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Background: The post-partum blues is a transient mood alteration affecting most women a few days after delivery. Its stereotypic pattern of symptoms and time course, peaking on post-partum day 3-5, is suggestive of biological determinants superimposed on psycho-social factors. This study was designed to evaluate the possible role of the serotonin system during this period through assessment of brain tryptophan availability., Methods: Blood samples from 50 women were collected just before (D0) and 3 days after (D3) delivery. Based on plasma concentration of tryptophan, amino acids competing with tryptophan for transport across the blood-brain barrier and on their respective affinities for this transporter, a brain tryptophan availability index (BTAI) was calculated and its variation correlated with the intensity of post-partum blues evaluated through the Kennerley and Gath score at D3., Results: The BTAI showed a -15% decrease between D0 and D3 (p < 0.01, paired t-test). This decrease was not supported by a drop in plasma tryptophan since its level rather increased (+19%). There was no evidence for change in placental indoleamine-2,3-dioxygenase activity since the variation in plasma l-kynurenine (+12%) paralleled the change in tryptophan level. The decreased BTAI appeared the consequence of a dramatic increase in plasma levels of most amino acids, particularly the competitor aminoacids leucine, isoleucine, valine and tyrosine, during the early post-partum. This decrease in brain tryptophan availability was concomitant to the post-partum blues, whose intensity significantly correlated with the amplitude of BTAI variation (Pearson's coefficient -0.283, p < 0.05)., Conclusion: This study suggests that generalized, large amplitude metabolic and/or nutritional changes occurring in the early post-partum result in a transient decrease in brain tryptophan availability, partly accounting for the mood alteration referred to as the post-partum blues, a model for the triggering of puerperal mood disorder in vulnerable women.

Background: Plasma homocysteine concentrations increase with age and remain an independent risk factor for vascular disease in the elderly. There are negative correlations between plasma homocysteine and serum folate and vitamin B12 concentrations. Two mechanisms, poor nutritional status, and chronic atrophic gastritis, could explain hyperhomocysteinemia., Objective: The purpose of the study was to determine prevalence and mechanisms of hyperhomocysteinemia in older hospitalized patients., Designs: During a 12-month period, all the consecutive hospitalized patients who underwent gastric endoscopy were recruited in this observational prospective study. Clinical, histological, and biological data concerning nutritional status, gastric analysis, homocysteine, vitamin B12, and folate concentrations were collected during the study for each included patient., Results: One hundred and ninety six patients (132 women and 64 men, mean age: 85.3 5.7 years) were included. Hyperhomocysteinemia (>or= 18 mmol/l) was diagnosed in 45.4 %, cobalamin deficiency in 13.3 %, and folate deficiency in 11.7 % patients. Hyperhomocysteinemia was significantly correlated to cobalamin deficiency (r = - 0.21; p = 0.005). In a sub group of patients without hypothyroidism, or chronic renal impairment, univariate and multivariate analysis showed a significant association between hyper homocysteinemia and low MNA (OR: 0.92; 95% CI 0.85-0.99), and low albumin (OR: 0.92; 95% IC: 0.83-0.99; p = 0.04). No correlation was found between homocysteine concentrations and chronic atrophic gastritis or Helicobacter pylori infection., Conclusion: Hyperhomocysteinemia seems to be frequent in the elderly and is associated with poor nutritional status rather than chronic atrophic gastritis.

