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Biomedical subjects

P H Groeneveld

Publications and source records attributed to P H Groeneveld.

At least 19 recordsLinked to original sources
PubMed2004

[Liver cirrhosis due to chronic use of nitrofurantoin].

A 74-year-old woman was admitted with jaundice. She was suffering from generalised liver failure with a highly prolonged prothrombin time, a low albumin level and ascites. Further anamnesis revealed that she had been taking nitrofurantoin as a prophylactic agent for recurrent urinary tract infections every day for 5 years. Because of the indications for liver damage due to nitrofurantoin, the drug was discontinued immediately on admission. After withdrawal of nitrofurantoin there was a very gradual clinical and biochemical improvement. Liver biopsies to confirm the diagnosis revealed extensive liver damage with cirrhosis such as may be seen following long-term use of nitrofurantoin. Nitrofurantoin should be prescribed with caution as a prophylactic agent in elderly women and patients with renal dysfunction because the risk of liver damage as a serious side effect of nitrofurantoin is greatly increased in these patients.

Aged↗
PubMed2003

[Unavoidable surgical intervention in two women with severe actinomycosis during IUD use].

Extensive abdominal infections with Actinomyces were diagnosed in two women aged 35 and 33 years respectively, who suffered from the nonspecific symptoms fever and abdominal pain. These infections occur more often in women with an intrauterine device. Development of an abdominal mass with ureter or bowel obstruction may cause hydronephrosis and mechanical ileus. The patients underwent a laparotomy and a double-J catheter was inserted, which could be removed later on (temporary stoma). Treatment included high-dose penicillin i.v. followed by oral amoxicillin. Both patients recovered. It may be difficult to establish this diagnosis: the first patient was diagnosed by histopathological examination, in the second Actinomyces had been found in a routine cervical smear a few years earlier.

Abdominal Pain↗
PubMed2001

Atrial natriuretic peptide infusion and nitric oxide inhalation in patients with acute respiratory distress syndrome.

AIM: To study the effects of infusion of atrial natriuretic peptide (ANP) versus the inhalation of nitric oxide (NO) in patients with an early acute respiratory distress syndrome (ARDS). METHODS: Ten patients with severe ARDS were studied in a crossover study design, within 72 hours after starting mechanical ventilation. We studied the effects of ANP infusion (10 ng/kg/min for 1 hour) and of inhalation of NO (20 ppm for 1 hour) on hemodynamic and respiratory patient parameters, as well as the effects on plasma levels of ANP, guanosine 3',5'-cyclic monophosphate, nitrate and endothelin-1. RESULTS: Despite an approximate 50% increase in mixed venous ANP plasma concentration (from 86 +/- 21 to 123 +/- 33 ng/l, P < 0.05) during ANP infusion, there were no changes in mean pulmonary artery pressure, pulmonary vascular resistance index, extravascular lung water index, or in pulmonary gas exchange. NO inhalation, in contrast, lowered mean pulmonary artery pressure (from 26 +/- 1.9 to 23.9 +/- 1.7 mmHg, P < 0.01), pulmonary vascular resistance index (from 314 +/- 37 to 273 +/- 32 dynes/cm5/m2, P < 0.05) and central venous pressure (from 8.2 +/- 1.2 to 7.3 +/- 1.1 mmHg, P < 0.02). Furthermore, NO inhalation improved pulmonary gas exchange, reflected by a decrease in alveolar-arterial oxygen gradient (from 41.9 +/- 3.9 to 40.4 +/- 3.6 kPa, P < 0.05), a small increase in oxygenation (PaO2/FiO2 from 17.7 +/- 1.4 to 19.7 +/- 1.1 kPa, P = 0.07) and a small decrease in venous admixture (Qs/Qt from 35.7 +/- 2.0 to 32.8 +/- 2.7%, P = 0.11). CONCLUSION: This study shows that, in contrast to NO inhalation, infusion of ANP neither improves oxygenation nor attenuates pulmonary hypertension or pulmonary edema in patients with severe ARDS.

Administration, Inhalation↗
PubMed2000

Endotoxin, cytokines, and procalcitonin in febrile patients admitted to the hospital: identification of subjects at high risk of mortality.

