Seasonal influences on groundwater arsenic concentrations in the irrigated region of the Cambodian Mekong Delta.

Similar to many southern and southeast Asian regions, the mobilisation of arsenic (As) from sediments has driven a widespread contamination problem for groundwater resources in the Cambodian Mekong Delta. For the first time, the seasonal changes in As concentrations and potential links to groundwater pumping for irrigation in shallow aquifers of the Cambodian Mekong Delta are investigated. Using environmental tracers (δ18O, δ2H, 3H, major/trace ions and rare earth elements) the natural and pumping-induced changes in hydrogeological processes are identified. Three conceptual models are proposed: Model 1, where there is limited local recharge or low recharge rates (3H mean residence time > 60 years) and groundwater has a large range in As concentrations (0.2 to 393.8 µg/L). In this semi-confined aquifer, only one of the six groundwater sites has As concentrations that increase (by 10.9 µg/L) potentially due to groundwater pumping and resultant mixing with high-As and low (Pr/Sm)NASC groundwater. However, data on groundwater extraction volumes is required to verify the link with irrigation practices. Model 2, where groundwater is recharged by evaporated surface waters (fractionated δ18O and δ2H). There are moderate As concentrations (64.1-106.1 µg/L) but no significant seasonal changes even though the recharging waters have relatively greater organic carbon contents during the dry season (reduced Ce/Ce*anomaly). Finally model 3, where groundwater is significantly recharged by wet season rainfall (~50% from δ18O data). There is a minor increase in As concentrations with recharge (by 6. µg/L). These combined results highlight an aquifer system in the irrigated region of the Cambodian Mekong Delta where As concentrations are largely impacted by natural rather than irrigation processes. Seasonal-scale recharge processes control As processes where the aquifer is not confined by shallow clay layers, and where the aquifer is semi-confined As concentrations largely reflect longer-term natural processes.

[Survival prognosis in pemphigoid. A cohort analysis of 78 patients]. / Pronostic vital de la pemphigoide. Analyse d'une cohorte de 78 malades.

INTRODUCTION: Bullous pemphigoid (BP) is the most frequent autoimmune bullous skin disease and usually affects elderly patients. Despite some conflicting data, vital prognosis is poor in BP, of which mortality rate after one year of treatment varies between 10 and 40 p. 100. To date, the factors influencing this prognosis remain to be determined. PATIENTS AND METHODS: A cohort of 78 consecutive patients with BP (mean age: 80 +- 4 years) has been prospectively selected on a six-year period (1987-1992) in Limoges. The diagnosis of BP was made on clinical criteria (using a standardized questionnaire), direct immunofluorescence (IF) findings (linear deposits of IgG and/or C3 along the basement membrane zone) and confirmed by direct immunoelectron microscopy and/or Western immunoblotting on epidermal extracts. RESULTS: The follow-up analysis (mean duration of follow-up: year of treatment (22 p. 100 in the first three months) with an actuarial survival curve inclined to be horizontal by the end of this first year of treatment. Therefore, we have studied the clinical or immunologic factors susceptible to influence the vital prognosis of BP according to this main criterion: death (or survival) at the end of the first year of treatment. None of the following factors has been found to be significantly linked to the vital prognosis in BP: age, sex, extent of skin lesions at presentation, presence of mucosal lesions, blood eosinophilia, presence of circulating basement membrane zone autoantibodies by indirect IF. The clinical factors of bad prognosis were an altered general condition and a history of coronaropathy. The presence of circulating autoantibodies against BP180 antigen (but not the one of autoantibodies against BP230) as detected by immunoblotting on epidermal extracts was found to be significantly more frequent (50 vs 22 percent) in BP patients who died within the first year of treatment (p < 0.02). DISCUSSION: Although modestly discriminating, the presence of circulating autoantibodies against BP180 represents the first vital prognosis factor demonstrated in BP. This result confirms the growing pathophysiologic importance of the anti-BP180 autoantibodies of which the pathogenic role has been recently formally demonstrated in BP using an animal model.

Serum levels of a negative regulator of cell proliferation (AcSDKP) are increased in certain human haemopathies.