Objectives: Juvenile peripheral obstructive arterial diseases (POAD) have been poorly investigated but account for 1 to 7% of POAD. We analyzed retrospectively a cohort of patients with onset before the age of 50 years., Patients and Methods: Seventy-three patients (60 males and 13 females) were divided into 4 groups (Buerger's disease: TAO, atheromatous PAOD, auto-immune POAD, arteriopathy of undetermined origin)., Results: The first symptoms occurred at 38 +/- 8 years of age. Fourteen patients (20%) had TAO, 51 (70%) atheromatous POAD, 4 (5%) POAD with systemic or autoimmune disease, and 4 (5%) undetermined POAD. Age of onset was earlier in TAO (35 +/- 8 vs 40 +/- 8 years, p=0.046), smoking greater in the atheroma group (33 +/- 16 vs 24 +/- 14 pack-years, p=0.033). Fifty-three POAD patients had dyslipidaemia and 26% hypertension. Regular cannabis intake was more frequent in the TAO group (21 vs 8%). At the time of medical care, Fontaine's stage was more frequently stage II in atheroma patients (57 vs 14%) and stage IV in TAO patients (86 vs 35%). TAO was diagnosed in 43% cannabis users and in 19% non users., Conclusion: The main etiology of juvenile POAD is atheroma, followed by TAO. Cannabis users account for at least 10% of these patients. They are characterized by lower tobacco intake, more distal lesions, more frequent involvement of the upper limbs. They present more frequently as TAO.

Homocystinuria is a genetically determined inborn error of the methionine amino acid pathway characterized by increased plasma homocysteine. In its major form, homocystinuria, is due to cystathionine beta synthase deficiency. Treatment of these adulthood patients lead physicians to call up on the skilled advices of pediatricians. But prevention and treatment of age related vascular and osteoporotic complications are still to be evaluated.

High-flux/high-efficiency (HF/HE) dialysis may have detrimental effects on micro-nutrients and water-soluble vitamins, such as vitamin B6, whose levels are lowered. Folate deficiency may increase cardiovascular risk through an increase in homocysteine (Hcy) serum levels. We therefore investigated the effects of dialysis with a high-flux (HF) membrane on folate and Hcy metabolism. Twelve patients without any folate supplementation, receiving dialysis with a low-flux membrane prior to the study (TO), were switched to dialysis using a HF triacetate membrane for four months (T1, T2, T3, T4) and received an oral daily folate supplementation during the two last months (T3, T4). Mean predialysis plasma folate levels fell dramatically after one month of HF dialysis (T1) and remained significantly lower than the initial level (p<0.05) at T2. Hcy concentrations were high in all patients at TO (mean 47.3 +/- 17.6 microM, normal range 5 to 15 microM). They did not change during the first two months of the study but dropped steeply after the beginning of oral folate supplementation. Folate supplementation should be used in HF/HE dialysis to avoid folate depletion. The combination of folate supplementation and HF/HE may lower Hcy levels and reduce cardiovascular morbidity and mortality in these patients.

HEREDITARY DISEASE: Hereditary anomalies of homocysteine metabolism are quite uncommon and manifest by very high homocysteine levels (> 100 mumol/l) and associated homocysteinuria. The risk of premature cardiovascular disease is high. Clinical, biological and epidemiological data accumulated since the 70 s have demonstrated that a moderately elevated serum homocysteine level favors the development of atherothrombosis. PROVEN RISK: The risk of coronary or cerebral events is 1.5 to 3-fold higher for fasting homocysteine levels above 15 mumol/l. These data show that moderately elevated homocysteine level is a powerful cardiovascular risk factor. Further information is however needed to ascertain its frequency in the population and determine whether it is a truly independent risk factor., Therapeutic Options: Most cases of moderately elevated homocysteine can probably be explained by gene-environment interactions. Homocysteine levels can be lowered by oral administration of vitamin cofactors implicated in homocystein metabolisms: folic acid, vitamin B6, vitamin B12.

Hyperhomocysteinaemia is a risk factor for premature atherosclerosis and venous thromboembolic disease. Supplementation with folic acid and vitamin B6 has been shown to decrease plasma homocysteine but data fail to assess an effect on the progression of vascular disease. We measured plasma homocysteine and two markers of endothelial injury (plasma soluble thrombomodulin and von Willebrand factor) at baseline and after 3 months of treatment with folic acid and vitamin B6. After this treatment there was a significant decrease in fasting soluble thrombomodulin (-15 ng/ml, 95%CI 5-22.2). Von Willebrand factor was significantly raised after methionine load at baseline but did not significantly rise after supplementation.

