[Thrombocytopenia associated with iron deficiency: a rare differential diagnosis of auto-immune thrombocytopenic purpura]. / Thrombopénie ferriprive : un diagnostic différentiel rare du purpura thrombopénique auto-immun.

INTRODUCTION: Iron deficiency is typically associated with microcytic anemia and thrombocytosis. It is a very uncommon cause of thrombocytopenia. CASE REPORT: A 17-year-old female presented with marked fatigue and dyspnea on exertion. Review of systems was only remarkable for abundant menstruations during the past two years. The hemogram revealed a profound microcytic anemia (4.4 g/dL, mean corpuscular volume [MCV] 49 fL) and a thrombocytopenia (33 G/L). Marked iron deficiency was also present: ferritinemia <3 µg/L. Investigations did not find any cause of iron deficiency anemia other than excessive menstrual loss. Bone marrow examination showed an increase number of megakaryocytes, compatible with an immune thrombocytopenia purpura. Iron supplementation completely normalized the platelet count within 48 hours. CONCLUSION: Iron affects thrombopoiesis. Because the number of megakaryocytes may then increase in the bone marrow, "iron deficiency thrombocytopenia" may be falsely diagnosed as immune thrombocytopenic purpura, leading to inappropriate corticosteroid therapy. Iron supplementation is the appropriate treatment of iron deficiency thrombocytopenia and allowed a rapid correction of the platelet count in all the 24 cases that have been previously reported with sufficient detail to be analyzed in the literature.

[Nonbacterial thrombotic endocarditis and gastric carcinoma]. / Endocardite marastique et adénocarcinome gastrique.

We report a 74-year-old woman with acute heart failure and recurrent ischemic strokes as the presenting features of a nonbacterial thrombotic endocarditis complicating a gastric adenocarcinoma. The treatment only allowed a few months remission. Diagnosis of nonbacterial thrombotic endocarditis is rarely obtained while the patient is alive. Coagulation abnormalities due to the tumoral process are responsible of the valvular thrombotic process. Anticoagulation with heparin is recommended. Valvular surgery remains controversial.

Galectin-3 gene (LGALS3) expression in experimental atherosclerosis and cultured smooth muscle cells.

The galectin-3 gene (LGALS3) encodes a beta-galactose binding lectin. LGALS3 expression is associated with neoplastic transformation and with differentiation of monocytes to macrophages. Factors involved in migration, proliferation, adhesion and differentiation of vascular smooth muscle cells (SMC) play a major role during atherosclerosis development. Expression of the galectin-3 gene was not detected in quiescent SMC but was activated in aortas of hypercholesterolemic rabbits, in aortas of rats after balloon injury and in cultured SMC. These results suggest that galectin-3 production is involved in the developmental process of atherogenesis.

[Severe hemorrhagic complications during treatment with low molecular weight heparin. Apropos of 2 cases]. / Accidents hémorragiques graves lors d'un traitement par héparine de bas poids moléculaire. A propos de deux observations.

Two cases of fatal bleeding in patients treated with low molecular weight heparin for deep vein thrombosis are reported. Risk factors for bleeding were: severe underlying disease (cancer in one case, morbid obesity and cardiac failure in the other), age over 80 years and worsening of renal insufficiency in both cases, recent surgical procedure in one case. Anti-Xa activity was beyond the therapeutic range at the time of bleeding in both cases. The usefulness of biologically monitoring the treatment of deep vein thrombosis with low molecular weight heparin is discussed.

Pharmacologic approaches to the treatment of atherosclerotic arterial obstruction.

Three consecutive periods in the natural history of atherosclerosis are amenable to medical treatment. Plaque development is the main target of prevention, which also aims at slowing the progression of already existing plaques. The control of several established risk factors (high blood cholesterol, high blood pressure, diabetes mellitus, tobacco smoking) has already yielded encouraging benefits, especially in the field of secondary prevention. More efficient prophylaxis is to be expected, either from the further improved control of these classic risk factors with earlier, stronger, and longer interventions or from the correction of newly established causal determinants of atherosclerosis. A plaque manifests itself clinically through progressive or abrupt obstruction of the arterial lumen, which can be avoided or retarded by interventions aimed at reducing thrombosis, at controlling plaque instability (the major cause of thrombosis), and at enhancing arterial remodeling (which allows compensatory enlargement of the arterial lumen). When ischemia has occurred, a third wave of palliative treatments aims at improving energy supply to the organ with compromised vascularization. Classic treatments reduce oxygen consumption or improve oxygen extraction by ischemic tissues. In addition, the design of drugs to enhance the development of collateral channels appears to be promising therapeutic approach.

