patients with onset before the age of 50 years.Seventy-three patients (60 males and 13 females) were divided into 4 groups (Buerger's disease: TAO, atheromatous PAOD, auto-immune POAD, arteriopathy of undetermined origin).The first symptoms occurred at 38 +/- 8 years of age. Fourteen patients (20%) had TAO, 51 (70%) atheromatous POAD, 4 (5%) POAD with systemic or autoimmune disease, and 4 (5%) undetermined POAD. Age of onset was earlier in TAO (35 +/- 8 vs 40 +/- 8 years, p=0.046), smoking greater in the atheroma group (33 +/- 16 vs 24 +/- 14 pack-years, p=0.033). Fifty-three POAD patients had dyslipidaemia and 26% hypertension. Regular cannabis intake was more frequent in the TAO group (21 vs 8%). At the time of medical care, Fontaine's stage was more frequently stage II in atheroma patients (57 vs 14%) and stage IV in TAO patients (86 vs 35%). TAO was diagnosed in 43% cannabis users and in 19% non users.The main etiology of juvenile POAD is atheroma, followed by TAO. Cannabis users account for at least 10% of these patients. They are characterized by lower tobacco intake, more distal lesions, more frequent involvement of the upper limbs. They present more frequently as TAO.

Distensibility is the ability of large elastic arteries to increase in diameter from diastole to systole. Pulse wave velocity (PWV) is one of the ways to measure this parameter. Several techniques, including QKd, are able to measure PWV.QKd is the time interval between the Q wave on EKG and auscultation of the second Korotkoff's sound at the brachial artery. QKd is measured by a specific apparatus that registers ambulatory blood pressure as well as EKG (normal200 ms). Arterial distensibility seems to be able to predict cardiovascular morbidity and QKd has been demonstrated to predict such morbidity in a sample of elderly hypertensives. Currently the relationship between QKd and prognosis is under investigation in systemic sclerosis (ERAMS study).QKd is a noninvasive ambulatory method that measures arterial distensibility as well as blood pressure.

We report a case of mitochondrial myopathy (MM), assessed by histological and biochemical studies. This illness was diagnosed in a 69-year-old patient with myocardiopathy revealed by ventricular arrhythmias. The originality of this case lies in the patient's age, the mode of onset and the biochemical features (i.e. normal mitochondrial enzymatic complexes but very low respiration when using glutamate as a substrate).

We 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 tilled 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.

Background In systemic lupus erythematosus (SLE), disease severity may be related to factors such as endothelial cell damage. Objectives We tested the hypothesis that anti-endothelial cell antibodies (AECA) and plasma markers of endothelial cell dysfunction would be related to disease severity in SLE. Methods Accordingly we measured AECA by human umbilical vein endothelial cell binding, endothelial markers von Willebrand factor, soluble thrombomodulin, soluble E-selectin by ELISA, and disease severity by SLEDAI and SLICC/ACR in 35 patients with SLE. Results Despite high levels of IgG AECA (p Conclusion We conclude that 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 only be related to excess inflammation in these patients.

Deep venous thrombosis is 50 times less frequent in upper than in lower limbs. Data remain poor in the literature. Forty consecutive patients (24 males, 16 females, mean age: 54.5 years) were retrospectively analysed from 161 subjects who underwent venous explorations of the upper extremity for a 3.5 year period in the same center. Diagnosis of thrombosis was made by duplex ultrasonography (n =37) or phlebography (n =3). Main clinical manifestations were edema (n =36) and pain (n =29). Location of thrombosis was humeral (n =1), axillary (n =2), or sub-clavian (n =37, 2 bilateral). The majority of thrombosis (n =29) were secondary to cancer and venous catheter (n =19, 15 implanted ports), to central catheter alone (n =3) or cancer alone (n =7). The 11 others were associated with thoracic outlet syndrome (n =6) or apparent primary thrombosis (n =5). Thrombophilia was identified in 6 out of these 11. During follow up [mean of 9 months (0,5-36)], two patients developed pulmonary embolism, 14 a post-thrombotic syndrome and 16 patients died. Initial therapy included heparin (n =36) or fibrinolysis (n =4). Upper extremity deep venous thrombosis are mostly associated with cancers and venous catheters. Thrombophilia is frequent in the other cases. Heparin followed by oral anticoagulation is the optimal therapy whose duration depends upon underlying condition. Fibrinolysis has not been useful for preventing post-thrombotic syndrome in our study.

