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Biomedical subjects

C J Doorenbos

Publications and source records attributed to C J Doorenbos.

At least 19 recordsLinked to original sources
PubMed2001

Successful treatment with recombinant factor VIIa of therapy-resistant severe bleeding in a patient with acquired von Willebrand disease.

We describe an elderly man who presented with life-threatening hematuria and gastrointestinal bleeding caused by acquired von Willebrand disease associated with monoclonal gammopathy of undetermined significance (MGUS). Standard therapy with desmopressin, von Willebrand factor-containing factor VIII concentrate, tranexamic acid, and immunoglobulin failed to achieve adequate hemostasis. However, treatment with recombinant activated factor VII (rFVIIa) arrested the bleeding completely. Since acquired von Willebrand disease can lead to life-threatening hemorrhage, clinicians should consider rFVIIa as an effective treatment option if standard therapy fails.

Aged↗
PubMed1999

[Nosocomial transmission of hepatitis C virus in a Dutch dialysis center].

OBJECTIVE: To describe the transmission of hepatitis C virus (HCV) in a dialysis centre in the Netherlands, to analyse risk factors and to redefine additional preventive measures. DESIGN: Descriptive. METHODS: The data of patients attending the dialysis centre of the Deventer Hospital, the Netherlands, who had participated in a national prospective survey on the epidemiology of HCV among Dutch dialysis patients, were examined. In addition, patients who developed signs of hepatic failure in the ensuing year were included in this study. To diagnose an HCV-infection serology as well as polymerase chain reaction were used. Genotyping and sequence analysis were used to assess phylogenetic relations. Infection control practices were audited. RESULTS: In the dialysis centre a cluster of four almost identical HCV isolates genotype 2a was found. Within a period of one year another cluster of four HCV-infected dialysis patients was detected in the same centre. These four isolates were almost identical to a fifth isolate, genotype 2b, found in the earlier study from another patient dialysing in the same unit. It was observed that possibly contaminating procedures were not strictly separated. Some of the shared medical equipment was not sterilised but only cleaned. Also blood-contaminated gloves might have played a role in the transmission of HCV. CONCLUSION: Nosocomial transmission plays an important role in the epidemiology of HCV in dialysis patients. Shared medical equipment and blood-contaminated gloves may constitute a potential route of transmission. There is a need for stringent implementation and regular auditing of infection control measures.

Cluster Analysis↗
PubMed1997

[Hyperthyroidism due to contamination of the alternative drug Ader-Rein (Vascu-Vitaal)].

A 52-year-old woman developed hyperthyroidism due to the alternative Vascu-Vitaal pills. She was suffering from nephrotic syndrome due to membranoproliferative glomerulonephritis and subclinical hypothyroidism, possibly due to renal loss of thyroid hormone. For peripheral vascular disease she took the non-registered Vascu-Vitaal pills on her own initiative. According to the product information, these pills contain multiple vitamins, minerals, amino acids and tissue extracts of bovine adrenals, hypophysis and thymus. The patient developed hyperthyroidism after starting on a new batch of the preparation; it subsided after stopping the treatment. A technetium thyroid scan showed decreased uptake and subsequently the Vascu-Vitaal pills were found to contain both thyroxine and triiodothyronine. The thyroid hormone contamination was probably caused by bovine thyroid tissue. It is suggested to require a health warning statement on the package of alternative therapeutics stating that production and contents are not subject to governmental supervision.

Animals↗
PubMed1992

Enalapril-induced anemia in two kidney transplant recipients.

Two renal transplant patients developed anemia during treatment of hypertension with enalapril medication. Hemoglobin levels normalized after administration of enalapril was stopped. In one patient, it was demonstrated that the discontinuation of enalapril was followed by a decrease in renal blood flow and a significant increase in the plasma erythropoietin levels that preceded the rise in hemoglobin. These observations are consistent with the hypothesis that angiotensin-converting enzyme inhibition may cause anemia by increasing renal blood flow and consequently decreasing erythropoietin levels.

Adult↗
PubMed1991

The acute and chronic antihypertensive effects of ketanserin cannot be explained by blockade of vascular serotonin, type 2, receptors or alpha 1-adrenergic receptors.

