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Biomedical subjects

H de Groot

Publications and source records attributed to H de Groot.

At least 55 records · Page 3Linked to original sources
PubMed1998

Occupational allergy caused by flowers.

We describe 14 consecutive patients with complaints due to the handling of flowers. The symptoms varied from allergic rhinoconjunctivitis and asthma to urticaria. Most patients had professions in the flower industry. Skin prick tests (SPT) were performed with home-made pollen extracts from 17 different flowers known to be the most commonly grown and sold in The Netherlands RAST against mugwort, chrysanthemum, and solidago was performed. The diagnosis of atopy against flowers was based on work-related symptoms due to the handling of flowers, positive SPT with flower extracts, and positive RAST. The concordance between SPT and case history was 74%, and that between SPT and RAST was 77% Extensive cross-sensitization was seen to pollen of several members of the Compositae family (e.g., Matricaria, chrysanthemum, solidago) and to pollen of the Amaryllidaceae family (Alstroemeria and Narcissus). Homemade flower extracts can be used to confirm IgE-mediated flower allergy. Mugwort can be used as a screening test for possible flower allergy. For most patients, the allergy led to a change of profession.

Adult↗
PubMed1998

Allergy to bumblebee venom. II. IgE cross-reactivity between bumblebee and honeybee venom.

To obtain more information on IgE cross-reactivity between bumblebee venom and honeybee venom, we tested sera from venom-sensitized patients for specific IgE against venoms from the European bumblebee (Bombus terrestris), the North American bumblebee (Megabombus pennsylvanicus), and the honeybee (Apis mellifera). RAST, RAST-inhibition, and immunoblotting experiments indicate that bumblebee venom and honeybee venom contain venom-specific IgE-binding epitopes. These results suggest that immunotherapy using honeybee venom may not be effective in all bumblebee venom-allergic patients. Our experiments also revealed differences in IgE binding for venom from European and American bumblebees.

Animals↗
PubMed1998

Tissue injury by reactive oxygen species and the protective effects of flavonoids.

Reactive oxygen species contribute decisively to a great variety of diseases. Flavonoids are benzo-gamma-pyrone derivatives of plant origin found in various fruits and vegetables but also in tea and in red wine. Some of the flavonoids, such as quercetin and silibinin, can effectively protect cells and tissues against the deleterious effects of reactive oxygen species. Their antioxidant activity results from scavenging of free radicals and other oxidizing intermediates, from the chelation of iron or copper ions and from inhibition of oxidases. For their free radical scavenging properties, scavenging of lipid- and protein-derived radicals is presumably of special importance. A non-radical reactive oxygen species effectively trapped by flavonoids is hypochlorous acid. In general, the antioxidative properties of flavonoids are favoured by a high degree of OH substitution. On the other hand, inhibition of enzymatic functions other than oxidases, e.g., inhibition of lipoxygenase and thus prevention of the formation of leukotrienes, may also participate in the cell and tissue protective properties of flavonoids.

Antioxidants↗
PubMed1998

Prevalence of natural rubber latex allergy (type I and type IV) in laboratory workers in The Netherlands.

The objective of the study was to study the prevalence of Type IV and Type I allergy to natural rubber latex (NRL) in a population at risk in the Netherlands. Laboratory workers regularly using gloves were invited to complete a questionnaire and to be tested. We performed patch tests with standard contact allergens, rubber additives, glove powder and pieces of 4 gloves; prick tests with inhalant allergens, glove extracts, glove powder and fruit extracts; and RASTs. Glove-related hand dermatitis was reported in 36.9% of the individuals interviewed. A positive patch test result for rubber additives was seen in only 6.6%. Glove-related urticaria, rhinoconjunctivitis and/or asthma were reported in 24.6% of all cases. Confirmation of an IgE-mediated reaction was achieved in 8.3% by prick test with glove extracts and 5.0% by RAST. No reaction to glove powder was noticed in patch testing or in prick testing. A high prevalence rate of glove-related symptoms and NRL Type I allergy was found in laboratory workers exposed to rubber gloves. Surprisingly, there was no co-existence of Type I and Type IV allergy in this population.

Adult↗
PubMed1998

Nitric oxide metabolites in cystic fibrosis lung disease.