HEREDITARY DISEASE: Hereditary anomalies of homocysteine metabolism are quite uncommon and manifest by very high homocysteine levels (100 mumol/l) and associated homocysteinuria. The risk of premature cardiovascular disease is high. Clinical, biological and epidemiological data accumulated since the 70 s have demonstrated that a moderately elevated serum homocysteine level favors the development of atherothrombosis. PROVEN RISK: The risk of coronary or cerebral events is 1.5 to 3-fold higher for fasting homocysteine levels above 15 mumol/l. These data show that moderately elevated homocysteine level is a powerful cardiovascular risk factor. Further information is however needed to ascertain its frequency in the population and determine whether it is a truly independent risk factor.Most cases of moderately elevated homocysteine can probably be explained by gene-environment interactions. Homocysteine levels can be lowered by oral administration of vitamin cofactors implicated in homocystein metabolisms: folic acid, vitamin B6, vitamin B12.

Hemorrhagic complications are the most frequent complications of antivitamin K (AVK) treatments and can be life-threatening. We report 75 patients from a University Hospital. They were 40 males and 35 females (median age 74 years, 20-94), and were classified into 3 grades according to clinical picture: grade 1 (no surgery or transfusion, grade 2: surgery or blood transfusion needed, grade 3: death). 43 patients had grade 1 complications, 27 grade 2, and 5 grade 3 complications. The most frequent complications were muscular hematomas (36 patients), sub-cutaneous hematomas (14 patients), digestive bleeding (13 patients), hematuria (12 subjects). Eight patients had intracerebral bleeding, of whom 3 died. The treatment time was very variable (1 to 988 weeks). Only half patients had a prothrombin rate (PR) below 20% but two thirds had an INR above 5. This study showed that PR was a poor predictor of hemorrhagic complications. INR was a better parameter. For 15 patients, we considered that the indication was unadapted or questionable, among whom 2 died. This work suggests that the promotion of AVK prescription rules should go on.

We report 6 cases of upper limb involvement in giant cell arteritis; upper limb involvement revealed the disease in 4 cases and clinical symptoms were present in 5 (upper limb pain, Raynaud's phenomenon). Upper limb pulses were not palpable and blood pressure unmeasurable in all. Duplex ultrasonography found signs of inflammatory arteriopathy in 4 cases (hypoechogenous halo of the arterial wall and acceleration of flow velocity). Arteriography was performed in 5 cases and showed long and regular stenoses. In the last case, arteriography was not done because the duplex exploration gave an easier diagnosis. With this technique, the diagnosis of upper limb involvement, frequent in autopsy series of giant cell arteritis, might be made more often. Corticosteroid therapy is indicated and surgery should be discussed only in emergency situations.

Patients 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-seropositive subjects with 100 microg 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 Willebrand factor and soluble thrombomodulin (both p0.01). 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.

Familial auto-immune hepatitis is unusual. We report a case in which hepatitis was associated with a deficiency in the C4 component of the complement.Type 1 auto-immune hepatitis A was diagnosed in a 38-year-old woman presenting with systemic lupus erythematosus. Her daughter had to undergo a splenectomy for immunologic thrombocytopenic purpura when she was 9 years old. When she turned 13, she further developed type 1 autoimmune hepatitis. During follow-up (4 and 8 years, respectively), both patients had a mild deficiency in C4.C4 deficiency is not only frequently observed in relatives of patients with auto-immune hepatitis, but also in familial systemic lupus. This abnormality may have had a crucial pathogenic role in these two patients.