The mechanism underlying the antihypertensive effect of acute and chronic administration of ketanserin was investigated in eight hypertensive patients. Intrabrachial artery infusions of serotonin and the selective alpha 1-adrenergic receptor agonist methoxamine were given before and 1 hour after a single oral dose of 20 mg ketanserin and after 4 weeks of treatment with 20 to 40 mg twice daily. Blood pressure was reduced by ketanserin both after the initial dose (p less than 0.01) and after 4 weeks of treatment (p less than 0.01). During placebo, serotonin, 1 ng/kg/min, increased forearm blood flow by 51% +/- 9% (p less than 0.01), whereas the highest dose induced a decrease in flow (-33% +/- 6%; p less than 0.01). Methoxamine elicited a vasoconstriction (p less than 0.001). These effects of serotonin and methoxamine were not influenced by either the initial dose of ketanserin or after 4 weeks of treatment. It is concluded that serotonin cannot be considered a general endogenous pressor agent in these patients. The antihypertensive effects of ketanserin cannot be attributed to either vascular alpha 1-receptor or serotonin, type 2, receptor blockade.

Adult↗
PubMed1991

Arterial and venous effects of atrial natriuretic peptide in the human forearm.

Atrial natriuretic peptide (ANP) has direct vasodilating properties in addition to its diuretic and natriuretic effects. Furthermore, vascular permeability may be influenced. Because relatively little is known about the venous and capillary actions of ANP in humans, we investigated the spectrum of vascular actions of ANP in the human forearm. In seven healthy subjects, ANP was infused intraarterially in consecutive doses of 0, 10, 50, and 250 ng/100 mL tissue/min together with vehicle or norepinephrine 1 ng/kg/min. In seven other subjects, 0.5 ng/kg/min angiotensin II and 10 ng/kg/min serotonin were used as a constrictor. Venous occlusion plethysmography was used to measure forearm blood flow, venous compliance, capillary filtration rate, and maximum venous outflow. Intraarterial infusion of ANP induced a dose-dependent increase of forearm blood flow but the relative increases were not influenced by concomitant vasoconstriction. Venous compliance was not affected by the infusions, but serotonin and angiotensin II decreased the changes of both forearm volume and venous pressure. ANP antagonized these effects of angiotensin II. Capillary filtration rate was not affected by ANP infusion. ANP alone had no effect on the maximum venous outflow, but it attenuated the decrease induced by norepinephrine and angiotensin II. These results indicate that in the human forearm ANP has predominantly arterial effects, whereas the venous actions become manifest only in the presence of vasoconstriction. The venous effect of ANP may therefore gain importance in disease states with elevated levels of vasoconstrictors, for instance, in congestive heart failure.

Adult↗
PubMed1991

Atrial natriuretic peptide.

In the past several years great progress has been made in the understanding of the (patho) physiology of ANP. Because an inhibitor of ANP is not available for human use, there is still discussion about the physiological role of ANP. Nevertheless, from the studies described above the evidence is accumulating that ANP has a role in protecting against fluid overload and hypertension by means of inducing natriuresis, inhibition of the renin-angiotensin-aldosterone system and vasopressin and by vasodilation. The therapeutic potential of modulation of the ANP system seems promising, but must await further research.

Animals↗
PubMed1990

Atrial natriuretic peptide and chronic renal effects of changes in dietary protein and sodium intake in man.

1. Plasma levels of atrial natriuretic peptide and several other hormones were measured and related to the renal responses to chronic changes in the dietary intake of protein and sodium, alone and in combination. Eight healthy subjects consumed four diets for 1 week: a basal diet containing 140 mmol of sodium/day and 1 g of protein day-1 kg-1, the same diet with isocaloric addition of 1 g of meat protein day-1 kg-1, the basal diet with addition of 170 mmol of sodium chloride/day and the basal diet with both additions. 2. Creatinine clearance was increased significantly both by protein and, to a smaller extent, by sodium. Plasma atrial natriuretic peptide and the urinary excretion of guanosine 3':5'-cyclic monophosphate were increased significantly by sodium but were not affected by protein. Protein induced a significant rise in plasma glucagon levels, whereas the rise in somatomedin C (insulin-like growth factor I) just failed to reach statistical significance. 3. These findings demonstrate that atrial natriuretic peptide does not mediate chronic protein-induced hyperfiltration, although it may contribute to the renal effects of sodium. Glucagon and somatomedin C (insulin-like growth factor I) may have contributed to chronic protein-induced hyperfiltration.