Although the activity of nitric oxide (NO) synthases are increased in lung tissue of patients with cystic fibrosis, the concentrations of nasal and exhaled NO have recently been found to be decreased in cystic fibrosis. This could either be due to reduced NO formation or metabolism of NO within airway fluids. In this study, the stable NO metabolites, nitrate and nitrite, were determined in the saliva and sputum of 18 stable cystic fibrosis patients, 21 cystic fibrosis patients during a pulmonary exacerbation, and in saliva and endotracheal secretions of normal controls. Median saliva concentrations of NO metabolites (nitrate plus nitrite) were 704 mumol/l (95% confidence interval (CI) 419 to 1477) in stable cystic fibrosis patients, 629 mumol/l (95% CI 382 to 1392) in cystic fibrosis patients presenting with pulmonary exacerbation, and 313 mumol/l (95% CI 312 to 454) in controls. Median sputum NO metabolite concentration in stable cystic fibrosis was 346 mumol/l (95% CI 311 to 504). This was not significantly different from cystic fibrosis patients presenting with pulmonary exacerbation (median 184 mumol/l, 95% CI 249 to 572), but significantly higher than in endotracheal secretions of controls (median 144 mumol/l, 95% CI 96 to 260). Sputum NO metabolite concentration in cystic fibrosis pulmonary exacerbation significantly increased during antibiotic treatment. A positive correlation was observed between sputum NO metabolites and lung function in stable cystic fibrosis, suggesting less airway NO formation in cystic fibrosis patients with more severe lung disease. These data indicate that decreased exhaled NO concentrations in cystic fibrosis patients may be due to retention and metabolism of NO within the airway secretions. However, sputum NO metabolites are not a useful marker of airway inflammation in cystic fibrosis lung disease.

Adolescent↗
PubMed1998

Specific IgE antibodies in the diagnosis of atopic disease. Clinical evaluation of a new in vitro test system, UniCAP, in six European allergy clinics.

A new immunoassay system utilizing new automatic instrumentation, new software for evaluation of data, and reagents updated for increased speed and accuracy was evaluated. Six clinical studies included 894 consecutive patients. Major symptoms were rhinoconjunctivitis, asthma, atopic dermatitis, and urticaria. The prevalence of inhalant allergy was 54-69%. Phadiatop, detecting atopic sensitization to common inhalant allergens, agreed with clinical diagnosis in 764/836 cases (91.4%). The clinical sensitivity and specificity were 93% and 89%, respectively. The clinical sensitivity and specificity of UniCAP specific IgE derived from 5170 comparisons with clinical diagnosis were 89% and 91%, respectively. Specific IgE measurements in UniCAP and in the Pharmacia CAP System agreed in 266/274 cases (97%). A comparison of the sensitivity and specificity of Pharmacia CAP System RAST in 1987 and with UniCAP specific IgE in 1995 showed equivalent performance without change of efficacy or degradation of IgE antibodies after 8 years. The systems were equivalent also in terms of measured values (r=0.96, slope=1.12), confirming the standardization of allergens and of assay calibration. UniCAP is an efficient laboratory system for routine diagnostic testing of allergy and a valuable tool for basic studies on allergens and antibodies.

Administration, Inhalation↗
PubMed1997

[Auxiliary liver transplantation for acute liver failure after intake of 3,4-methylenedioxymethamphetamine ("Ecstasy")].

HISTORY AND CLINICAL FINDINGS: An 18-year-old patient had for 6 days been suffering from right upper abdominal pain, weight loss, vomiting and yellow discoloration of the skin. For the preceding 8 months he had been regularly taking 1-2 tablets of "ecstasy" (3,4-methylenedioxymethamphetamine--MDMA) per week, the last 8 days before the onset of the described signs. Physical examination was unremarkable, except for pain on pressure over the right upper abdomen and the jaundice. INVESTIGATIONS: The activities of SGOT (756 U/I), SGPT (1450 U/I). gamma GT (164 U/I) and lactate dehydrogenase (539 U/I) as well as total bilirubin level (7.5 mg/dl) were elevated. The synthesising functions of the liver were impaired (thromboplastin time 47%, fibrinogen 116 mg/dl). Abdominal sonography was unremarkable. All virological tests (hepatitis A, B, C and D; Epstein-Barr virus; cytomegalovirus; HIV 1 and 2) were negative. TREATMENT AND COURSE: The suspected diagnosis was acute liver failure after "ecstasy" intake. The cholestasis and the parameters of liver synthesis and hepatocellular functions deteriorated under symptomatic treatment. 15 days after onset of the first symptoms progressive hepatic encephalopathy occurred and required heterotopic auxiliary liver transplantation (piggy-back technique). 5 months later hepatobiliary sequential scintigraphy demonstrated regenerating of the patient's own liver an atrophy of the transplanted liver. Immunosuppression with cyclosporin A and prednisolone was gradually reduced, and the transplant was removed 6 months postoperatively because of an abscess in it. 11 months after the transplantation liver functions is normal and the patient well. CONCLUSION: In young patients with jaundice of unknown origin toxic hepatitis after "ecstasy" intake should be considered. Auxiliary liver transplantation can lead to regeneration during temporary relief of the patient's own liver. After its function has been restored immunosuppression is no longer needed.

