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Biomedical subjects

R O von Vigier

Publications and source records attributed to R O von Vigier.

At least 19 recordsLinked to original sources

[Urinary hormone analysis].

Urinary hormone analysis is applied to detect an altered steroid hormone metabolism, an elevated production of biogenic amines and to non-invasively determine the protein hormone human beta-choriogonadotropin indicating a pregnancy. Occasionally, these determinations need to be complemented by plasma- or serum hormone analysis. Clinical data including current drug therapy and urinary creatinine as reference are required to interpret any urine analysis. Diseases to be investigated by steroid hormone analysis are excess production of a typical or atypical mineralocorticoid active steroid hormones, the hormonal activity of adrenal or ovarian tumors, acne of unknown origin, hirsutism, a PCO-, an adrenogenital or a suspected Cushing syndrome. Biogenic amines should be determined in suspected secondary or refractory arterial hypertension, in case of pheochromocytoma- or paraganglioma-associated symptoms or if a serotonin-producing tumor is suspected. In children genetically determined diseases are the primary background to perform an analysis.

Endocrine System Diseases↗

[Hemolytic uremic syndrome in childhood: not so rare in Swiss children].

Fifty years after the first report by Gasser and Gautier, hemolytic, uremic syndrome is rather rare but severe childhood disease. A recent survey demonstrates that more than 90% of the cases occurring in Switzerland are caused either by Escherichia coli that produces shigatoxin or by Streptococcus pneumoniae.

Escherichia coli Infections↗

[Electrolyte imbalances in infancy and childhood].

Electrolyte disturbances are frequently encountered in pediatric patients, not only in those with critical illness. They can manifest as lethargy, seizures, vomiting and cardiac arrhythmias. In many cases, electrolyte abnormalities are secondary to other underlying conditions, therefore clinical signs and symptoms can be predominated by the primary disease and not by the electrolyte imbalance. Clinical and laboratory evaluation must consist of a detailed history including any drug treatment, evaluation of volume status, acid-base balance, electrolytes as well as plasma and urine osmolality. Before initiating treatment, potential risks of both, the electrolyte disorder itself and the treatment must be considered. Therefore, long lasting (chronic) disorders must in general be corrected very slowly, whereas in acute disturbances rapid correction is better tolerated.

Child↗

[Vesico-ureteral reflux, reflux nephropathy and terminal renal failure].

Vesicoureteric reflux is subcategorized into primary and secondary. Secondary vesicoureteric reflux results from increased bladder pressure duo to anatomic outlet obstruction or neuropathic disturbances. Primary vesicoureteric reflux was felt to result from a congenitally short mucosal tunnel length but this concept has been thrown into question. Recent studies suggest an association between lower urinary tract dysfunction and primary vesicoureteric reflux. Primary vesicoureteric reflux is often associated with kidney damage. It has been traditionally assumed that in children with primary vesicoureteric reflux kidney damage results from reflux of infected urine into the renal tissue. While there is unarguable proof that kidney damage can be acquired by the reflux of infected urine, the extent of reflux nephropathy explained by this mechanism has been overemphasized. Recent observations indicate that there are two categories of primary reflux disorder: a mild reflux associated with an acquired renal scarring secondary to infections which affects most females and a proportion of males; and a prenatal high-grade vesicoureteric reflux with a congenital nephropathy characterized by generalized hypodysplastic features which almost exclusively affects boys. Treatment options of primary vesicoureteric reflux range from surgical ureteric reimplantation to antimicrobial prophylaxis. Findings from comparative trials of prophylactic antibiotics and surgical management of children with high-grade vesicoureteric reflux do not show difference in renal growth and acquisition of new scars or renal function for 10 years. The factors accounting for the outcome in the mentioned studies are that most damage occurs at a very early stage and that severely damaged kidneys will either remain stable or progress to end-stage kidney disease, despite all efforts to cure the reflux.

Age Factors↗

Antihypertensive efficacy of amlodipine in children with chronic kidney diseases.

In adults the calcium antagonist amlodipine given once a day has proved to be an attractive addition to the antihypertensive armamentarium. The present report describes our experience in 43 paediatric outpatients (26 boys and 17 girls, aged between 1.1 and 19, median 9.8 years) with chronic kidney diseases. The patients were given amlodipine for 16 weeks as part of their antihypertensive treatment. Before amlodipine arterial pressure was 150 (142-163)/90 (84-95) mm Hg (median and interquartile range). Six patients withdrew from amlodipine because of oedema, flushing or headache. In the remaining patients amlodipine 7.7 (6.9-9.4) mg/m(2) body surface area once a day significantly decreased arterial pressure by 17 (13-22)/10 (7-13) mm Hg. The efficacy of amlodipine was more pronounced in girls than in boys. No changes in heart rate, body weight and circulating haemoglobin, sodium, potassium and creatinine were noted. In none of the patients circulating potassium, sodium or creatinine changed by more than 0.5 mmol/l, 5 mmol/l respectively 20%. In 11 patients concomitantly treated with cyclosporine the dosage and the trough-level of this agent were stable throughout the trial. In conclusion the present experience in paediatric outpatients with chronic kidney diseases supports the view that amlodipine is an effective and rather well tolerated antihypertensive drug when given once a day.

