PubMed Health⌕ Search

Biomedical subjects

C J van den Hamer

Publications and source records attributed to C J van den Hamer.

At least 19 recordsLinked to original sources
PubMed1998

The value of methods to determine zinc deficiency in patients with Crohn's disease.

BACKGROUND: The serum zinc concentration is frequently applied for the assessment of zinc deficiency, but this concentration is also influenced by other factors. The aim of this study was to compare various methods of assessing the zinc status in patients with Crohn' s disease. METHODS: Serum levels of zinc, serum alkaline phosphatase activity, and zinc in various types of cells were related to factors potentially inducing zinc deficiency: the number of liquid stools, weight loss, bowel resection, and the extent and severity of inflammation. RESULTS: Thirty-one patients with more or less active Crohn's disease were included. In 68% of these patients the serum zinc concentration was less than the reference level, and it was correlated with the extent of bowel resection and the van Hees Index but not with the Crohn's Disease Activity Index. Serum alkaline phosphatase activity was correlated with bowel resection. Zinc in blood cells was poorly correlated with factors inducing zinc deficiency. CONCLUSION: A decrease of serum zinc concentration is frequently seen in active Crohn's disease. This study suggests that the determination of zinc in blood cells is not superior to the determination of the serum zinc concentration and serum alkaline phosphatase activity.

Adult↗
PubMed1996

Serum alkaline phosphatase activity during zinc deficiency and long-term inflammatory stress.

A decrease in serum zinc can be caused by a real zinc deficiency but can also be caused by an apparent zinc deficiency, e.g. in inflammatory stress. The aim of this study was to evaluate the diagnostic power of serum alkaline phosphatase (AP) activity in the discrimination between pathophysiologic states of "real" and "apparent" zinc deficiency. A decrease in serum zinc was induced in growing and adult rats, by providing a diet low in zinc and by causing inflammatory stress. AP activity was determined using reagents low or enriched in zinc. Serum AP was decreased in zinc-deficient adult rats (P < 0.01). In zinc-deficient growing rats AP activity was not different from normal rats but AP activity decreased rapidly. In the same growing rats a significant difference was found in AP activities determined using buffers low and enriched in zinc (P < 0.001) between both groups of rats. After inducing inflammatory stress a decrease in AP activity (P < 0.01) and serum zinc (P < 0.001) was seen during the first few days. After the initial phase of inflammation AP activity normalized, serum zinc showed a rise which after correction for the decrease in serum albumin reached the level of the control rats. A difference in AP activity in buffers low and enriched in zinc was observed only during the first few days after induction of inflammatory stress (P < 0.001). Probably the method of measurement of the difference in enzyme activity, using buffers low and enriched in zinc, can be used as an indication for zinc deficiency in situations with changing AP enzyme concentrations. AP activity is decreased during the initial phase of inflammatory stress due to a decrease in serum zinc.

Alkaline Phosphatase↗
PubMed1992

Zinc uptake by blood cells of rats in zinc deficiency and inflammation.

In zinc deficiency, the function of leukocytes is impaired. However, the results of studies on the zinc concentration of blood cells in zinc deficiency are conflicting, probably in part because of technical and analytical problems. The aim of this study was to investigate, under standard conditions, the uptake of 65Zn-labeled zinc by blood cells, taken from zinc-deficient rats and from rats in which an inflammation is induced. In both conditions, the serum zinc concentration is reduced. In clinical practice, this makes it difficult to determine whether the decrease in serum zinc is the result of a real or an apparent zinc deficiency. In stress, like an inflammatory disease, the decrease of zinc reflects an apparent zinc deficiency because of redistribution of serum zinc into the liver and because of decrease in serum albumin concentration. Over 70% of the serum zinc is bound to albumin. Blood cells from zinc-deficient and control rats were isolated using a discontinuous Percoll gradient and incubated under nearly physiological conditions in a 65Zn-containing medium. A significant increase in the in vitro uptake of 65Zn-labeled zinc by the blood cells of zinc-deficient rats was seen: erythrocytes 1.3, mononuclear cells 2.0, and polymorphonuclear cells 2.6 times the control values. During inflammation, no change in 65Zn-labeled zinc uptake by erythrocytes and mononuclear cells was demonstrated after 2 d, although the serum zinc and albumin concentrations were decreased, but a small but significant increase in zinc uptake by polymorphonuclear cells was observed. This study of 65Zn uptake in vitro under standard conditions may prove of value for distinguishing in patients real zinc deficiency from apparent zinc deficiency owing to, e.g., stress, although additional experiments should be performed.