Adolescent↗
PubMed1997

Decrease of ischemic injury to the isolated perfused rat liver by loop diuretics.

Recent studies suggest a major role played by sodium in the pathogenesis of ischemic liver injury: in these studies, sodium-free media have been shown to offer protection against hypoxic injury to isolated hepatocytes. As sodium-free perfusions of the isolated rat liver proved impossible because of extensive vasoconstriction, we assessed the effects of two inhibitors of the Na+-K+-2Cl- cotransporter, the loop diuretics furosemide and bumetanide, on ischemic liver injury. In untreated control livers lactate dehydrogenase (LDH) efflux immediately after reperfusion after 60 minutes of ischemia at 37 degrees C was 1666 +/- 473 U/L. When livers were pretreated with furosemide or bumetanide before the ischemic period, LDH efflux was only 773 +/- 292 U/L and 702 +/- 183 U/L respectively (P < .01). LDH activity in the effluent of the pretreated livers remained significantly below the values of ischemic control livers for the whole reperfusion period of 90 minutes. Bile flow in the postischemic phase was improved by pretreatment with furosemide or bumetanide. The increase in intracellular sodium, as measured by 23Na-NMR, was attenuated from 193% +/- 71% during 60 minutes of ischemia in controls to 148% +/- 80% after bumetanide application (P < .05). Also, after 120 minutes of warm ischemia, LDH and aspartate aminotransferase release were significantly decreased and bile flow increased by pretreatment with bumetanide. Thus, both furosemide and bumetanide showed a clear benificial effect on rat livers subjected to warm ischemia. These data suggest that one means by which sodium ions are accumulated during liver ischemia might be the Na+-K+-2Cl- cotransporter, which is blocked by furosemide and bumetanide.

Animals↗
PubMed1997

Oxygen-free radical-mediated injury to cultured rat hepatocytes during cold incubation in preservation solutions.

We have previously shown that the injury to cultured liver endothelial cells during cold incubation in University of Wisconsin (UW) solution is energy-dependent and is mediated by reactive oxygen species. Here we demonstrate that this reactive oxygen-mediated injury is specific neither to endothelial cells nor to UW solution: cultured hepatocytes incubated in cold (4 degrees C) UW solution or histidine-tryptophan-ketoglutarate (HTK) solution were injured under normoxic conditions (loss of viability, 63% +/- 10% after 48 hours of cold incubation in UW solution and 82% +/- 11% after 24 hours of cold incubation in HTK solution), whereas hypoxia was protective (loss of viability, 29% +/- 12% [UW] and 13% +/- 3% [HTK] after the same cold incubation times). The injury under normoxic conditions was also largely decreased by adding either the spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO) or the flavonoid silibinin to the solutions, or by preincubating the cells with the iron chelator deferoxamine before the hypothermic incubation. Marked lipid peroxidation was observed during cold incubation in both preservation solutions. These results suggest that the injury to cultured hepatocytes during cold incubation in UW and HTK solutions is mediated by reactive oxygen species as is the injury to cultured liver endothelial cells.

Adenosine↗
PubMed1997

Preservation of pig liver allografts after warm ischemia: normothermic perfusion versus cold storage.

Warm ischemia is known to induce substantial damage to the liver parenchyma. With respect to clinical liver transplantation, the tolerance of the liver to warm ischemia and the preservation of these organs have not been studied in detail. In isolated reperfused pig livers we proceeded according to the following concept: Livers were subjected to 1 or 3 h of warm ischemia. Subsequently, these organs were preserved by either normothermic perfusion or cold storage (histidine-tryptophan-alpha-ketoglutarate, HTK) for 3 h each. After storage, liver function was assessed in a reperfusion circuit for another 3 h. Parameters under evaluation were bile flow, perfusion flow, oxygen consumption, enzyme release into the perfusate (creatine kinase, glutamic oxaloacetic transaminase (GOT), lactic dehydrogenase, and glutamic pyruvic transaminase), and histomorphology. Damage to the liver was lowest after warm ischemia of 1 h. The results after cold storage were superior to those after normothermic perfusion (GOT: 3.2 +/- 0.3 and 2.6 +/- 0.2 U/g liver; cumulative bile production: 14.7 +/- 2.1 and 9.4 +/- 1 ml, respectively; P < 0.05). In contrast, we found substantial damage at the end of reperfusion in livers undergoing 3 h of warm ischemia under both preservation techniques with severe hepatocellular pyknoses and essentially altered nonparenchymal cells. The results suggest that pig livers undergoing 1 h of warm ischemia and cold storage for 3 h with HTK solution may lead to functioning after transplantation.