We prospectively examined 464 febrile patients (median age, 61 years) for predictors of in-hospital death, by use of univariate and multivariate logistic regression using clinical data (age, underlying disease, duration of fever, chills, and shock on admission) and plasma endotoxin, TNF-alpha, IL-6, IL-10, and procalcitonin levels. The mortality rate was 4.6-fold higher (95% confidence interval [CI], 1.8-12) in 31 patients with shock on admission, 7 of whom died; the strongest association with mortality was the endotoxin concentration (relative risk, 13.7; 95% CI, 1. 4-136), which predicted 5 of the deaths with a 5% false-positive rate. For 433 patients without shock on admission, mortality (26 deaths) was associated with age and underlying disease: clinical data predicted 30% of the deaths, whereas IL-6 and procalcitonin levels identified an extra 10% with a 5% false-positive rate. When febrile patients are screened on hospital admission to identify those with a high risk for mortality, clinical judgment on the basis of age, underlying disease, and recent history outweighs the predictive value of endotoxin, cytokine, and procalcitonin levels. Only in patients who present with shock will measurement of endotoxin levels help predict those who will likely die at the cost of few false-positive results.

Adolescent↗
PubMed2000

Interleukin-10 has different effects on proliferation of Listeria monocytogenes in livers and spleens of mice.

The aim of this study was to investigate the effect of interleukin-10 (IL-10) on the course of Listeria monocytogenes infection in naive and immune mice. Treatment with IL-10 during the course of a primary infection significantly decreased the number of bacteria in the spleen and did not affect the number in the liver. During a secondary infection in immune mice treated with IL-10, the number of bacteria was significantly lower in the spleen but significantly higher in the liver in comparison to mock-treated immune mice. IL-10 treatment during a primary Listeria infection decreased the concentration of gamma interferon (IFN-gamma) in plasma and the toxoplasmastatic activity of macrophages, whereas it increased the percentage of mildly CD3-positive T cells in the spleen. During a secondary infection, the concentration of IFN-gamma in plasma was decreased on day 1 but remained unaffected during later days of infection. From these results, we conclude that IL-10 has different effects on the proliferation of L. monocytogenes in the spleen and liver during primary and secondary Listeria infections.

Animals↗
PubMed1999

Decreased expression of zeta molecules by T lymphocytes is correlated with disease progression in human immunodeficiency virus-infected persons.

In human immunodeficiency virus type 1 (HIV-1) infection, functional activities of T lymphocytes are impaired. Analogous to tumor-infiltrating T lymphocytes from cancer patients, in whom poor proliferative responses are associated with fewer zeta molecules, this study compared expression of CD3zeta molecules by T lymphocytes from HIV-infected persons and healthy controls. Flow cytometry and immunoblotting revealed significantly diminished zeta expression by CD3, CD4, and CD8 T lymphocytes from AIDS patients but not from persons without AIDS. zeta-mRNA levels were also decreased in cells from AIDS patients. CD3zeta expression correlated significantly with CD4 cell counts and HIV-1 RNA levels; impaired expression of CD3zeta molecules appeared to be reversible upon virus load reduction following highly active antiretroviral treatment (HAART). Thus, reduced expression of CD3zeta molecules by T lymphocytes from HIV-infected persons correlates with disease status. Investigations into CD3zeta expression by subpopulations of peripheral T lymphocytes and by T lymphocytes in lymphoid tissues will contribute to the understanding of immune reconstitution of HIV-infected patients following HAART.

AIDS-Related Opportunistic Infections↗
PubMed1999

Antibiotic-induced cell wall fragments of Staphylococcus aureus increase endothelial chemokine secretion and adhesiveness for granulocytes.

Antibiotics release inflammatory fragments, such as lipoteichoic acid (LTA) and peptidoglycan (PG), from the cell wall of Staphylococcus aureus. In this study, we exposed S. aureus cultures to a number of beta-lactam antibiotics (imipenem, flucloxacillin, and cefamandole) and protein synthesis-inhibiting antibiotics (erythromycin, clindamycin, and gentamicin) and investigated whether supernatants of these cultures differ in their capacity to stimulate endothelial cells (EC). After 24 h of incubation, endothelial adhesiveness for leukocytes, surface expression of various adhesion molecules, and secretion of the chemokines interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) were measured. Supernatants of beta-lactam-exposed cultures (designated beta-lactam supernatants) enhanced the adhesiveness of EC for granulocytes, whereas those of protein synthesis-inhibiting antibiotic-exposed cultures (designated protein synthesis-inhibitor supernatants) did not. This hyperadhesiveness coincided with a higher intercellular adhesion molecule-1 expression on the surface of the stimulated EC. In addition, EC stimulated with beta-lactam supernatants secreted significantly higher concentrations of the chemokines IL-8 and MCP-1 than those stimulated with protein synthesis-inhibitor supernatants. The finding that the concentrations of LTA and PG in beta-lactam supernatants were much higher than those in protein synthesis-inhibitor supernatants suggests that the observed differences in stimulatory effect between these supernatants are a result of differences in the release of cell wall fragments, although the presence of other stimulatory factors in the supernatants cannot be excluded. In conclusion, our results argue for a release of LTA and PG from S. aureus after exposure to beta-lactam antibiotics that enhances the development of a systemic inflammatory response by stimulating EC such that adhesiveness for granulocytes is increased and large amounts of IL-8 and MCP-1 are secreted.