We report a series of seven patients who had scleroderma renal crisis. Their primary clinical and laboratory features along with the details of their management were compared with those of similar cases from the literature. The seven patients died within one to four months of the diagnosis with a pattern of acute renal failure, left ventricular failure and malignant hypertension. Histopathologic examination was performed in four of the patients, in two of whom it revealed thickening of the wall of the interlobular arteries related to the scleroderma, and in the other two patients nonspecific lesions of malignant hypertension. This histopathologic particularity led us to propose, on the basis of multiple renal biopsies performed in patients with scleroderma, a lesion chronology of the kidney in patients with scleroderma. Nevertheless, the triggering factors and pathophysiologic mechanisms of scleroderma renal crisis remain unclear and its prognosis is severe. Early treatment with angiotensin-converting enzyme inhibitors and other vasodilatators administered intravenously can prevent death and dialysis.

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.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.In our observation, endothelium activation or antiphospholipid antibodies might be responsible for thrombosis.

We investigated the possible role of antiphospholipid (APA) and anti-human 2-glycoprotein I (beta2-GPI) antibodies (Ab) in thrombosis and atherosclerosis in human immunodeficiency (HIV)-positive patients, in whom they seem to be more frequent.We measured APA and anti-beta2-GPI Ab in 58 HIV-positive patients together with markers of disease progression, circulating beta2-GPI, plasma lipids, biological markers of endothelial activation and integrity (plasma thrombomodulin, von Willebrand factor, vascular cell adhesion molecule 1) and with antimalonic dialdehyde antibodies (anti-MDA Ab).We found a 41% frequency of IgG APA in the HIV-positive patients. APA IgMs were rarely positive (7%), and anti-beta2-GPI IgGs were positive in 3-4% patients. There was no correlation between APA or anti-beta2-GPI Ab and the presence of opportunistic infections. Although plasma thrombomodulin, von Willebrand factor and vascular cell adhesion molecule 1 were significantly increased in the HIV-positive patients, APA was correlated only with vascular cell adhesion molecule 1, suggesting that APAs are correlated with endothelial activation but not with vascular endothelial lesions. A correlation between APA and anti-MDA IgG was demonstrated using multivariate analysis (r=0.542, P0.0001), suggesting a relationship between the targets of these antibodies. Finally, IgG APAs are frequent in HIV infection but are not correlated with biological markers of endothelial injury.Our results do not support a role for APA or anti-beta2-GPI in HIV-associated silent vascular endothelial damage. However, the role of these autoantibodies in clinically relevant thrombotic events should be investigated in HIV-positive patients.

Giant cell arteritis is an inflammatory disease that can affect the arteries anywhere in the body. Two cases are reported in which the arteries of the lower limbs were involved. Intermittent claudication with a walking distance of only 30 m was the inaugural manifestation in both cases. A biopsy of the superficial femoral artery provided the diagnosis in the first case. Ergotamine toxicity was considered initially in the second case. Acute ischemia and gangrene requiring amputation can complicate giant cell arteritis of the lower limbs and consequently corticosteroid therapy in an effective dose should be given as soon as the diagnosis is made. The inflammatory arterial lesions improve under therapy, but irreversible fibrosis with stenosis can develop if treatment is initiated late.

Objectives. To evaluate the distensibility of large arteries in patients with systemic sclerosis (SSc). Design. Prospective case-control study including unselected patients with SSc. Setting. One cardiology and two internal medicine units in a teaching hospital. Subjects. Eighteen patients with SSc and controls matched for age, sex, height, weight and 24-h ambulatory blood pressure (BP). Intervention. The timing of Korotkoff's sounds (QKD interval), a newly described noninvasive ambulatory method was used to measure arterial distensibility during 24 h. Main outcome measures. Two endpoints were used: QKD 100–60 (normalized for a heart rate of 100 beats min-1 and a systolic BP of 100 mmHg) and the slope of QKD against pulse pressure. Results. The patients with SSc had a lower slope of QKD against pulse pressure than the controls (median 0.55, range 0–1.21, versus 0.92, range 0.5–1.34, respectively; P=0.003), and a lower QKD 100–60 (medians/ranges respectively 191 [162–216] and 203 [169–231]; P=0.01). Conclusions. These results indicate that arterial distensibility of large arteries is decreased in SSc.

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.

