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of HS [2] : serum alanine aminotransferase (ALAT) level usually rises within 30 min after HS and peaks within 3-4 d. The risk of ALF during HS must be emphasized, because its incidence appears to be higher than is indicated in this study. Irreversible ALF is rare and may require liver transplantation [3] . We have already reported some of our clinical data [4,5] , from a cohort of 50 male subjects (which now consists of 110 cases); all investigated after EHS were confi rmed by clinical and biological data, study of muscle metabolism by magnetic resonance spectrophotometry, muscle biopsy for pharmacodynamic tests, and pathology. Twenty-fi ve of these consecutive patients (aged 25 ± 4 years) with EHS and ALF were compared with 25 other EHS patients, who were age-matched but without ALF (ALAT 3563 ± 1313 vs 590 ± 742 IU/L; factor V 30% ± 12% vs 66% ± 20%; P < 0.001 for each). ALF was defi ned as ALAT > 10 times the upper limit, and coagulopathy (factor V lower than 50%).Age, body mass index, physical fitness, background, climatic conditions, drug and alcohol intake, clinical manifestations and laboratory fi ndings were analyzed with reference to their prognostic signifi cance in ALF. A logistic regression model was used. In 22 of 25 patients, ALAT level returned to normal within 10 d, but three patients died of ALF. Univariate analysis found that poor fi tness (P = 0.02), hygrometry > 86% (P = 0.03), creatininemia > 160 μmol/L (P < 0.001) and hypophosphatemia < 0.5 mmol/L (P < 0.001) were significant predictors of ALF. In multivariate analysis, on admission, hypophosphatemia < 0.5 mmol/L was the only independent predictive factor of ALF (RR 3.8, 95% CI 1.1-6.2).In conclusion, ALF is not uncommon in EHS of which we assert, as Weigand et al [1] , that this one is an underestimated cause.This ALF is strongly associated with early hypophosphatemia, of which a value < 0.5 mmol/L is predictive. However, there is no evidence that hypophosphatemia by itself causes important liver dysfunction [6] . Massive liver cell necrosis results from thermal shock, circulatory disruption, endotoxinemia (heat sepsis), high blood concentration of cytokines and acute-phase proteins.Therefore, in EHS, measurement of phosphatemia, ALAT and factor V should be systematic on admission, and 3-4 d later. Phosphorus supply, usual in an intensive care unit, has not been evaluated in this situation. REFERENCES AbstractAcute liver failure (ALF) is relatively frequent during heat stroke (HS). This risk must be emphasized, because its incidence is higher than is usually thought. In a recent study by Weigand et al , two cases were reported in which liver failure was the leading symptom. We have confirmed their conclusion in a study of 25 cases of HS with ALF, compared with 25 other cases without ALF. Moreover, we observed that hypophosphatemia on admission could predict occurrence of ALF during HS. As for clinical and other biological parameters, phosphatemia should be monitored for at least 3 d in all cases of HS, even when it is thought to be mild.

The aim of this study was to ascertain if hyperhomocysteinemia is associated with the metabolic syndrome. The metabolic syndrome is a cluster of cardiovascular risk factors. Hyperhomocysteinemia is an obvious independent risk factor for atheroma, and thrombosis morbidity and mortality. EPIMIL is a prospective epidemiological survey, which began with a crosssectional study of cardiovascular risk factors in a French male population, followed by monitoring for 10 years. Initial data collection, blood pressure measurement, ECG, and blood samples have been performed. For the metabolic syndrome, we used the criteria of the Third Report of the National Cholesterol Education Program-Adult Treatment Panel III (NCEP ATP III) on detection, evaluation, and treatment of high blood cholesterol in adults. Out of 2045 men aged 20-58 years (37.7 +/- 8.7 years), 185 (9%) have metabolic syndrome (at least three criteria), 587 (29%) have a plasma homocysteine level of >/=12 micromol/L, and 202 (10%) have a level of >/=15 micromol/L. Mean homocysteinemia is 10.97 +/- 5.01 micromol/L for the whole population and does not differ significantly with (11.4 +/- 6 micromol/L) or without (10.9 +/- 5 micromol/L) the metabolic syndrome, as does its value distribution. Nor does it correlate with the Body Mass Index (BMI), waist and hip measurements, or blood glucose, HbA1c, insulin resistance, and cardiovascular risk markers (CRPus, microalbuminuria). It weakly correlates with systolic and diastolic blood pressure, creatinine clearance, tobacco use, cholesterolemia, triglycerides, and free fatty acids, but not with HDL and LDL fractions, or lipoprotein(a) (Lp(a)). It contributes slightly to the 10-year vascular risk according to the Framingham equations or Score system. In this male population, homocysteinemia and the prevalence of hyperhomocysteinemia do not differ with or without the metabolic syndrome. Plasma homocysteine level does not correlate with its main criteria. Hyperhomocysteinemia is not associated with the metabolic syndrome; nevertheless, it should be monitored in high-risk cardiovascular patients.

Hairy cell leukemia (HCL) is a rare, chronic, B-cell, lymphoproliferative disorder. Treatment has been revolutionized by the advent of interferon (IFN)-α and purine analogs (PA). First-line therapy with PA yields complete response rates of 75–100%, with many long-lasting remissions. In the event of profound neutropenia and/or infectious complications, a short sequence of IFN-α may precede PA treatment. Because of the excellent results achieved with PA therapy, the potential role of rituximab (an anti-CD20 monoclonal antibody that is highly effective against most B-cell lymphomas) in HCL has yet to be elucidated. Six HCL cases treated with rituximab are reported herein with a view to elucidating the potential role of the drug in HCL. The indications essentially consist of relapsing or refractory disease, avoiding the cumulative toxicity of PA, consolidation therapy in order to eradicate minimal residual disease, and first-line therapy for patients with contraindications to PA and IFN-α.

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