Albumine sérique et maladies cardiovasculaires : une revue approfondie de la littérature

Cardiovascular diseases are the leading cause of death worldwide. Conceptually, endothelial dysfunction, inflammatory status and oxidative stress are at the forefront in the onset and development of most cardiovascular diseases, particularly coronary artery disease and heart failure. Serum albumin, the most abundant plasma protein, has many physiological properties, including anti-inflammatory, antioxidant and antiplatelet aggregation activity. It also plays an essential role in the fluid exchange across the capillary membrane. Definite evidence is that hypo-albuminemia is a powerful prognostic marker in the general population as well as in many pathological settings. In the more specific context of cardiovascular diseases, serum albumin is independently associated with the development of a variety of deleterious conditions such as coronary artery disease, heart failure, atrial fibrillation and stroke. Serum albumin has also emerged as a powerful prognostic parameter in patients with coronary artery disease, heart failure, congenital heart disease, infective endocarditis, cardiovascular surgery and stroke, regardless of usual prognostic markers. This prognostic value probably refers mainly to the malnutrition-inflammation syndrome and the severity of comorbidities. Nevertheless, hypo-albuminemia may act as an unknown and modifiable risk factor that contributes to the emergence and the pejorative evolution of cardiovascular diseases, mainly by exacerbation of inflammation, oxidative stress and platelet aggregation, and by pulmonary and myocardial edema. This article provides an overview of the physiological properties of serum albumin, the prevalence, causes, prognostic value and potential contribution to the emergence and aggravation of cardiovascular disease of hypoalbuminemia, as well as its clinical implications.     

Botulisme : à propos d’un cas et revue de la littérature

IntroductionBotulism is a rare syndrome resulting from the action of a neurotoxin produced by Clostridium botulinum, that it is potentially life threatening if diagnosis is delayed.Case reportWe report a 26-year-old woman who presented an acute onset of bilateral cranial neuropathies associated with an anticholinergic syndrome in the absence fever leading to consider and confirm the diagnosis of botulism. At the end of follow-up, 7 weeks later, the outcome was favorable with an almost complete neurologic recovery.ConclusionAlthough botulism is uncommon, better awareness of its manifestations and high clinical suspicion should shorten diagnostic delay that makes the use of specific antitoxin ineffective. An acute onset of a bilateral oculomotor palsy, a fixed pupillary dilation and descending weakness in the absence of fever is typical of botulism. Outcome is usually favorable with a slow but full neurological recovery.     

Entéropathies exsudatives : à propos de cinq observations et revue de la littérature

Objective

Protein-losing enteropathy (PLE) is a rare entity with multiple etiologies. The diagnosis is confirmed by the elevation of faecal alpha-1-antitrypsin clearance. We report five cases of PLE and review the clinical characteristics and prognosis factors.

Methods

We retrospectively reviewed the medical report of 5 patients with PLE seen at the Department of internal Medicine between Hedi Cheker Hospital between 1996 and 2012.

Results

Five women with a mean age of 44.8 years (25–70 years) were studied. The initially suggestive clinical symtomatology was lower edema was in 3 cases, ascites in a patient while EE was discovered incidentally in another case. There were no gastrointestinal symptoms in all cases. Biologically, hypoproteinemia with hypoalbuminemia was found in all patients, hypogammaglobulinemia in 3 patients and lymphopenia in 3 cases. Hypocalcemia was present in one case, moreover, there was no digestive malabsorption in others cases. Renal function was normal without proteinuria in all cases. PLE was confirmed by the elevation of the clearance of alpha -1-antitrypsin in all patients. The investigations revealed systemic lupus erythematosus (SLE) in one case, a duodenal lymphangiectasia associated with non specific ulcerative ileitis in another. Celiac disease was highly likely in a patient, an iatrogenic origin was implicated in another (magnesium hydroxide). However, no cause was found in the fifth patient. All patients received a high-protein diet with specific treatment in three cases. The outcome was good in four patients with resolution of edema and correction of laboratory abnormalities.

Conclusion

PLE is a rare entity with digestive or nondigestive causes. Dietary measurement is generally indicated associated with the treatments of the more common causes.     

Syndrome de Budd-Chiari primaire: à propos de quatre observations et revue de la littérature

Introduction

Budd-Chiari syndrome results from obstruction of hepatic venous drainage from the hepatic venules to the distal inferior vena cava. It is a rare condition whose causes are multiple.

Materials and methods

We report four clinical observations collected at the Service of Internal Medicine, Hospital University Center Hassan II, Fez, between December 2004 and February 2007.

Results

These two cases of Budd-Chiari syndrome secondary to Behcet’s disease, occurred in the first observation after ten years of disease progression. In addition, thrombosis of hepatic veins was discovered fortuitously in Observation number 4 during an abdominal scan, performed before the presence of an inflammatory syndrome. The Budd-Chiari syndrome was secondary to a primary antiphospholipid syndrome in the second observation and a paroxysmal nocturnal hemoglobinuria in the third case.

Conclusion

The Budd-Chiari syndrome is associated in two thirds of cases with one or more underlying prothrombotic disorders, including myeloproliferative disorders, which are the main primitive in about 50% of the cases, mutation of factor V Leiden or a deficiency of protein C in about 25% of the cases, antiphospholipid syndrome in about 20% and paroxysmal nocturnal hemoglobinuria or Behçet’s disease in about 5% of the cases. The Budd-Chiari syndrome may be asymptomatic, discovered incidentally by an abdominal doppler ultrasound or an abdominal scan, found in 20% of cases. The chronic form of Budd-Chiari syndrome is reported in 60% of the cases.