Animals↗
PubMed1992

Changes in zinc metabolism after burns: observations, explanations, clinical implications.

Zinc in plasma and urine and serum albumin and alpha 2-macroglobulin were measured in 48 patients with burns. Mean total burned surface area amounted to 18%, ranging from 2 to 55%, and mean hospitalization time amounted to 35 days, ranging from 10 to 124 days. All parameters showed a decrease during the first two post-burn days. Minimal values were reached on days 2 and 3 for plasma and urine zinc, and between days 5 and 10 for the proteins. Thereafter, values increased, rapidly for both plasma and urinary zinc, more slowly for albumin and alpha 2-macroglobulin. The ratio R of the total plasma zinc minus the alpha 2-macroglobulin concentration to the albumin concentration is postulated as an indicator for zinc deficiency. From values of R and of the urinary zinc excretion, conclusions can be drawn about various processes of the zinc metabolism that may occur during the acute stage following the thermal accident and during the stages of tissue demarcation and of recovery. These processes are discussed in terms of possible temporary and/or local zinc deficiency. Evidence is presented that zinc administration in only indicated during the final stages of recovery in case of inadequate dietary intake.

Adolescent↗
PubMed1991

Zinc sulphate therapy for Wilson's disease after acute deterioration during treatment with low-dose D-penicillamine.

A 30-year-old woman with Wilson's disease was treated with low-dose D-penicillamine. After 12 days, treatment was changed to zinc sulphate because of severe neurological deterioration. The patient subsequently improved within a few days. During a follow-up period of 20 months, the effectiveness of therapy was evaluated by measuring copper and zinc levels in plasma and urine, and by 64Cu-loading tests. We conclude that sulphate therapy may be a satisfactory alternative, even when rapid deterioration occurs in the early stages of D-penicillamine treatment.

Adult↗
PubMed1990

Urinary zinc excretion in a patient with burns: a caveat when using bladder catheters in urine zinc studies.

The results of a longitudinal study on plasma and urine zinc concentrations in a patient with 68 per cent burns are described. Special attention was paid to possible zinc contamination due to the use of bladder catheters for urine sampling. The course of the plasma and urine zinc concentrations during the first 50 days in hospital was comparable to those reported in the literature. It was shown that surgery was associated with a pronounced rise in urine zinc level, while catheter replacement caused no significant increase in urinary zinc content in this particular patient. However, measurements of zinc content of and zinc release from three types of bladder catheters showed that the two types of latex-based catheters contained about 0.25 per cent zinc, versus 0.01 per cent in the siliconelastomer equivalent. During an 8 h perfusion latex catheters released about 1.2 mumols zinc (2.5 mumols/l). Possible errors in urine zinc determinations due to zinc contamination from catheters are calculated. Recommendations are made for minimizing these errors.

Adult↗
PubMed1990

Iodine-129 as a protein label for studies of plasma protein turnover and its measurement with neutron activation analysis.

Iodine-129 (t 1/2 = 1.57 x 10(7) y) was used as a protein label for the measurement of the turnover rate of albumin in two human subjects. Plasma samples were assayed for 129I using destructive neutron activation analysis. The experiment entailed an estimated radiation dose of 0.2 muSv to the total body of the subjects. The turnover parameters showed reasonable agreement with literature values. When in a rabbit the catabolism of (129I + 131I)-labeled autologous albumin was followed, the results obtained with both labels agreed well.

Animals↗
PubMed1989

Selenium-induced protection against cis-diamminedichloroplatinum(II) nephrotoxicity in mice and rats.

The influence of selenium on cis-diamminedichloroplatinum(II) (c-DDP) nephrotoxicity in mice and rats was assessed, using single doses of both compounds. Sodium selenite, 2 mg of selenium per kg, given 1 h before c-DDP, greatly reduced blood urea nitrogen and creatinine levels and morphological kidney damage in both BALB/c mice and Wistar rats, while administration 1 h after c-DDP did not. Liver toxicity of selenium was evaluated by measuring serum glutamic pyruvate transaminase and serum glutamic oxalate transaminase and by routine histology. No liver damage was observed in animals treated with sodium selenite, 2 mg of selenium per kg, and physiological saline or c-DDP. Pretreatment with sodium selenite did not reduce the antitumor activity of c-DDP against MPC 11 plasmacytoma or Prima breast tumor in BALB/c mice. The present results indicate that sodium selenite may provide protection against c-DDP nephrotoxicity, when it is given before c-DDP. Moreover, selenium has an antineoplastic activity against several tumors. The combination of these qualities may open new perspectives in cancer chemotherapy.