One of the first known effects of the endogenous peptide N-acetyl-Ser-Asp-Lys-Pro (AcSDKP) is to inhibit entry into DNA synthesis of pluripotent haematopoietic stem cells (CFU-S) in mice. A specific anti-AcSDKP polyclonal antibody allows the level of the tetrapeptide by to be determined by enzyme immunoassay with good sensitivity and specificity. We present results demonstrating the presence of AcSDKP in humans: serum levels of 34 healthy controls were found to be between 0.7 and 2.5 pm/ml, regardless of age and sex. High levels were found in 44% of asymptomatic controls but only in 8% of AIDS patients out of a total of 37 patients with HIV. Subsequently, studies of serum levels were performed before treatment in 121 subjects with disorders of the nonlymphoid and the lymphoid lineages. Our results did not demonstrate any decrease in serum levels, however a moderate or marked increase was noted in one-third of the subjects, which was greater in disorders of the non-lymphoid lineages (48% of 72 patients) than the lymphoid lineage (21% of 50 patients). The most significant differences were observed between controls versus patients with myeloproliferative disorders (MPD, 24 patients: p < 0.001), controls versus patients with acute myelogenous leukaemia (AML, 15 patients: p < 0.02), as well as patients with AML versus patients with primary myelodysplastic syndromes (PMDS, 10 patients: p < 0.05). The pathophysiology of these abnormalities is discussed.

[Isolated inflammatory syndrome: think of benign tumors of the liver]. / Syndrome inflammatoire isolé: penser aux tumeurs bénignes du foie.

The authors report seven cases of benign tumors of the liver revealed by elevated acute phase reactants. They show that these elevated acute phase reactants are not linked with a particular histological diagnosis, the presence of tumor necrosis and that they disappear with the chirurgical cure of the tumor.

[Death in Horton disease. Prognostic factors]. / Les décès dans la maladie de Horton. Facteurs de pronostic.

The authors reported causes of death and searched for prognosis factors in Giant Cell Arteritis (GCA). The diagnosis was confirmed by temporal biopsy in all cases. Fourteen patients died during treatment; thirty-six patients had completely recovered (follow up > 6 months after withdrawal of steroid therapy). The commonest causes of death were cardiovascular (n = 7) and digestive (n = 4); they occurred after an average of 195 days of treatment, half of them during the first three months. One death was due to GCA (autopsy) and five deaths were attributed to the treatment with corticosteroids. The prognosis factors were searched for by comparing age, sex, clinical signs, laboratory data before treatment, past medical history in the both series; further more initial dose of Prednisone and the dose after 180 days of steroid therapy were compared in the two groups. The adverse prognosis factors revealed by this study were: advanced age (p < 0.01), previous ischaemic heart disease (p < 0.05) and higher dose of corticosteroids administered at 6 months of treatment (< 0.01).

[Inflammation proteins in Horton's disease. Prospective study of 25 patients]. / Protéines de l'inflammation dans la maladie de Horton. Etude prospective sur 25 malades.

In a study of 25 giant cell arteritis patients, whose diagnoses were made by temporal artery biopsy, the authors compared the evolution of the erythrocyte sedimentation rate (ESR) with those of the acute phase proteins (APP): fibrinogen (F), C reactive protein (CRP), orosomucoid (O), haptoglobin (H) and alpha 2-globulins (alpha 2-G), before, during and after corticotherapy; 165 laboratory analyses were made. Prior to treatment, ESR was increased in 96% of the patients, O and H in 100%, F and CRP in 96% and alpha 2-G in 92%. CRP showed the greatest mean increase (21x). Statistically significant positive correlations were found between ESR and alpha 2-G, F, CRP and O. No significant relationship was observed between APP and the occurrence of ophthalmological complications or the length of treatment. The CRP level returned to normal within the first week of steroid therapy for 76% of the patients, before ESR, F and O. During the withdrawal phase of corticotherapy, an ESR greater than 30 mm almost always corresponded to an inflammatory syndrome and an ESR of less than 15 mm to its absence (kappa coefficient = 0.64, p less than 0.001); however, an ESR between 15 and 30 mm did not enable us to draw a conclusion as to the absence or presence of such a syndrome. After terminating steroid therapy, the relationship between ESR and an inflammatory syndrome was weaker (kappa coefficient = 0.57, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Unilateral diaphragmatic dysfunction in blunt chest trauma.

This study was undertaken to evaluate unilateral diaphragmatic dysfunction within ten days after blunt chest trauma. Thirty patients with unilateral chest injury, or predominantly one-sided injuries, were investigated in the supine position, under analgesia. Right and left hemidiaphragm displacement (DD) was measured, using digital subtraction radiography, during quiet and forced breathing. The diaphragmatic contribution to breathing was determined by rib cage and abdominal circumference measurement changes. In both breathing modes, DD of the injured side was lower than DD of the uninjured side (p less than 0.01, p less than 0.001). Six patients had complete diaphragmatic motionlessness. The inspired air volume due to diaphragmatic motion (Vab) was reduced when compared to normal subjects and Vab/VT ratio was always found to be less than 0.65. The degree of diaphragmatic dysfunction appeared related to injury location and is most severe in injuries of the lower chest which implies direct diaphragm muscle injury, although other mechanisms may be implicated. Diaphragmatic dysfunction can contribute to respiratory failure in these patients, and should be considered.