Adult↗
PubMed1990

The effects of dietary excesses in animal protein and in sodium on the composition and the crystallization kinetics of calcium oxalate monohydrate in urines of healthy men.

Dietary excesses in animal protein and/or salt have been implicated as risk factors in calcium oxalate urolithiasis. The underlying physicochemical mechanism is, however, not known. Eight healthy men were given four different diets varying in animal protein and in sodium content for 1 week each. On a high protein intake (2 g/kg.day) significant changes in urinary calcium, uric acid, and citrate excretion rates were found. Similar changes in calcium and citrate were induced by a high sodium intake (310 mmol/day). The changes were more pronounced when a high protein was combined with a high sodium diet. Urinary calcium increased from 3.79 +/- 0.31 to 6.42 +/- 0.61 mmol/24 h and urinary uric acid from 4.69 +/- 0.26 to 8.0 +/- 0.47, whereas urinary citrate decreased from 3.93 +/- 0.53 to 2.79 +/- 0.34 mmol/24 h. All three dietary regimens induced a significant decrease in the ability of urines to inhibit calcium oxalate monohydrate crystal agglomeration, which was most marked during the combined diet (from 345 +/- 39 to 205 +/- 28 min). The ability of urines to inhibit crystal agglomeration was related to their citrate content (r = 0.69, P less than 0.0001). These results show that high animal protein and/or sodium intake decrease the ability of urines to inhibit the agglomeration of calcium oxalate crystals and provide a possible physicochemical explanation for the adverse effects of dietary aberrations on renal stone formation.

Adult↗
PubMed1989

The effect of acute ACE inhibition on atrial natriuretic peptide.

1. The effect of acute angiotensin converting enzyme (ACE) inhibition on the plasma concentrations of atrial natriuretic peptide (ANP) was investigated in a single-blind placebo controlled crossover study in healthy volunteers. 2. Intravenous infusion of 2 mg cilazaprilat resulted in a significant and short lasting inhibition of ACE as evidenced by a decrease of plasma angiotensin II and an increase in plasma renin activity. 3. When compared with placebo cilazaprilat lowered diastolic pressure and increased heart rate significantly. 4. No effect of cilazaprilat was found on plasma ANP levels, suggesting that angiotensin II does not mediate ANP release.

Adult↗
PubMed1989

Correlates of plasma atrial natriuretic peptide levels in renal transplant recipients.

Plasma atrial natriuretic peptide (ANP) levels were measured with a radio-immunoassay in 56 patients, 3 weeks to 16 1/2 years after renal transplantation. At the time of the study their renal function was stable, with creatinine clearances ranging from 10 to 101 ml/min. Plasma ANP levels ranged from 1 to 941 pg/ml and were found to correlate positively with both age and systolic blood pressure. Moreover, a negative correlation was found between plasma ANP levels and creatinine clearance. We conclude that in renal transplant recipients neither renal denervation nor the use of immunosuppressive therapy abolishes the influence of age, systolic blood pressure and renal function on the plasma levels of ANP.

Adolescent↗
PubMed1988

Effects of posture and saline infusion on atrial natriuretic peptide and haemodynamics in patients with Bartter's syndrome and healthy controls.

In order to explore the role of atrial natriuretic peptide (ANP) in Bartter's syndrome, five patients and five healthy controls matched for age and sex were studied. The study was designed to stimulate and suppress ANP secretion by manipulation of right atrial pressure with different body positions and mild volume expansion with saline. Other vasoactive hormones were also measured, and heart rate and blood pressure were recorded at 5-min intervals. Plasma ANP levels increased after head-down tilt and returned to baseline in the upright position. Infusion of saline failed to increase plasma ANP both in the control group and in four of the patients. No significant differences were found in plasma atrial natriuretic peptide concentrations between both groups. In view of previously reported elevated plasma ANP levels, Bartter's syndrome may be heterogeneous in this respect. Plasma renin activity was higher in the patients, but plasma aldosterone, adrenaline and noradrenaline were similar in both groups. Mean arterial blood pressure was similar in both groups, but rose significantly in the upright position in the control group only, while changes in heart rate were similar in both groups. We conclude that atrial natriuretic peptide does not seem to play a causal role in our patients with Bartter's syndrome.

Adult↗