National study of obliterative arterial disease of the lower limbs involving general practitioners in France: Artemio study.

A national survey was performed in France from May to June, 1993. The aim of this study was to evaluate general practitioners' attitudes and behaviors when diagnosing and managing patients with lower extremity arterial disease (LEAD). One thousand general practitioners, randomly drawn from an exhaustive list, were contacted to participate in a telephone interview concerning the last patient with intermittent claudication seen in their practice. Four hundred seventy-six general practitioners participated. Risk factors noted for these 476 patients with intermittent claudication were in agreement with the literature: 86% were men aged 64 +/- 10 years (mean +/- SD) and 14% were women aged 73 +/- 8 years. Sixty-two percent had a pain-free walking distance of between 100 and 500 meters at diagnosis. Forty-five percent were former smokers and 37% currently smoked; 55% had hypertension, 14% diabetes, and 56% disturbances of lipid metabolism. A majority of them were hypercholesterolemic. The diagnosis of the disease was based primarily on a clinical assessment, confirmed for 33% by Doppler or echo Doppler. The mean duration of diagnosis was 4.4 +/- 4.1 years. Management of the disease was mainly by prescription of vasodilators (91%), antiplatelet agents (59%), and anticoagulants (8%). Use of Doppler or echo Doppler was recommended once a year. Infection was observed in 27% of patients. Thirty-eight percent had had a cardiac incident (angina pectoris or myocardial infarction) and 10% a cerebrovascular accident. They differed significantly from those with LEAD alone for the following parameters: age (68.5 +/- 9.2 vs. 63.2 +/- 10.3 years; p < 0.001); duration of LEAD (5.6 +/- 4.6 vs. 3.6 +/- 3.5 years; p < 0.001); hypertension (65% vs. 50%; p < 0.01); and current smoking (29% vs. 43%; p < 0.01). This survey confirmed the feasibility of telephone interviewing, on a large sample of general practitioners in France. The high level of association with other cardiac incidents was, for these patients, a much higher risk of mortality and morbidity than LEAD alone. It would be interesting to validate the associations observed with a prospective study of comorbidity.

[Inflammatory mechanisms of atherosclerosis: pathogenic and etiologic inferences]. / Mécanismes inflammatoires de l'athérosclérose: inférences pathogéniques et étiologiques.

Inflammation is the reaction of a vascularized living tissue to local injury. At its chronic stage, inflammation displays 4 characteristic features that are all to be found in atherosclerotic plaques: lympho-monocytic infiltration; sclerosis; cellular proliferation; vascular proliferation. This view sheds new light and opens new avenues for research on atherosclerosis. That is true for pathogenesis which progressively integrates the mass of information that has accumulated about the cellular and molecular mechanisms of inflammation. That is also true fort the aetiology of atherosclerosis where the causal enigmas are approached with a more open mind, much wider than the traditional concepts of degeneration and overloading that have prevailed for so long. In the near future, some promising therapeutic clues should derive from this renewed approach of atherosclerosis.

[Staphylococcus aureus endocarditis: an unusual clinical picture]. / Endocardite à Staphylococcus aureus: présentation clinique inhabituelle.

We describe an unusual presentation of bacterial endocarditis due to Staphylococcus aureus in a 50 year-old woman with mitral insufficiency. The disease began by a vascular purpura without fever and a digital embolism. The source of infection was anal ulcerations. Diagnosis of endocarditis was made possible by trans-oesophagus echocardiography but not by trans-thoracic echocardiography. The patient was successfully treated by surgery associated with antibiotherapy. This observation emphasizes the indications of surgery at the acute phase of endocarditis. The anal source of endocarditis is original, no other case has been found in the literature.

[Leukocytes and arteriosclerosis]. / Leucocytes et athérosclérose.

