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Biomedical subjects

R Lauwerys

Publications and source records attributed to R Lauwerys.

At least 217 records · Page 12Linked to original sources

Potentiation of carbon-tetrachloride hepato-nephrotoxicity by phenobarbital in man, a case report.

A 47 year-old male epileptic who had been treated for eight years with variable doses of phenobarbital and valproate was hospitalized in the intensive care unit with the following clinical and biological features: coma grade 2, metabolic acidosis, acute renal and hepatic failure. The recent clinical history revealed that he had been using CCl4 to clean paintings for the last three days in a confined atmosphere. Upon admission, the recent absorption of CCl4 was confirmed by the detection of the solvent in blood and adipose tissue. Cellular lipoperoxidation was suggested by the presence of an increased concentration of pentane in expired air. Evidence of microsomal enzyme induction was provided by the relative preservation of aminopyrine demethylation as indicated by the 14C-aminopyrine breath test and also by the morphological evidence of endoplasmic reticulum proliferation at liver biopsy. Supportive therapy, repeated haemodialysis and administration of antioxidant drugs resulted in a complete recovery. The unusual severity of CCl4-induced liver and renal injury observed in this case is best explained by the induction of CCl4 microsomal activation due to phenobarbital therapy.

Barbiturates↗

Development of a quantitative test for hand tremor measurement. Study of factors influencing the response in a control population.

The frequency spectrum of hand tremor amplitude was investigated in a group of 15 control subjects under four different conditions (rest position, wrist loading with 2 kg, pointer directed to a target, and wrist loading with 2 kg, pointer directed to a target, and wrist loading plus pointer). The series of four tremor recordings was repeated on three different days. The hand tremor pattern was recorded using an accelerometer connected to a tape recorder through a precision sound level meter. The tremor signals were subsequently analyzed with a real time spectrum analyzer. Different parameters (peak frequencies, acceleration amplitudes, moments, displacements, and velocities) have been determined and their variability has been characterized. The method described for hand tremor recording is suitable for field application.

Adult↗

Comparison of retinol-binding protein and beta 2-microglobulin determination in urine for the early detection of tubular proteinuria.

The specificity, sensitivity and stability of beta 2-microglobulin (beta 2-m) and retinol-binding protein (RBP) in urine as indices of tubular proteinuria were compared. In vitro experiments show that RBP in urine is stable down to pH 4.5, whereas beta 2-m degrades below pH 5.5. This was confirmed by the relationships between pH and the concentration of both proteins in the urines from 150 healthy subjects. Urinary RBP was independent of pH (r = 0.125) but in contrast at pH below 6, beta 2-m concentration was inversely correlated with pH (r = 0.54, p less than 0.05). The comparison of urinary excretion of RBP and beta 2-m in 68 patients with renal diseases shows that in absence of a pH effect, the sensitivity and specificity of both proteins as indices of tubular proteinuria are rather similar. Therefore, in view of its greater stability in urine, RBP appears to be a more practical and reliable index of proximal tubular function than beta 2-m.

Adult↗

The possible role of direct ingestion on the overall absorption of cadmium or arsenic in workers exposed to CdO or As2O3 dust.

Six volunteers (two office and four cadmium (Cd)-exposed workers, all nonsmokers) from an electric condenser factory participated in a study involving the measurement of cadmium in air and in dust, the evaluation of hand and mouth contamination by cadmium, and the determination of fecal cadmium. The mean levels of total airborne cadmium measured with static and personal samplers were for the exposed workers 9.5 and 16.7 microgram/m3, respectively, and for the office workers 0.3 and 0.5 microgram/m3, respectively. In the office workers, hand contamination by Cd hardly changes over the workday (less than 10 microgram/hand), whereas in the exposed workers important hand contamination by Cd was observed (up to 1,200 microgram/hand during the workday and up to 300 microgram/hand before lunch or before leaving the factory). Mouth contamination by Cd is rather similar in both groups on Monday morning, but increases 20- to 50-fold on Friday afternoon in the Cd workers against a slight increase for the office workers. The concentration of Cd in the feces was not much different between Sunday and Friday in the office workers, whereas in the exposed workers it was higher on Friday than on Sunday. There is suggestive evidence from a comparative study of fecal cadmium in two Cd-exposed volunteers who carried out their jobs with and without gloves that direct cadmium intake from hand contamination may contribute to the overall Cd absorption. A limited study in a glassware factory (As2O3 exposure) involving the measurement of total airborne arsenic, the determination of urinary arsenic, and the evaluation of hand and mouth contamination by arsenic before and after the workshift suggests that the high urinary arsenic levels (300 microgram/g creatinine) are likely to be more related to an increased oral intake from contaminated hands than to an increased absorption from the lungs.

Air↗

Comparison of renal function and psychomotor performance in workers exposed to elemental mercury.