Alanine Transaminase↗
PubMed1997

Metabolites of nitric oxide in the lower respiratory tract of children.

UNLABELLED: Nitric oxide (NO) is produced in the upper and lower respiratory tract and can be detected in exhaled air of both healthy individuals and subjects with pulmonary diseases. Recent studies have shown that exhaled NO is mainly derived from the upper airways. There is, however, evidence that in aqueous solutions NO is rapidly converted to distinct oxides of nitrogen. We therefore studied the stable NO metabolites nitrate and nitrite in broncho-alveolar lavage (BAL) fluid and serum as indicators of NO formation in the lower respiratory tract. The study population consisted of 31 healthy children undergoing elective surgery for non-pulmonary illnesses and 13 immunosuppressed children with pneumonia. Nitrate and nitrite were determined photometrically. Nitrate was found in BAL fluid of all children. In children with pneumonia, nitrate concentrations in BAL fluid were significantly higher than in healthy children. A significant correlation was observed between nitrate in BAL fluid and serum of immunosuppressed children with pneumonia. Nitrite was not detected in any of the BAL fluid or serum samples. CONCLUSIONS: Our results suggest that in the lower airways significant amounts of NO are metabolised to nitrate. Studies on NO in pulmonary diseases should therefore include determination of nitrate in lower airway fluids.

Bronchoalveolar Lavage Fluid↗
PubMed1997

Involvement of reactive oxygen species in the preservation injury to cultured liver endothelial cells.

We have previously demonstrated an energy-dependent injury to cultured liver endothelial cells during cold incubation in University of Wisconsin (UW) solution. In the present study, we report experimental evidence for the involvement of reactive oxygen species in this injury: LDH release during 48 h of cold incubation in UW solution was decreased from 40-55% under aerobic conditions to less than 20% under hypoxic conditions or by the presence of KCN (1 mM). Similar protection was achieved by the addition of the spin trap 5,5-dimethyl-1-pyrroline N-oxide, the hydroxyl radical scavenger dimethyl sulfoxide, or the flavonoid silibinin to UW solution under aerobic conditions. Preincubating the cells with the iron chelator deferoxamine even decreased the injury to less than 5%. The residual injury (as observed after longer incubation times) under hypoxic conditions or in cells preincubated with deferoxamine was no longer energy dependent. The amount of thiobarbituric acid-reactive substances markedly increased during cold incubation of the cells in UW solution. This increase was not observed in UW solution to which KCN had been added, i.e., under the conditions of energy depletion. These results suggest that an iron-dependent generation of reactive oxygen species with subsequent lipid peroxidation is involved in the pathogenesis of the injury to cultured liver endothelial cells in cold UW solution.

Animals↗
PubMed1997

Injury to cultured liver endothelial cells after cold preservation: mediation by reactive oxygen species that are released independently of the known trigger hypoxia/reoxygenation.

When cultured liver endothelial cells were incubated in cold University of Wisconsin (UW) solution under hypoxic conditions, 3 +/- 2% of cells had lost viability after 25 h. Simulating reperfusion by returning the cells to normal cell culture conditions increased the injury to 30 +/- 11% after 3 h of recultivation. An injury of similar time course was observed after cold normoxic incubation in UW solution when the loss of viability increased from 20 +/- 5% after the cold incubation to 60 +/- 8% during a 3 h recultivation period. The loss of viability during recultivation was decreased by hypoxia, by the addition of 5,5-dimethyl-1-pyrroline N-oxide or of dimethyl sulfoxide to the cell culture medium, or by preincubating the cells with deferoxamine. The injury was accompanied by lipid peroxidation and was dependent on the period of cold incubation in UW solution. These results suggest the occurrence of a cold-preservation-induced "recultivation injury" mediated by reactive oxygen species. This cold-preservation-induced injury--occurring independently of hypoxia/reoxygenation--is likely to constitute an additional component of reperfusion injury after cold preservation of the liver.

Animals↗
PubMed1996

Determination of hepatocellular enzymes in effluent of human liver grafts for preoperative evaluation of transplant quality.