Adolescent↗

Fluid resuscitation in infantile hypertrophic pyloric stenosis.

UNLABELLED: The purpose of this analysis was to investigate biochemical disturbances at presentation and initial fluid resuscitation before surgery in infantile pyloric stenosis. The charts of 139 consecutive infants (113 boys and 26 girls) between 7 d and 20 wk of age with hypertrophic pyloric stenosis were reviewed. The infants were treated at the Department of Pediatric Surgery, University of Bern, Switzerland, in the period between 1987 and 1997. A trend towards hypokalaemia (13 of the 139 patients), hypochloraemia (39 patients) and especially metabolic alkalosis (98 patients) was frequently noted on admission. In 84 patients, data on fluid management and on circulating sodium, potassium, chloride and the acid-base balance immediately before surgery were also available. In these patients a significant correlation was found between the parenteral chloride dose given for fluid repair (y = 0.310 x; r = 0.54; p < 0.001) and the changes in plasma bicarbonate. The equation indicates that a chloride dose of 10 mmol/kg body weight is required to reduce plasma bicarbonate on average by 3 mmol/. CONCLUSION: Since assessment of the fluid volume stated by physical examination and history is inaccurate in infants with vomiting, the severity of metabolic alkalosis helps to define the amount of fluid required for repair.

Alkalosis↗

Pulmonary renal syndrome in childhood: a report of twenty-one cases and a review of the literature.

In adults, the term specific pulmonary renal syndrome describes disorders with pulmonary and glomerular manifestations and includes Wegener's granulomatosis, Goodpasture disease, and systemic lupus erythematosus. Nonspecific pulmonary renal syndrome refers to either pulmonary disease complicating glomerular disease, or glomerular diseases following pulmonary disease. Since little is known regarding pulmonary renal syndrome in childhood, we reviewed the charts of 21 pediatric patients with pulmonary renal syndromes treated by the Department of Pediatrics, University of Bern between 1991 and 1998; we also reviewed the pediatric literature that deals with specific pulmonary renal syndromes. Specific pulmonary renal syndrome was noted in 3 children with systemic vasculitis (Wegener granulomatosis, N = 2; microscopic polyangiitis, N = 1) and 2 with systemic lupus erythematosus. Nonspecific pulmonary renal syndrome was observed in 12 patients with pulmonary edema (N = 9), pulmonary thromboembolism (N = 2), and pulmonary infection (N = 1) complicating the course of a glomerular disease, and in 4 children with a pulmonary disease followed by a glomerular disease. Review of the literature disclosed 52 cases of specific pulmonary renal syndrome other than systemic lupus erythematosus: Wegener granulomatosis (N = 28), Goodpasture disease (N = 13), and Henoch-Schönlein purpura (N = 11). In addition, hemolytic uremic syndrome complicated pneumococcal pneumonia in 32 cases. We conclude that pulmonary renal syndromes need to be looked for in childhood. Apart from Wegener granulomatosis, Goodpasture disease, and systemic lupus erythematosus, Henoch-Schönlein purpura and hemolytic-uremic syndrome occasionally have both pulmonary and renal features.

Adolescent↗

Preliminary experience with the angiotensin II receptor antagonist irbesartan in chronic kidney disease.

UNLABELLED: Blocking the formation of angiotensin II with converting enzyme inhibitors is an established intervention for kidney disease. The advent of antagonists of the angiotensin II receptor has increased the options for inhibiting the renin-angiotensin-aldosterone system. In adults, angiotensin II antagonists have antihypertensive and antiproteinuric effects similar to those of converting enzyme inhibitors and an adverse effect profile similar to that of placebo. In children, no information is available on angiotensin II antagonists. A total of 20 children (aged 4 to 17 years) with chronic kidney disease received the angiotensin II antagonist irbesartan given once daily. They had hypertension (n = 11), overt proteinuria (n = 3), or both (n = 6). At last follow-up, 2 to 17 months after starting irbesartan (median dosage: 3.3 mg/kg body weight daily), arterial pressure was significantly reduced: the systolic value by 16 [6-22] and the diastolic value by 11 [4-22] mmHg (median and interquartile range). In nine patients with proteinuria, the urinary albumin/creatinine ratio significantly decreased by 145 [105-209] mg/mmol. The frequency of reported adverse events was similar before and with irbesartan. CONCLUSION: In children with chronic kidney disease the effects of the angiotensin II antagonist irbesartan on arterial pressure and proteinuria mimic those observed with the converting enzyme inhibitors. The effectiveness of a single daily dose and the paucity of side-effects suggest that angiotensin II antagonists expand therapeutic options for inhibiting the renin-angiotensin-aldosterone system in children.

Adolescent↗

Non-infectious causes of uveitis in 70 Swiss children.