Anti-Bacterial Agents↗
PubMed1998

Antibiotic-induced release of lipoteichoic acid and peptidoglycan from Staphylococcus aureus: quantitative measurements and biological reactivities.

Antibiotics with different mechanisms of action may vary with respect to their effects on the release and immunostimulatory activities of cell wall fragments from gram-positive bacteria. Therefore, after Staphylococcus aureus was cultured for 4 h in the absence of antibiotics (control) and in the presence of beta-lactam antibiotics (imipenem, flucloxacillin, or cefamandole) and protein synthesis-inhibiting antibiotics (erythromycin, clindamycin, or gentamicin), the lipoteichoic acid (LTA) and peptidoglycan (PG) levels in the bacterial supernatants were measured. beta-Lactam antibiotics greatly enhanced the release of LTA and PG (4- to 9-fold and 60- to 85-fold, respectively), whereas protein synthesis inhibitors did not affect PG release and even inhibited the release of LTA compared to the amount of LTA released in control cultures. The capacity of beta-lactam supernatants to stimulate the production of tumor necrosis factor alpha and interleukin-10 in human whole blood was significantly higher than that of protein synthesis inhibitor or control supernatants; the amounts of these cytokines released were directly proportional to the concentrations of PG and LTA in the supernatants. Enzymatic degradation of PG in the supernatants indicated that PG was mainly responsible for the observed biological reactivity.

Anti-Bacterial Agents↗
PubMed1998

Antibiotic-induced lipopolysaccharide (LPS) release from Salmonella typhi: delay between killing by ceftazidime and imipenem and release of LPS.

It has been suggested that the antibiotic-induced release of lipopolysaccharide (LPS) is an important cause of the development of septic shock in patients treated for severe infections caused by gram-negative bacteria. Beta-lactam antibiotics change the integrity of the bacterial cell envelope by binding to penicillin-binding proteins (PBP) in the membrane and thus may affect the amount of LPS that is released and the kinetics of that release. In this respect, ceftazidime at intermediate concentrations binds with a high affinity to PBP 3 and PBP 1a and thus can induce filament formation in addition to killing, whereas imipenem preferentially binds to PBP 2 and PBP 1b, leading to spheroplast formation and rapid cell lysis. We investigated the effects of these antibiotics on the killing and the release of the radioactively labelled LPS of Salmonella typhi Ty 21A. A mathematical model was developed to calculate the delay between bacterial killing and LPS release, designated the lag time. At antibiotic concentrations inducing equal killing, the amount of LPS released was the same for both antibiotics. Only after 6 h of incubation at antibiotic concentrations above 0.5 microg/ml, the amount of 3H-LPS released was slightly higher (approximately 1.2-fold) in incubations with ceftazidime than in those with imipenem, and the maximum releases of the total label were 33.2% +/- 0.89% and 27.1% +/- 0.45%, respectively. Despite the clear concentration-dependent effect on the bacterial killing and subsequent LPS release, the lag time was independent of the antibiotic concentration. For ceftazidime as well as imipenem the lag time amounted to approximately 60 min. In conclusion, our findings imply that the mechanism of antibiotic-induced LPS release is independent of the PBP affinities for these beta-lactam antibiotics. Furthermore, once the organism is killed by either imipenem or ceftazidime, the rate of LPS release from S. typhi does not differ according to the antibiotic with which the organism is killed, and there is little difference in the relative amount of LPS released.

Anti-Bacterial Agents↗
PubMed1997

Relation between pro- and anti-inflammatory cytokines and the production of nitric oxide (NO) in severe sepsis.