Renal function and psychomotor performance (eye-hand coordination, arm-hand steadiness) of a group of 43 workers exposed to mercury vapor were examined. Their mean age an average duration of exposure to mercury were 38 and 5 years, respectively. The results were compared with those in a matched group of 47 control workers. Increased proteinuria and albuminuria were found slightly more prevalent in the Hg-exposed group than in the control workers. These results are in agreement with those found during a previous study carrier out in another group of workers also exposed to elemental mercury (Buchet et al. 1980). The scores of the psychomotor tests were less satisfactory in the Hg workers than in the control workers, the arm-hand steadiness test being more discriminative than the eye-hand coordination test. Preclinical changes in psychomotor function can be detected independently of the presence of signs of renal dysfunction. No clear-cut relationships were found between the prevalence of abnormal psychomotor scores and the level of mercury in blood (HgB) or in urine (HgU). Increased prevalences of abnormal psychomotor scores seem however to occur for HgB between 1 and 2 micrograms/100 and for HgU between 50 and 100 micrograms/g creatinine. Therefore, a biologic threshold limit value of 50 micrograms/g creatinine in proposed for urinary mercury to prevent the development of preclinical effects on the central nervous system. A similar critical HgU level based on renal dysfunction prevalences has been suggested in a previous study.

Adult↗

Release of nickel into fluid stored in the reservoir of Dermo-Jets.

Release of nickel into triamcinolone acetonide suspensions stored in the reservoir of a Dermo-Jet was demonstrated by electrothermal atomic absorption spectrometry. Increased urinary nickel excretion was found for three days following intradermal injections (with the Dermo-Jet) of triamcinolone acetonide in patients suffering from alopecia areata. The dimethylglyoxime test showed that the internal rod of the reservoir as well as metallic internal parts of the nozzle leached appreciable amounts of nickel, even before any clinical use.

Alopecia Areata↗

Severe and prolonged poisoning by fenthion. Significance of the determination of the anticholinesterase capacity of plasma.

A case of acute poisoning by oral ingestion of fenthion is reported. The different clinical signs, especially the delayed and prolonged symptomatology, are described. The various types of therapeutic measures (gastric lavage with charcoal, administration of atropine, Toxogonine, lyophilized human cholinesterase, and fresh plasma and exchange transfusion) are discussed. Correlation studies between clinical signs and plasma and erythrocyte cholinesterase activities are presented together with plasma fenthion levels and the anticholinesterase capacity of the patient's plasmas.

Adult↗

Evolution of cadmium-induced renal dysfunction in workers removed from exposure.

A retrospective examination of the medical records gathered during several surveys carried out among cadmium workers has permitted the identification of a group of 19 workers who had been examined before and after removal from cadmium exposure. All the workers had been exposed for more than 15 a (range 15.6-41.7 a). Their last examination took place from 0.3 to 7.9 a after the date of removal from cadmium exposure. At that time, all the workers exhibited sign(s) of cadmium-induced renal dysfunction. Comparison of the renal function parameters (serum creatinine, total proteinuria, aminoaciduria, albuminuria, beta 2-microglobulinuria, and the urinary excretion of retinol-binding protein) before and after the cessation of exposure indicated that cadmium-induced renal lesions, albeit of slow progression, are not reversible when exposure ceases.

Adult↗

[Cadmium toxicity: summary of personal studies].

Occupational and environmental exposure to cadmium leads to a progressive and almost irreversible accumulation of the metal in the body. The epidemiological and experimental studies carried out by the authors allow them to draw the following conclusions: 1) the kidney is usually the critical organ i.e. the organ exhibiting the first signs of adverse effects following long term moderate exposure to cadmium by inhalation or by ingestion. 2) Cadmium interferes not only with the tubular reabsorption process(es) for low molecular weight proteins (e.g. beta 2 . microglobulin, retinol binding protein) but also with the glomerular or tubular mechanism determining the excretion of high molecular weight proteins (e.g. albumin, transferrin). Both types of proteinuria may occur independently. 3) The renal functional disturbances induced by cadmium and compatible not only with a tubular dysfunction but also a glomerular dysfunction. 4) The early detection of renal disturbances induced by cadmium should not rely only on the determination of total proteinuria but necessitates the analysis in urine of at least one low molecular weight protein (beta 2-microglobulin or retinol binding protein) and one high molecular weight protein (albumin). 5) Before the occurrence of renal dysfunction and providing the intensity of exposure to cadmium is moderate, urinary cadmium reflects mainly the body burden whereas blood cadmium reflects mainly the last few months exposure. 6) In adult male workers occupationally exposed to cadmium, the critical concentration of cadmium in the renal cortex is in the order of 200 ppm. The corresponding critical urinary level is approximately 10 micrograms/g creatinine. The critical level of cadmium in the renal cortex is not reached if the exposure is kept at a level where cadmium in blood does no exceed 1 microgram/100 ml. 7) Comparison of literature data on current exposure of the general population to cadmium and the critical exposure level indicates that some groups of the general population absorb daily amounts of cadmium closed to the critical level. 8) The critical biological levels indicated under (6) do not necessarily prevent an exacerbation of the age-related decline in renal function. 9) A preliminary study performed in Belgium suggests that cadmium might play a role in the increased mortality by renal diseases in a population living in an area polluted by cadmium. More detailed studies are necessary to confirm this hypothesis.