Hyperhomocysteinaemia has been associated with arterial and venous thrombosis possibly by causing damage to the endothelium. We hypothesised that an oral load in methionine, that increases plasma homocysteine, would also result in an increase in biological markers of endothelial or platelet dysfunction. Then we investigated two groups of patients with arterial or venous occlusive disease: 17 with hyperhomocysteinemia and 12 without hyperhomocysteinemia. We measured in both groups plasma soluble thrombomodulin, von Willebrand factor, P-selectin and tissue factor plasma inhibitor before and 6 hours after a load with 100 mg/kg oral methionine. Methionine load resulted in a significant increase in von Willebrand factor in both groups (P<0.02), suggesting that endothelial dysfunction occurs during the load.

Mild hyperhomocysteinemia, due to genetic or to environmental factors, is now recognized as a risk factor for premature arterial disease, including peripheral arterial occlusion, thrombotic stroke and myocardial infarction. It is defined by either an increased level of fasting homocysteine or by an increased level after loading with methionine, which is more frequently altered than the former. We studied the hemostatic parameters in 88 patients with premature arterial disease (mean age 43 +/- 11 years). We confirmed previously known hemostatic alterations described in vascular patients when compared to controls, but found that, among patients, some of these parameters were more altered in hyperhomocysteinemic patients. When fasting homocysteine was increased, higher alterations were found in factors VIIIc, von Willebrand and thombin-antithrombin complexes were more elevated. When post-methionine load homocysteine was increased, alterations in fibrinolytic parameters were more pronounced.

Glyphosate containing herbicides are an alternative to paraquat and are widely used throughout the world. Despite animal studies showing a low mammalian toxicity, human fatalities are reported after suicidal ingestions of glyphosate. Among the numerous analytical methods proposed, the reference method is the HPLC Monsanto procedure which is available in very few laboratories. The Monsanto procedure consists of a pre-column derivatization with detection of the resulting chromophore by HPLC with a variable wavelength UV/VIS detector. We propose a simple and rapid method for the diagnosis and monitoring of glyphosate poisoning. This method uses an aminoacid analyzer (Beckman 6300) with the program for biological fluids. With this procedure the glyphosate and amino methyl phosphoric acid retention times are respectively 1.75 and 3.54 min. This method gives a rapid result. The time between collecting the sample and completing the result is 45 min. This method may be useful for the diagnosis and monitoring of glyphosate poisoning and is easy to perform with an apparatus usually available in every laboratory involved in aminoacid analysis.

In 14 of 23 patients seen with coeliac disease thrombocytosis was present (range: 420,000 to 789,000 platelets per cubic mm) and was unrelated to iron deficiency or inflammatory syndrome. Among patients with thrombocytosis (group I), 6 had an associated autoimmune disease; this association was absent in patients without thrombocytosis (group II). There was no correlation between thrombocytosis and lymphocyte count, plasma IgA, IgG, IgM and fibrinogen levels, presence of HLA B8 antigen or histological stage. On the other hand, group I patients had a lower plasma level of albumin, phosphorus and folates. We conclude that thrombocytosis is useful in the assessment of patients with coeliac disease and reflects an enhanced activity of the disease. Moreover, the presence of thrombocytes in these patients' blood may indicate a major risk of associated autoimmune disease.

To evaluate nephrotoxicity of dibekacin among elderly patients, we studied the daily urinary excretion of NAG and determined isoenzyme levels in the urine of 36 patients (mean age 80 yrs) treated with dibekacin (3 mg.kg-1.day-1). Only two patients developed transient acute renal failure during the first 10 days of treatment. Total NAG urinary activity was however important (304.5 +/- 38.6 U/mmol creat), due primarily to isoenzymes A (58.8 +/- 2.0%) and I (30.8 +/- 1.5%), while B-form excretion was moderately increased (10.3 +/- 1.0%). These results were compared with those obtained with gentamicin (28 patients, 11 transient acute renal failure). The rate of A-form was identical for both antibiotics while excretion of the B-form was significantly higher with gentamicin (p less than 0.001). These results show that nephrotoxic risk is linked to the excretion of the B-form, and allow us to oppose the notion of "functional" enzymuria (low nephrotoxic risk) linked with A- and I-forms with the notion of "lesional" enzymuria (high nephrotoxic risk) linked with the B-form.