The aim of the present study was to investigate the relationship between the levels of pro-inflammatory [interleukin 6 (IL-6), IL-8, tumour necrosis factor alpha (TNF-alpha)], anti-inflammatory cytokines [IL-10, soluble TNF receptor type I (TNFsrI), TNFsrII], and the production of nitric oxide (NO) during a 1-week period in 23 patients with severe sepsis. The highest levels of pro-inflammatory cytokines and nitrate, the stable metabolite of NO, were found during the first day after inclusion and gradually declined thereafter. Detectable levels of IL-10, TNFsrI and TNFsrII were present in all patients at study entry but did not significantly change during the study period [analysis of variance (MANOVA); P > 0.05]. Serum nitrate levels correlated significantly with both pro-inflammatory cytokines (IL-6, IL-8, TNF-alpha) as well as anti-inflammatory cytokines (IL-10, TNFsrI, TNFsrII). Serum nitrate levels over time were higher in patients with positive blood cultures (n = 4) (MANOVA; P < 0.005), as compared to patients without proven bacteraemia. These data support the concept of an acute phase of sepsis that is characterized by an excess of pro-inflammatory cytokines, while anti-inflammatory cytokines are predominantly present during the secondary phase. The present findings indicate that pro-inflammatory cytokines are related to the induction of excessive NO production during the first phase of sepsis and that reduction of NO production occurs during the secondary phase. This may suggest that anti-inflammatory cytokines are able to diminish the production of NO in patients with severe sepsis.

Antigens, CD↗
PubMed1997

Combination of flucloxacillin and gentamicin inhibits toxic shock syndrome toxin 1 production by Staphylococcus aureus in both logarithmic and stationary phases of growth.

Production of exotoxins by staphylococci and streptococci may lead to the development of toxic shock syndrome (TSS). Because clindamycin inhibits exotoxin production, its use has been advocated for the treatment of TSS. However, the bacteriostatic action of clindamycin might be a disadvantage for the treatment of overwhelming infections. We investigated the effects of flucloxacillin and gentamicin on exotoxin production, because incubation with these antibiotics combines bactericidal action with protein synthesis inhibition. Staphylococcus aureus during the logarithmic and stationary phases of growth was incubated with either clindamycin, flucloxacillin, or a combination of flucloxacillin and gentamicin at concentrations of 2 or 10 times the MIC. In logarithmic-phase cultures clindamycin had a static effect on bacterial growth. After incubation with flucloxacillin, either alone or in combination with gentamicin, a rapid and large reduction in the number of viable bacteria was demonstrated. In stationary-phase cultures none of the antibiotics significantly changed the number of viable bacteria. TSS toxin 1 (TSST-1) production during logarithmic-phase growth was inhibited by > or =95% by all antibiotics. In stationary-phase cultures, clindamycin, flucloxacillin, and the combination of flucloxacillin and gentamicin inhibited TSST-1 production by 95, 30, and 75%, respectively, compared with the level of exotoxin production in the controls. The present results indicate that clindamycin inhibits TSST-1 production and exerts bacteriostatic activity in both bacterial growth phases. Because the combination of flucloxacillin and gentamicin combines the inhibition of exotoxin production with high bactericidal activity at least in logarithmic-phase cultures, it should be considered an alternative to clindamycin for the treatment of exotoxin-mediated diseases, especially in patients with overwhelming infections.

Anti-Bacterial Agents↗
PubMed1997

Elimination of resident macrophages from the livers and spleens of immune mice impairs acquired resistance against a secondary Listeria monocytogenes infection.

During a secondary Listeria monocytogenes infection in mice, the bacteria are eliminated more rapidly from the liver and spleen than during a primary infection. This acquired resistance against a secondary infection is dependent on T lymphocytes, which induce enhanced elimination of bacteria via stimulation of effector cells such as neutrophils, resident macrophages, exudate macrophages, and hepatocytes. The aim of the present study was to determine the role of the resident macrophages in acquired resistance against a secondary L. monocytogenes infection in mice. Mice which had recovered from a sublethal primary infection with 0.1 50% lethal dose (LD50) of L. monocytogenes intravenously (i.v.), i.e., immune mice, received a challenge of 1 LD50 of L. monocytogenes i.v. to induce a secondary infection. At 2 days prior to challenge, immune mice were given an i.v. injection of liposomes containing dichloromethylene-diphosphonate (L-Cl2MDP) to selectively eliminate resident macrophages from the liver and spleen. Control immune mice received either phosphate-buffered saline (PBS) or liposomes containing PBS (L-PBS). Treatment of mice with L-Cl2MDP effectively eliminated resident macrophages from the liver and spleen but did not affect the number of granulocytes, monocytes, or lymphocytes in peripheral blood or their migration to a site of inflammation. Phagocytosis and killing of L. monocytogenes by peritoneal exudate cells elicited with heat-killed L. monocytogenes were similar in all groups of immune mice. On day 3 of a secondary infection, the number of L. monocytogenes organisms in the livers and spleens of L-Cl2MDP-treated immune mice was 4 log10 units higher than in immune mice treated with PBS or L-PBS. The concentration of reactive nitrogen intermediates in plasma, a measure of the severity of infection, was 70-fold higher for L-Cl2MDP-treated immune mice than for PBS- or L-PBS-treated immune mice. Treatment with L-Cl2MDP significantly increased the number of inflammatory foci in the liver and spleen, decreased their size, and affected their structure. From these results, we conclude that resident macrophages are required for the expression of acquired resistance against a secondary L. monocytogenes infection in mice.