In 50 human livers harvested for transplantation, injury was assessed by determination of liver enzymes (lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, glutamate dehydrogenase, and creatine kinase) and of thrombomodulin in the effluent perfusate after cold ischemia. The results were compared with the morphology and the clinical course after transplantation. Whereas the release of the markers of endothelial cell injury correlated neither with the history of the graft nor with the postoperative course, the release of hepatocellular enzymes into the perfusate did indicate the severity of liver injury, even when biopsy showed normal liver tissue. Seven of 12 livers with high activities of hepatocellular enzymes in the effluent (activity of more than twice the median) showed delayed onset of function or primary nonfunction. In the other 38 livers with enzyme activities below this borderline, no delayed functioning or primary nonfunction was observed. Thus, determination of liver enzyme activities in the effluent makes it possible to identify those livers in which initial nonfunction is very unlikely, a potential that is especially valuable in livers shown by anamnesis or morphology to be of borderline quality.

Biomarkers↗
PubMed1996

Injury to hepatocytes and non-parenchymal cells during the preservation of human livers with UW or HTK solution: a determination of hepatocellular enzymes in the effluent perfusate for preoperative evaluation of the transplant quality.

In 50 livers harvested for transplantation, injury was assessed by determination of the enzymes in the effluent perfusate after cold ischemia. The results were compared to the histology and the clinical course after transplantation. Whereas the release of the markers of endothelial cell injury did neither correlate with the history of the graft nor with the postoperative course, the release of hepatocellular enzymes in the perfusate did indicate preexisting damage of the liver even when the biopsy showed normal liver tissue. Of 12 livers with high activity of hepatocellular enzymes in the effluent (activity of more than twice the median), 7 showed delayed onset of function or a primary non-function. In the other 38 livers with an enzyme activity below this borderline no delayed function or primary non-function was observed. Because of additional influences a prognosis of the function after transplantation was not possible, but the determination of the enzymes in the effluent of marginal livers probably allows the preoperative recognition of organs which will do well.

Adenosine↗
PubMed1996

Scavenging of reactive oxygen species and inhibition of arachidonic acid metabolism by silibinin in human cells.

The effects of the flavonoid silibinin, which is used for the treatment of liver diseases, on the formation of reactive oxygen species and eicosanoids by human platelets, white blood and endothelial cells were studied. Silibinin proved to be a strong scavenger of HOCI (IC50 7 microM), but not of O2- (IC50 > 200 microM) produced by human granulocytes. The formation of leukotrienes via the 5-lipoxygenase pathway was strongly inhibited. In human granulocytes IC50-values of 15 microM and 14.5 microM silibinin were detected for LTB4 and LTC4/D4/E4/F4 formation, respectively. In contrast to this, three- to fourfold silibinin concentrations were necessary to half maximally inhibit the cyclooxygenase pathway. For PGE2 formation by human monocytes an IC50-value of 45 microM silibinin was found. IC50-values of 69 microM and 52 microM silibinin were determined for the inhibition of TXB2 formation by human thrombocytes and of 6-K-PGF1 alpha formation by human omentum endothelial cells, respectively. Thus, the deleterious effects of HOCI that can lead to cell death, and those of leukotrienes that are especially important in inflammatory reactions, can be inhibited by silibinin in concentrations that are reached in vivo after the usual clinical dose. Silibinin is thought not only to display hepatoprotective properties but might also be cytoprotective in other organs and tissues.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Inhibition of Kupffer cell functions as an explanation for the hepatoprotective properties of silibinin.

The flavonoid silibinin, the main compound extracted from the milk thistle Silybum marianum, displays hepatoprotective properties in acute and chronic liver injury. To further elucidate the mechanisms by which it acts, we studied the effects of silibinin on different functions of isolated rat Kupffer cells, namely the formation of superoxide anion radical (02-), nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha), prostaglandin E(2) (PGE(2)), and leukotriene B(4) (LTB(4)). Production of 02- and NO were inhibited in a dose-dependent manner, with an 50 percent inhibitory concentration (IC(50)) value around 80 micro mol/L. No effect on TNF-alpha formation was detected. Opposite effects were found on the cyclooxygenase and 5-lipoxygenase pathway of arachidonic acid metabolism. Whereas no influence on PGE(2) formation was observed with silibinin concentrations up to 100 micro mol/L, a strong inhibitory effect on LTB(4) formation became evident. The IC(50)-value for inhibiting the formation of this eicosanoid was determined to be 15 micro mol/L silibinin. The strong inhibition of LTB(4), formation by silibinin was confirmed in experiments with phagocytic cells isolated from human liver. Hence, while rather high concentrations of silibinin are necessary to diminish free radical formation by activated Kupffer cells, significant inhibition of the 5-lipoxygenase pathway already occurs at silibinin concentrations which are achieved in vivo. Selective inhibition of leukotriene formation by Kupffer cells can at least partly account for the hepatoprotective properties of silibinin.

Animals↗