Our aim was to study the lipoprotein (a) (Lp(a)) levels in various pathological states.This investigation was prospective and included a healthy control group.This study was carried out in two internal medicine and angiology services in teaching hospitals.505 patients were included with various diseases: 66 acute infections, 9 HIV infections, 25 cancers, 86 diabetes, 36 systemic diseases, 94 atheromatous vascular disease, 27 arterial hypertensions. A control group was composed of 21 healthy subjects.There was no therapeutic intervention but cardiovascular treatments were recorded.Serum Lp(a), total cholesterol, triglycerides, HDL-cholesterol, calculated LDL-cholesterol, apolipoproteins A-I and B were measured together with inflammatory parameters, serum creatinine, proteinuria, serum aminotransferase activity.There was no difference in Lp(a) levels between controls and each patient group. However, a correlation was found in systemic diseases between Lp(a) and C reactive protein (r = 0.371, p = 0.026) or serum albumin concentration (r = 0.453, p = 0.006). In hypertension, Lp(a) correlated with serum creatinine (r = 0.420, p = 0.03). In the whole patient population, Lp(a) was correlated with cholesterol (r = 0.156, p = 0.0001), apolipoprotein B (r = 0.215, p = 0.0001), age (r = 0.108, p = 0.015), arterial events (r = 0.174, p = 0.0001) and platelet anti-aggregant drugs (r = 0.169, p = 0.0001).Lp(a), was related to atheromatous events and in systemic diseases to inflammation, suggesting that Lp(a) might vary in some patients in a manner similar to acute phase proteins.

The authors describe the third case in the literature of superior mesenteric artery's thrombosis occurring in the course of the Behçet's syndrome according to Mason and Barnes classification. Clinical manifestations in the patient were represented by intestinal angor. The literature data concerning vascular involvement in Behçet's disease, particularly thrombosis are reviewed. The value of noninvasive paraclinic arterial digestive explorations is discussed.

In 34 patients with peripheral occlusive arterial disease, circulating levels of endothelial cell markers were compared with the ischemic status. Unlike tissue plasminogen activator and plasminogen activator inhibitor, plasma levels of thrombomodulin were closely related to both transcutaneous oxygen pressure (p = 0.01) and the graded clinical stages of disease (p = 0.02). Levels of von Willebrand factor were correlated only with the transcutaneous oxygen pressure (p = 0.04). Since thrombomodulin and von Willebrand factor constitute markers of endothelial cell damage, the extent of endothelial injury would appear to be determined by the ischemic status.

Objective: To investigate red blood cell (RBC) and plasma fatty acids (FA) in HIV-positive patients in relation to oxidative stress and nutritional or immunologiical status. Design and Methods: FA, plasma selenium, vitamins A and E were measured in 95 patients divided into four groups according to CD4 cells. Results: Poly- and di-unsaturated FA (PUFA, DUFA) decreased and saturated FA (SFA) increased in RBC in the patients below 400/mm3 and in plasma in the patients below 50/mm3 RBC SFA correlated to CD4 cells, PUFA to MDA. Unlike vitamin E, plasma vitamin A and selenium decreased in most groups. Plasma SFA and MUFA correlated negatively to selenium and PUFA and DUFA to vitamin E. No correlation was found between PUFA and nutritional markers. Conclusion: FA seem to be modified during HIV infection by oxidative stress and disease evolution, but not by denutrition.

Antiphospholipid/cofactor antibodies are detected in only 60% of patients with systemic lupus erythematosus (SLE) with thrombosis.1 Therefore, we studied thrombophilia factors and their relation with thrombosis in patients with SLE. Forty eight consecutive patients with SLE were included (39 women, 9 men), 15 with and 33 without past thrombosis (Th and NTh group, respectively). Twenty thrombotic events were identified: 17 deep venous and 1 arterial thrombosis, 2 osteonecrosis. Both groups had comparable clinical, biological, therapeutic data, and mean (SD) SLE disease activity index (SLEDAI) (5 (4.6) v 5.3 (4.8)). Patients were examined at least one month after thrombosis (>3 months in 11 out of 15). The following parameters were determined: protein C, total and free …