Human atherosclerotic plaques contain two type of leucocytes: 1. Monocytes/macrophages comprise almost two thirds of the cells in the center of the lesion (lipid core), and a quarter of the cells in its periphery (fibrous cap); 2. T lymphocytes comprise 10 to 15% of the plaque cells. Polymorphonuclear granulocytes are only present in very small number. The abundance of leucocytes, together with sclerosis and proliferation of mesenchymatous cells (arterial smooth muscle cells), confer to atherosclerosis the aspect of a chronic inflammatory reaction, a fact which has been recognised for a long time. Monocytes/macrophages may contribute to the development of atherosclerosis in several ways: stimulation of the fibro-muscular reaction, endothelial injury, accumulation of intimal lipids. The role of T lymphocytes is still poorly understood. According to some observations, they might be involved in an immunological reaction of the arterial wall which could be determinant in the evolution of the lesion. Arterial leucocytes have somewhat complicated, but also widened our pathogenic hypotheses of atherosclerosis. A major issue now is to identify the nature of the arterial aggressions which provoke the involvement of leucocytes, and the reasons why the defences they oppose are overwhelmed to result eventually in severe thrombo-occlusive events. Recent evidence has strengthened the possibility that viral infection plays a role in atherosclerosis. Beyond their pathogenic interest, these acquisitions might soon provide interesting therapeutic approaches.

[Viruses and atherosclerosis]. / Virus et athérosclérose.

Our understanding of the pathogenesis and aetiology of atherosclerosis remains incomplete. An infection by herpesviruses is among the plausible hypotheses. In chicken, inoculation with Marek's disease virus provokes arterial lesions closely resembling atherosclerotic plaques. Experiments done on cultured arterial cells have shown that herpesviruses might enhance atherogenesis. Herpesviruses molecules (proteins, messenger ribonucleic acid, deoxyribonucleic acid) are commonly found in the human arterial wall. According to a recent study using gene amplification by the polymerase chain reaction, the complete cytomegalovirus genome can be detected in 90 p. 100 of the samples from atherosclerotic plaques and in 53 p. 100 of the samples from normal arterial wall. Cytomegalovirus infection appears to increase the risk and severity of atherosclerotic lesions which develop in heart grafts and compromise their survival. These data are not sufficient to prove that herpesviruses, especially cytomegalovirus, play a causal role in human atherosclerosis. The viral hypothesis, however, must be considered as serious and is certainly worth further investigations.

[New concepts of atherogenesis]. / Notions nouvelles sur l'athérogenèse.

The main advances since 1980 in our understanding of atherosclerosis can be summarised under four headings. 1) The migration and proliferation of smooth muscle cells from the media into the intima are key-events of atherogenesis, and probably also of restenosis following percutaneous transluminal coronary angioplasty. The experimental study of their regulations, especially looking for inhibitors, has therefore gained increased interest as it may provide original approaches to the prevention of post-angioplasty restenosis. 2) The histiocytes/macrophages, derived from blood monocytes, also take a major part in the initiation of atherosclerotic lesions. An intensive research activity is now being devoted to elucidating the many facets of their participation in atherogenesis. 3) Brown and Goldstein's discoveries have explained the biochemical mechanisms of the increased plasma low-density lipoprotein (LDL) concentration found in familial hypercholesterolemia (type IIa), although they did not completely solve the enigma of lipid deposition in the arterial wall. The metabolic handling of modified LDLs appears to be crucial to the foamy transformation of macrophages and, possibly, of smooth muscle cells. 4) Risk factors identified by epidemiology are usually held responsible for atherosclerosis. Yet this causal interpretation is not entirely satisfactory, and alternative or complementary hypotheses are being but forward. Among them, the most consistent submits that a viral aggression of the arterial wall is involved in the genesis and progression of atherosclerosis.

[Epidemiology and risk factors of cerebral arterial accidents]. / Epidémiologie et facteurs de risque des accidents artériels cérébraux.

In France, available epidemiologic data (mortality statistics, Paris prospective study)--although still insufficient--indicate: 1) that arterial strokes account for about 13 per cent of all deaths, and 2) that their annual incidence in men aged 40 to 60 is around 0.6 per thousand and increases sharply thereafter. These results are comparable to those of other industrialized countries, with the exception of Japan where the actual incidence of arterial strokes seems to be higher. Age and high blood pressure are the major risk factors and causes of the various types of ischaemic and haemorrhagic arterial strokes. Several studies suggest that the treatment of hypertension significantly decreases the incidence of arterial strokes.