Thrombose veineuse cérébrale après ponction lombaire et stéroïdes intraveineux chez deux patients souffrant d'une sclérose en plaques [Cerebral venous thrombosis after lumbar puncture and intravenous steroids in two patients with multiple sclerosis]

Two patients affected with a multiple sclerosis developed cerebral venous thrombosis after lumbar puncture and treatment with intravenous methylprednisolone. In one case, the course was favorable. The second patient died in spite of intracerebral thrombolysis. The autopsy confirmed the diagnosis of cerebral venous thrombosis and multiple sclerosis. We discuss the relationship between lumbar puncture, steroid treatment and cerebral venous thrombosis.

Alvéolite aux isocyanates chez une couturière [Isocyanate-induced alveolitis in a furniture manufacture worker]

A 41-year-old woman who worked in a furniture plant was admitted to hospital for acute dyspnea that had developed a few hours she marked pieces of "Alcantara" material with a heated metallic blade. The chest x-ray showed a restrictive syndrome. The lymphocyte count was high in the bronchioalveolar lavage fluid with a CD4/CD8 ratio of 0.11, leading to the diagnosis of alveolitis. Investigations at the work place allowed identification and evaluation of the causal agent. Alcantara is a synthetic fabric composed of 70% polyurethane fibers, which when burned produces isocyanate monomers. After eliminating exposure and institution of corticosteroid therapy, the outcome was good with complete recovery. The risk was eliminated by changing the work procedure. This risk has not been reported earlier for furniture manufacture.

Exacerbations aiguës au cours de la fibrose pulmonaire idiopathique [Acute exacerbations of idiopathic pulmonary fibrosis].

Although generally considered as a slowly evolving disease, idiopathic pulmonary fibrosis (IPF) is also characterized by episods of rapid deterioration with worsening of dyspnea and hypoxemia, and new ground glass opacities at imaging. These events called "acute exacerbations" (AE) are responsible for half of all deaths in IPF. Pathophysiologic mechanisms of AE are poorly understood. The effectiveness of corticosteroids and immunosuppressive agents appears limited. The mortality of AE is 60-70%. Preventing or controlling AE could improve the overall prognosis of IPF. AE also exist in other interstitial lung diseases.

Hormonal and metabolic changes following severe head injury or noncranial injury.

In order to evaluate the effect of head injury in severely traumatized patients on the response of plasma cortisol, glucagon, insulin, glucose, and FFA as well as urinary N and catecholamines excretions, 36 patients were prospectively studied over 5 consecutive days following injury. They were divided into three groups: group I, severe isolated head injury (n = 14); group II, multiple injury combined with severe head injury (n = 12); group III multiple injury without head injury (n = 10). The results demonstrate similar hormonal and metabolic changes between these three groups of patients, characterized by elevated urinary adrenaline, noradrenaline excretion, increased cortisol, glucagon, insulin plasma levels throughout the study and elevated N urinary excretion with strongly negative N balances during the first 5 days postinjury. A significant correlation was observed between N intake and 5 day cumulated N balance (r = 0.63, p less than 0.001). In addition, N balance was negatively correlated with urinary excretion of adrenaline (r = -0.47, p less than 0.01) and noradrenaline (r = -0.44, p less than 0.05) as well as plasma levels of glucagon (r = -0.44, p less than 0.05). Isolated severe head injury seems to induce a full response in the secretion of the catabolic counterregulatory hormones comparable to that encountered in patients with multiple injury and associated with a marked increase in protein catabolism; additional noncranial major injury does not seem to enhance these responses.

Prise en charge de l'asthme en médecine de premier recours [Management of asthma in primary care medicine].

The international recommendations issued by GINA (Global Initiative for Asthma) have undergone considerable adaptations over the last years. This article proposes the local adaptation of those guidelines bearing on the practical aspects of the treatment for the general practitioner's use. One of the fundamental changes in these new guidelines on good practice relates to the permanent adaptation of the treatment on the basis of symptom control rather than on the severity of the asthma. Another change from the old recommendations concerns the manner in which the asthma is categorised into different phases.

Hirsutisme: que faire [Hirsutism, what can be done?]