Animals↗
PubMed1987

Evaluation of the EDTA-washed diet for use in the experimental production of zinc deficiency in human subjects.

Ethylenediaminetetraacetate (EDTA) is known to bind zinc (Zn) and other metals. EDTA-washed soy protein-based diet has been extensively used as a dietary model for the production of Zn-deficiency in human subjects as well as in experimental animals. The present study was conducted to test this diet for possible contamination with EDTA (inhereted by washing procedure) and also to evaluate it for its acceptability and palatibility by human subjects. In the first experiment, EDTA-washed soy protein-based diets were prepared as previously described (repeated washing with EDTA-sodium salt followed by washing with deionized water and filteration), but 14C-EDTA was used. Scintillation counter analysis showed no traces of 14C in the prepared diet (100% of the 14C activity was recovered in the filtrate). In the second experiment, the diets were prepared using inactive EDTA, then fed to 10 volunteers for sensory evaluation. Results of this trial showed that the palatibility and acceptability of these diets are generally very poor. In conclusion, the use of EDTA-washing procedure did not result in any contamination of the soy assay protein with the EDTA. However, the present dietary model may not be used to induce zinc deficiency in human volunteers on a long term basis since the palatibility of the washed product is poor.

Diet↗
PubMed1985

Copper responsive anemia, induced by oral zinc therapy in a patient with acrodermatitis enteropathica.

Normocytic anemia with granulocytopenia occurred in a 23 year old man with acrodermatitis enteropathica who received high doses of zinc sulphate orally for 12 months. Copper deficiency was suspected to be the cause of this anemia when extreme hypocupremia and hypoceruloplasminemia were found. Oral zinc therapy was stopped and intravenous supplements of copper were followed by reticulocytosis and complete correction of the anemia and granulocytopenia. Plasma copper and ceruloplasmin levels normalized. Up to now copper deficiency has never been reported during zinc treatment in acrodermatitis enteropathica. We conclude that the copper status should be monitored during oral zinc therapy in this condition.

Acetates↗
PubMed1985

Trace element uptake in liver cells. 2. Effect of different proteins in the medium on the uptake of copper and zinc by hepatoma cells.

Cultured rat hepatoma cells (HTC-cells) were used to study the uptake of copper and zinc from a minimal salt-glucose medium, supplemented with albumin from different species or with ovalbumin. Competitive equilibrium dialysis showed that at low molar ratios of metal/protein (less than 1) the affinity for copper of human and bovine albumin was about equal, but that of dog albumin or ovalbumin was much lower. Only a small difference in affinity for zinc could be detected between human albumin and ovalbumin. Supplementing the medium with the different proteins the rate of copper uptake in the cell at a given molar Cu/protein ratio increased as follows: human albumin congruent to bovine albumin less than dog albumin less than ovalbumin. When the molar Cu/protein ratio was increased, a discontinuity was seen with all three albumin species at a ratio of about 1. In contrast, the zinc uptake mimics that of Cu/ovalbumin, and no discontinuity was observed using different molar Zn/protein ratios. These results indicate that the rate of copper and zinc uptake depends strongly on its affinity for the protein: a low affinity leads to a high uptake. The results suggest further that at physiologic concentrations zinc is taken up by a mechanism different from that for copper.

Animals↗
PubMed1984

Trace metal uptake in liver cells. 1. Influence of albumin in the medium on the uptake of copper by hepatoma cells.

Cultured rat hepatoma cells (HTC-cells) were used to study the transfer of copper from a well-defined medium to and across the cell membrane and particularly the role of albumin in this process. HTC-cells, maintained in a minimal salt-glucose medium, accumulated far more copper than when maintained in the same medium, but supplemented with albumin. In the latter case, the Cu uptake strongly depended on the molar Cu/albumin ratio. The results suggest a role of albumin in the uptake of trace metals. The results indicate the presence of two types of binding sites for copper on the cell membrane. The sites of the first type bind copper very strongly and are probably responsible for the uptake of copper under physiological conditions. Their number was estimated to be about 10(6) per cell. Those of the second type only bind copper when the molar Cu/albumin ratio exceeds a value of about 1, i.e., under extreme, unphysiological conditions. Furthermore, the results suggest a direct interaction of the Cu-albumin complex with these strong binding sites as a first step in Cu uptake processes.

Animals↗