Search

Patients infected with the human immunodeficiency virus (HIV) appear to have a high risk of ischaemic cerebral events. We observed two cases of cerebral infarction in patients with acquired immune deficiency syndrome (AIDS). In the first case, a 38-year-old homosexual with no cardiovascular risk other than smoking presented with rapidly progressive hemiparesia. Brain CT-scan visualized two infarcts in the territory of the right sylvian artery and the arteriography an occlusion of the internal carotid artery. In the second, a 37-year-old homosexual, hospitalization was required for a left-sided pure sensitive epilepsy seizure. There was no cardiovascular risk other than smoking. Magnetic resonance imaging showed parietal ischaemia and thrombus in the left atrium without atrial hypertrophy was seen at transoesophageal echocardiography. In both cases, there was no evidence of endocarditis, dissection of the neck vessels or disseminated intravascular coagulation nor of associated viral or bacterial infectious complication of AIDS. Angiographic findings eliminated cerebral vascularitis. Among the perturbed haemostasis factors previously reported in HIV+ patients, we observed free proteins S deficiency (68 and 43%) and heparin cofactor II deficiency (54 and 40%). Serum albumin was 33 and 32 g/l respectively. Outcome was favourable in both cases with anticoagulant therapy. These coagulation anomalies would not appear sufficient to explain cerebral infarction. Other mechanisms including immune complexed deposition, direct HIV toxicity for endothelial cells or the effect of cytokines on smooth muscles fibres and fibroblasts are probably more important causal factors.

We report the case of a 23 year-old Caribbean woman with sarcoidosis who developed specific skin ulcerations. Ulcerative lesions in sarcoidosis are distinctly unusual, generally multiple, painless, with preponderant location on the lower limbs. The diagnosis is difficult. The pathogenesis is discussed. The most successful therapy is hydrochloroquine with corticosteroids.

A 3-year old boy was referred to a paediatric psychiatry out-patient clinic for major disorders consisting of hyperphagia, intolerance to frustrations and instability since the age of one year, and pica (i.e. the indigestion of non-edible substances) since the age of two years. These symptoms developed in a context of greatly disturbed parent-child relations, predominantly made of ambivalence and inability to define limits and interdictions. Conversations with the family are restoring the parental roles and improving the child's symptoms.

Type IV glycogen storage disease, also termed Andersen's disease or amylopectinosis, is a rare autosomic recessive hereditary disease usually caused by a deficit in glycogen branching enzyme. We report our observation of two siblings with type IV glycogen storage disease who had normal branching enzyme activity. The initial symptom was severe heart failure. A 14-year-old boy, born to consanguinous parents, was seen for severe global heart failure. Growth retardation had been diagnosed since the age of 6 and abnormal fatigability since the age of 12. Muscle and endomyocardium biopsies revealed abnormal glycogen storage with normal branching enzyme activity. The patient's condition improved after symptomatic treatment, but death occurred due to infectious complications after orthoptic heart transplantation. One year later, the proband's 12-year-old sister, with an uneventful personal medical history, was hospitalized for severe left ventricular failure. Muscle and liver biopsies demonstrated the same anomalies, again without branching enzyme deficiency in the liver. Heart failure was controlled with symptomatic care and the patient's current condition remains satisfactory. This observation demonstrates the clinical expression of familial type IV glycogen storage disease in patients with normal branching enzyme activity. Age at onset is quite variable, reported from 5 to 70 years, as is the clinical course before diagnosis.

The concept of Internal Medicine was introduced recently and stems from the Internal Pathology which dates back to Antiquity. This concept spread out during the XIXth century with the concomitant progress of clinical science and heurism within a global and humanistic medicine. In France, Internal Medicine was not recognized until 1966. The criteria of eligibility for certification in this specialty were issued in 1970. The Syndicat National des Médecins Spécialistes de Médecine Interne, the Société Nationale Française de Médecine Interne and the diploma of certification in Internal Medicine were respectively created in 1975, 1979, 1984. The field of interest of Internal Medicine is wide and ambiguous. It includes a specific hard core and less specific allocations that encroach on "organ" specialties. French internist practitioners are not numerous and most of them are practising in hospitals. Internal Medicine is highly regarded in Anglo-Saxon countries and in Germany. In the European Community, the future of this medical specialty depends on the success of the harmonization of training programs and the development of medical students exchange. There is currently a controversy about the recognition of Internal Medicine as a full specialty. To bring out this specialty, French internists should benefit from reforms at several levels: university, hospital and French health service contract.

During the last few years the fluoroquinolone class has been profoundly reshaped. The development of mutation-acquired resistance, principally from staphylococci and Gram-negative bacteria responsible for nosocomial infections has restricted the use of these antibiotics as first-line monotherapy to some community-acquired infections (urinary tract, gastrointestinal, sexually transmitted infections), while defects in their antibacterial spectrum (pneumococci, streptococci and anaerobes) have reduced the possibility of use against respiratory infections. Future developments concern compounds that are active against Gram-positive cocci and some intracellular bacteria (e.g. mycobacteria) and possibly against certain parasites. Problems of tolerance are important in clinical trials of the new compounds.

Bartter's syndrome, sometimes a familial autosomal recessive condition, is characterized by hypokalaemia with normal kaliuresis, hyperreninaemia with secondary hyperaldosteronism, vascular resistance to angiotensin and overproduction of prostaglandins by the kidneys. This syndrome is rare but sometimes envisaged in patients with unexplained hypokalaemia, the main difficulty being to exclude intoxication with diuretics which is very similar in all respects. Its physiopathology is unknown, and the various hypotheses put forward since it was first described (vascular insensitiveness to angiotensin, defect of sodium or chloride reabsorption, excess of atrial natriuretic factor, general abnormality of membrane permeability) were unable to demonstrate their primary character, each disorder described seeming, subsequently, secondary to another. For this reason, treatment is difficult and disappointing, but although the hypokalaemia is sometimes worrying, Bartter's syndrome is usually a benign condition.