Many diseases are linked with uveitis, but few studies have specifically looked at the noninfectious triggers of childhood uveitis in Central Europe. The charts of 70 paediatric patients with non-infectious uveitis admitted to the Department of Pediatrics, University of Bern, Switzerland, between 1983 and 1998 were therefore reviewed. In the patients the age at presentation with uveitis ranged between 0.3 and 16 y, median 8.5 y. Based on the localization, uveitis anterior was diagnosed in most cases (n = 40; 57%), followed by panuveitis (n = 20; 29%) and uveitis posterior (n = 10; 14%). Uveitis was chronic in 54 (77%) and acute in 16 (23%), bilateral in 38 (54%) and unilateral in 32 (46%) cases. An associated condition was noted in 32 (46%) cases: juvenile idiopathic arthritis in 24 cases, sarcoidosis and juvenile spondyloarthropathy in 3 cases, and Sjögren's syndrome and Behçet's disease in 1 case each. In the remaining 38 (54%) patients, no associated condition was diagnosed. It is concluded that in Swiss children, uveitis can be due to a wide spectrum of non-infectious diseases, juvenile idiopathic arthritis being the leading cause. In the majority of the children, no associated condition was recognized.

Acute Disease↗

Acute community-acquired diarrhea requiring hospital admission in Swiss children.

In order to ascertain the prevalence of agents that cause childhood diarrheal illness, stool specimens of 312 consecutive children with community-acquired diarrhea requiring admission were evaluated. Pathogens were detected in 166 (53%) of the 312 children (>/=2 pathogens in 28 children): Rotavirus (n=75), Salmonella spp. (n=37), Campylobacter spp. (n=24), Shigella spp. (n=5), Giardia spp. (n=4), Yersinia spp. (n=2), Aeromonas spp. (n=15), Cryptosporidium (n=15), enteropathogenic Escherichia coli (n=13), enterotoxigenic E. coli (n=7), and enterohemorrhagic E. coli (n=5). In conclusion, acute childhood diarrheal illness pathogens, such as Aeromonas, Cryptosporidium, and diarrheagenic E. coli, account for a large proportion of patients with a microbiologically positive stool specimen.

Adolescent↗

Hypomagnesaemia-hypercalciuria-nephrocalcinosis: a report of nine cases and a review.

BACKGROUND: The cardinal characteristics of primary hypomagnesaemia-hypercalciuria-nephrocalcinosis include renal magnesium wasting, marked hypercalciuria, renal stones, nephrocalcinosis, a tendency towards chronic renal insufficiency and sometimes even ocular abnormalities or hearing impairment. METHODS: As very few patients with this syndrome have been described, we provide information on nine patients on follow-up at our institutions and review the 42 cases reported in the literature (33 females and 18 males). RESULTS: Urinary tract infections, polyuria-polydipsia, renal stones and tetanic convulsions were the main clinical findings at diagnosis. The clinical course was highly variable; renal failure was often reported. The concomitant occurrence of ocular involvement or hearing impairment was reported in a large subset of patients. Parental consanguinity was noted in some families. CONCLUSIONS: The results indicate an autosomal recessive inheritance. The diagnosis of primary hypomagnesaemia-hypercalciuria-nephrocalcinosis deserves consideration in any patient with nephrocalcinosis and hypercalciuria.

Adolescent↗

Aminoglycosides and renal magnesium homeostasis in humans.

BACKGROUND: The use of aminoglycosides has been linked with hypomagnesaemia in scattered reports. The objective of the study was to measure prospectively the effect of treatment with the aminoglycoside amikacin on renal magnesium homeostasis. METHODS: Twenty-four cystic fibrosis patients (aged 9-19 years) admitted because of exacerbation of pulmonary symptoms caused by Pseudomonas aeruginosa were treated with the aminoglycoside amikacin and the cephalosporin ceftazidime for 14 days. Renal values and plasma and urinary electrolytes were measured before and at the end of the systemic anti-pseudomonal therapy. RESULTS: In the patients with cystic fibrosis, treatment with amikacin and ceftazidime did not modify plasma creatinine or urea and plasma or urinary sodium, potassium and calcium. Treatment with amikacin and ceftazidime significantly decreased both plasma total magnesium (from 0.77 (0. 74-0.81) to 0.73 (0.71-75) mmol/l; median and interquartile range) and ionized magnesium (from 0.53 (0.50-0.55) to 0.50 (0.47-0.52) mmol/l) concentration and increased fractional urinary magnesium excretion (from 0.0568 (0.0494-0.0716) to 0.0721 (0.0630-0.111)) and total urinary magnesium excretion (from 30.7 (26.5-38.0) to 38.5 (31. 5-49.0) micromol/l glomerular filtration rate). CONCLUSIONS: The present study demonstrates that systemic therapy with amikacin plus ceftazidime causes mild hypomagnesaemia secondary to renal magnesium wasting even in the absence of a significant rise in circulating creatinine and urea.

Adolescent↗