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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.

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.