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INTRODUCTION: New-onset diabetes mellitus (NODM) has important implications for long-term outcome following liver transplantation. AIM: To evaluate the impact of conversion from tacrolimus to cyclosporine in liver transplant patients presenting NODM. METHOD: In a 12-month pilot study, 39 liver transplant patients with NODM were converted from tacrolimus to cyclosporine. Most patients (59%) were receiving antidiabetic therapy (18% insulin, 41% oral) and all patients had received dietary advice prior to the study. RESULTS: At month 12, NODM had significantly resolved (FBG<7 mmol/L without treatment) in 36% of patients (95% CI 20.8-51.0%). In the 16 patients not receiving antidiabetic drugs at baseline, mean FBG decreased from 8.1 mmol/L to 6.6 mmol/L (P=0.008) and mean HbA(1c) decreased from 6.4 to 6.0% (P=0.05). Steroids were stopped rapidly in the nine patients receiving steroids at inclusion but NODM resolution was observed in only one of these nine patients. No significant factors were identified that could have affected NODM resolution. There were three episodes of biopsy-proven acute rejection (7.7%), no graft losses and one death. Overall, cyclosporine tolerance was good with no significant change in creatinine clearance at month 12. Total cholesterol increased from 4.6 mmol/L to 5.1 mmol/L (P<0.001). CONCLUSIONS: These results suggest that liver transplant patients with NODM may benefit from conversion to cyclosporine from tacrolimus through improved glucose metabolism. Confirmation in a prospective, randomized comparative study is required.

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The idiopathic hypereosinophilic syndrome is defined by the combination of prolonged eosinophilia and evidence of tissue damage including heart and nervous system. Cardiac disease is the major cause of mortality. The idiopathic hypereosinophilic syndrome is a heterogeneous collection of disorders. Products of activated eosinophils could exert toxicities on specific organs; it is a diagnosis of exclusion. There is no specific tests diagnostics. The development of a comprehensive diagnosis and therapeutic approach ensure from a better understanding of the pathogenesis.

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BACKGROUND: The antiphospholipid syndrome was individualized 12 years ago. Treatment was initially based on steroids, immunosuppressive drugs and intravenous immunoglobulin therapy. More recently, several retrospective studies have established that in most clinical conditions therapeutic doses of oral vitamin K antagonists (INR > or = 3) are sufficient to control the disease. THE ROLE OF IMMUNOGLOBULIN THERAPY: However, high dose immunoglobulin therapy is still indicated in a few cases, especially in life-threatening immune peripheral thrombocytopenia, and in recurrent foetal loss: in the latter indication, immunoglobulin therapy alone is efficient in 80% of cases. FUTURE PROSPECTS: Prospective studies are needed to assess the efficacy of intravenous immunoglobulin therapy in neurological complications occurring in spite of anticoagulant therapy, and in the context of repeated foetal losses when antithrombotic therapy with aspirin and subcutaneous heparin has failed.

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The autonomic cardiovascular control was investigated in 10 patients with septic shock, 10 patients with sepsis syndrome, and six tilted healthy subjects. Overall variability, high- and low-frequency components (AUC, HF, and LF, beats/min(2)/Hz or mm Hg(2)/Hz) from heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressures spectra were obtained from 5-min recordings. LF(HR)/HF(HR) and the square root of LF(SBP)/LF(HR) (alpha) were used as indices of sympathovagal interaction and baroreflex control of the heart, respectively. Compared with tilted control subjects and patients with sepsis syndrome, septic shock is characterized by reduction in: (1) HR variability, i.e., decreased AUC(HR) (p = 0.007), LF(HR) (p = 0.002), and LF(HR)/HF(HR) (p = 0.0002); (2) DBP variability, i.e., decreased AUC(DBP) (p = 0.003) and LF(DBP) (p = 0.001), (3) alpha (p = 0.003). In septic shock, LF(HR)/HF(HR), alpha, and LF(DBP) correlated with mean blood pressure (r = 0.67, p = 0.04, r = 0.64, p = 0.03, and r = 0.88, p = 0.0008, respectively), and with plasma norepinephrine levels (r = -0.65, p = 0.03, r = -0.79, p = 0.006, and r = -0.69, p = 0.03, respectively). In conclusion, onset of septic shock is characterized by high concentrations of circulating catecholamines but impaired sympathetic modulation on heart and vessels, suggesting that central autonomic regulatory impairment contributes to circulatory failure.

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The effect of Guillain-Barré syndrome (GBS) on the short-term variability of blood pressure and heart rate was evaluated in six patients presenting with a moderate form of the syndrome, i.e. unable to stand up unaided and without respiratory failure, at the height of the disease and during recovery. The patients were compared with six age-matched healthy volunteers. During the acute phase of the syndrome, GBS patients exhibited a significant heart rate elevation (+26 beats/min compared with healthy subjects), but the acceleratory response to atropine, or to 60 degrees head-up tilt, was maintained. Resting plasma noradrenaline levels were high in acute GBS, but the secretory response to tilt was preserved. Desensitization to noradrenaline was observed in acute GBS with a reduced pressor action of this alpha-adrenoceptor agonist. Blood pressure levels were normal and head-up tilt did not induce orthostatic hypotension in this moderate form of GBS. Power spectral analysis demonstrated marked alterations in cardiovascular variability. The overall heart period variability was markedly reduced with the reduction predominantly in the high-frequency (respiratory) range (-73%). The low-frequency component of heart period variability was also reduced (-54%). This cardiovascular profile of moderate GBS at the height of the disease could result from a demyelination of the reflex loop controlling respiratory oscillations in heart rate and from a desensitization of the arterial tree to an elevated plasma noradrenaline. Sympathetic nervous activation may contribute to the high resting heart rate in acute GBS.

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A sixty-three year old French man presented with isolated late-onset amyloid cardiomyopathy proven by endomyocardial biopsy. There was no known family history of amyloidosis. Immunohistochemistry of cardiac deposits suggested that amyloi fibrils were derived from transthyretin. DNA sequencing revealed a point mutation in exon 2 of the transthyretin gene responsible for a novel amyloidogenic variant Asp42.

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The beneficial effects of physical exercise on the blood pressure are widely recognised. Nevertheless, some athletes remain hypertensive and the treatment of this population makes special demands with respect to treatment efficacy and tolerability, the respect of athletic performance and problems of proscribed substances. For example, the Athletic Boards have prohibited betablockers and diuretics in competitive athletes. The aim of this study was to assess nicardipine LA 50 mg administered twice daily in the special context of hypertensive athletes. Thirty-eight athletes with mild or moderate hypertension undergoing endurance training were included in this double blind trial versus placebo. After two months treatment, the systolic and diastolic blood pressures were significantly lower at rest in the nicardipine than in the placebo group (delta SBP = -18.9 vs -4.1 mmHg, p less than 0.001; delta DBP = -15.7 vs -4.1 mmHg, p less than 0.01). In addition the maximum SBP on effort was significantly lower in the nicardipine group (200 vs 215 mmHg, p less than 0.05). On the other hand, no difference was observed between the two groups as regards the maximum oxygen consumption (delta VO2 max = 6.2 vs -0.4 ml/min/kg, NS) and duration of effort (13.75 vs 12.32 min, NS), showing that athletic performance was unchanged in the group treated by nicardipine LA. These results suggest that treatment with nicardipine LA fulfills the special criteria of hypertensive athletes.

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