Cadmium↗

Comparison of the urinary excretion of arsenic metabolites after a single oral dose of sodium arsenite, monomethylarsonate, or dimethylarsinate in man.

The urinary elimination of the metabolites of arsenic has been followed up as a function of time in volunteers who ingested a single oral dose of arsenic (500 microgram As) either as sodium arsenite (Asi), monomethylarsonate (MMA), or cacodylate (DMA). The excretion rate increased in the order Asi less than DMA less than MMA. After 4 days, the amount of arsenic excreted in urine represents 46, 78, and 75% of the ingested dose in the case of Asi, MMA and DMA, respectively. With regard to the in vivo biotransformations, it is concluded that DMA is excreted unchanged; MMA is slightly (13%) methylated into DMA while roughly 75% of the arsenic excreted after ingestion of Asi is methylated arsenic (about 1/3 as MMA and about 2/3 as DMA).

Adult↗

Characterization of the proteinuria induced by prolonged oral administration of cadmium in female rats.

Female Sprague-Dawley rats were given 200 ppm cadmium (Cd) in the drinking water for 11 months. Total proteinuria and the concentrations of Cd in blood, urine, liver and kidney cortex were determined monthly. The proteinuria was characterized by Sephadex G-75 chromatography and by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. From the 8th month of treatment, the Cd concentration in the kidney cortex levels off at a value of about 250 microgram/g wet wt and this phenomenon coincides with the occurrence of proteinuria. The proteinuria was characterized by an increased urinary excretion of high molecular weight (HMW) proteins, particularly gamma-globulins. Aminoaciduria also increased which suggests the existence of a slight tubular dysfunction. The renal dysfunction induced by chronic oral administration of Cd seems different from that observed in a previous study in which Cd was administered by the i.p. route (1 mg Cd/kg, 5 times a week for 2 months). For the same level of Cd in the kidney cortex the proteinuria induced by i.p. injection of Cd was usually of mixed type and in some cases of the tubular type. The development of this proteinuria was coincident with the levelling off of Cd concentration in the kidney cortex and in the liver. The saturation of liver by Cd is very likely at the origin of he extensive tubular lesion and of the mixed type proteinuria observed in the i.p. experiment. These results demonstrate the importance of mode of Cd administration on the nature of the Cd-induced proteinuria in animal. They support also our proposal that both low and HMW proteins should be determined in urine for the early detection of renal damage occurring in man chronically exposed to cadmium.

Administration, Oral↗

The metabolism of arsenic in humans acutely intoxicated by As2O3. Its significance for the duration of BAL therapy.

The urinary excretion of inorganic arsenic and of its less toxic metabolites [monomethylarsonic acid (MMA) and dimethylarsinic acid (DM)] has been followed-up in five cases of acute oral intoxication by As2O3. In addition to supportive therapy all patients were given BAL. The proportion of the three species of urinary arsenic (inorganic, MMA, DMA) changes markedly with time. During the first 2 to 4 d after the intoxication, arsenic is excreted mainly as its unmetabolized inorganic form but this is rapidly followed-up by a progressive increase of the proportion excreted as MMA and DMA. The time at which the majority of arsenic is excreted as its organic metabolites depends on the severity of the intoxication but in all the cases, more than 95% of th excreted arsenic is in the organic form after 9 d, the dimethylated derivative being preponderant. Speciation of arsenicals in urine might be useful to determine the duration of BAL treatment.

Adult↗

Assessment of renal function of workers simultaneously exposed to inorganic lead and cadmium.

The renal function of a group of workers (n = 62) exposed simultaneously to lead and to cadmium has been examined. The results were compared with those obtained in a earlier study of three groups of workers - one exposed to lead only, one exposed to cadmium only and one not exposed to either of these metals (control group). The results obtained in the earlier study have been published previously. No interaction between lead and cadmium is evidenced. The signs of renal dysfunction found in the group exposed simultaneously to lead and to cadmium can be ascribed to cadmium only. The results of this study have confirmed the authors' previous observations, that is, a moderate exposure to lead (plumbemia less than 62 micrograms/100 ml and average duration of exposure = 13.2 years) does not seem to influence renal function; in adult male workers the critical levels of cadmium in blood and in urine are 1 microgram/100 ml whole blood and 10 micrograms/g creatinine, respectively; the renal dysfunction induced by cadmium is both glomerular and tubular.

Adult↗