Hirsutism is a relatively frequent condition in an ambulatory setting affecting about 4% of women. A rational clinical and biochemical diagnostic approach assures an optimal treatment directed at etiologic and pathogenetic factors. The diagnosis of hyperandrogenism is evaluated considering the pathophysiologic mechanisms responsible for excessive growth of hair. Ovarian and adrenal tumors are the most serious diseases that have to be excluded by clinical and biochemical tests. The other causes for hirsutism are treatable by a great variety of modalities, available drugs can inhibit pituitary gonadotropins, the hypothalamo-pituitary axis and the conversion of testosterone into biologically active substrate. Finally the binding of androgens to its receptor can be blocked. These possibilities for treatment and their indications for the different etiologies of hirsutism are discussed.

Lésions cutanées et infiltrats pulmonaires d'évolution défavorable sans cause infectieuse [Progressive cutaneous and pulmonary lesions without infectious etiology: two cases reports of sweet syndrome with pulmonary involvement].

Sweet syndrome is a non infectious febrile disease with a neutrophilic infiltrate of dermis. Extracutaneous involvement can occur. We report two cases of Sweet syndrome with cutaneous and pulmonary involvement and give a short review of the literature of pulmonary involvement in Sweet syndrome.

Mineralocorticoid receptor is essential for corticosteroid-induced up-regulation of L-type calcium currents in cultured neonatal cardiomyocytes.

Despite the fact that mineralocorticoid receptor (MR) antagonist drugs such as spironolactone and eplerenone reduce the mortality in heart failure patients, there is, thus far, no unambiguous demonstration of a functional role of MR in cardiac cells. The aim of this work was to investigate the activation pathway(s) mediating corticosteroid-induced up-regulation of cardiac calcium current (ICa). In this study, using neonatal cardiomyocytes from MR or glucocorticoid receptor (GR) knockout (KO) mice, we show that MR is essential for corticosteroid-induced up-regulation of ICa. This study provides the first direct and unequivocal evidence for MR function in the heart.

Cibles rétiniennes d'action des médicaments [Retinal drug targets].

Retinal effects of systemically administered drugs are rare due to the hematoretinal barriers that protect the retina from circulating active principles. However, some compounds may have direct or indirect toxic effects on the retina through direct interaction with a specific receptor or due to their accumulation within pigment of uveal cells. In the latter case, toxicity is dose-dependent and may be observed years after cessation of medication, as observed with antimalarial drugs. Anti-infective and anti-inflammatory agents, particularly glucocorticoids, are currently injected peri- or intraocularly. The mechanisms and the exact toxicity of glucocorticoids on the retina remain poorly understood. More recently, anti-VEGF has been specifically developed for the treatment of retinal diseases. However, the long-term blockade of VEGF on normal retinal physiology should be determined taking into account VEGF and VEGF receptors expression in the normal and pathologic retina. Whilst enormous advances are made in the treatment of retinal diseases, basic research is still required to define more accurately the molecular targets of drugs to improve their benefits and reduce their potential side effects.

Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis.

Central serous chorioretinopathy (CSCR) is a major cause of vision threat among middle-aged male individuals. Multimodal imaging led to the description of a wide range of CSCR manifestations, and highlighted the contribution of the choroid and pigment epithelium in CSCR pathogenesis. However, the exact molecular mechanisms of CSCR have remained uncertain. The aim of this review is to recapitulate the clinical understanding of CSCR, with an emphasis on the most recent findings on epidemiology, risk factors, clinical and imaging diagnosis, and treatments options. It also gives an overview of the novel mineralocorticoid pathway hypothesis, from animal data to clinical evidences of the biological efficacy of oral mineralocorticoid antagonists in acute and chronic CSCR patients. In rodents, activation of the mineralocorticoid pathway in ocular cells either by intravitreous injection of its specific ligand, aldosterone, or by over-expression of the receptor specifically in the vascular endothelium, induced ocular phenotypes carrying many features of acute CSCR. Molecular mechanisms include expression of the calcium-dependent potassium channel (KCa2.3) in the endothelium of choroidal vessels, inducing subsequent vasodilation. Inappropriate or over-activation of the mineralocorticoid receptor in ocular cells and other tissues (such as brain, vessels) could link CSCR with the known co-morbidities observed in CSCR patients, including hypertension, coronary disease and psychological stress.