Animals↗
PubMed1996

Nitric oxide (NO) production correlates with renal insufficiency and multiple organ dysfunction syndrome in severe sepsis.

OBJECTIVE: To investigate whether the production of nitric oxide (NO) relates to the development of renal insufficiency and multiple organ dysfunction syndrome (MODS) in patients with severe sepsis. DESIGN: Prospective study in 23 patients with severe sepsis. SETTING: Medical and surgical intensive care units (ICU) of three hospitals. MEASUREMENTS AND RESULTS: Serum nitrate levels, as an indirect parameter of the production of NO in vivo, and scores for renal insufficiency and MODS were determined in patients with severe sepsis during a 1-week period after admission to the ICU. The highest serum nitrate levels were found at 4 h (mean 52 +/- 16 mumol/l) after entry into the study and the levels gradually declined thereafter. Patients with renal insufficiency had considerably higher serum nitrate levels during the study period that patients who did not develop renal sufficiency (MANOVA, p < 0.05). Serum nitrate levels correlated with scores for renal insufficiency (r = 0.60, p < 0.001), and far exceeded the levels that can be explained solely by reduced renal clearance of nitrate. Further analysis showed that serum nitrate levels significantly and positively correlated with scores for MODS (r = 0.44, p < 0.001). CONCLUSION: Our results indicate that the production of NO correlates with renal insufficiency and MODS in patients with severe sepsis and that this reactive nitrogen intermediate could be involved in the pathogenesis of organ failure in these critically ill patients.

Adult↗
PubMed1996

Acquired resistance against a secondary infection with Listeria monocytogenes in mice is not dependent on reactive nitrogen intermediates.

During an infection, inflammatory mediators can induce the production of nitric oxide, a reactive nitrogen intermediate (RNI) which plays a role in antimicrobial activity against a wide variety of pathogens. In vitro experiments have shown that release of RNI by macrophages is mediated by tumor necrosis factor alpha (TNF). Since TNF is essential for acquired resistance during a secondary Listeria monocytogenes infection in mice, the aim of the present study was to determine whether RNI are also involved in the course of such an infection. Mice which had recovered from a sublethal primary infection with 0.1 50% lethal dose of (LD50) L. monocytogenes were infected intravenously with 10LD50 of L. monocytogenes. During a primary infection, the number of bacteria in the liver and spleen, as well as the concentration of RNI in plasma, increased. During a secondary infection, the number of bacteria in the liver and spleen decreased whereas no significant increase in the concentration of RNI in plasma was observed. Neutralization of endogenously produced TNF and gamma interferon by subcutaneous injection of alginate-encapsulated monoclonal antibody-forming cells during a secondary infection resulted in an increase in the number of bacteria in the liver and spleen an increase in the concentration of RNI in plasma. When the production of RNI was inhibited by treatment of mice with competitive NO-synthase inhibitor N omega-nitro-L-arginine methyl ester hydrochloride (L-Name) and an iota-arginine-deficient diet during a secondary infection, the proliferation of L. monocytogenes in the liver and spleen was not affected whereas the concentration of RNI in plasma of these mice was significantly reduced. Our findings that inhibition of RNI formation during a secondary infection does not affect the proliferation of L. monocytogenes in the liver and spleen and that enhanced elimination of bacteria from these organs is not accompanied by an increase in the concentration of RNI in plasma led to the conclusion that resistance against a secondary infection with L. monocytogenes is not dependent on RNI.

Animals↗