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Biomedical subjects

M G Bianchetti

Publications and source records attributed to M G Bianchetti.

At least 37 records · Page 2Linked to original sources

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↗

Systemic, pulmonary, and renal hemodynamic effects of endothelin ET(A/B)-receptor blockade in patients with maintained left ventricular function.

Endothelin-1 (ET-1) regulates vascular tone in congestive heart failure and modulates renal function. Its role in patients with normal left ventricular (LV) function and its renal effects are unclear. Cardiac and renal hemodynamics were studied in 24 patients with normal LV function and coronary arteries after single-dose, double-blind, randomized administration of TAK-044 (25, 50, or 100 mg, i.v.), an ET(A/B)-receptor antagonist, or placebo. Hemodynamics were monitored using Swan-Ganz and arterial catheters, and ET levels were measured. Renal function was assessed by clearance techniques. In the absence of a dose-response relation, TAK-044 patients were analyzed as a single group. Most hemodynamic effects occurred during the first 4 h. TAK-044 reduced mean arterial (-9.3 mm Hg, p < 0.001), pulmonary (-1.8 mm Hg, p = 0.01), and pulmonary capillary wedge pressure (-1.6 mm Hg, p < 0.001) between 30 min and 4 h. Mean reduction in systemic vascular resistance was 279 dyne/s/cm2 (p < 0.001), whereas heart rate increased 6.1 beats/min (p < 0.001) and cardiac index by 0.37 L/m2 (p = 0.01). Stroke volume index, right atrial pressure, and pulmonary vascular resistance did not change. TAK-044 increased renal plasma flow in proportion to the increase in cardiac output (+119 ml/min, 4 h after TAK-044; p < 0.05) and ET-1 levels (2.5-fold; p < 0.05). No serious side effects were noted. In patients with normal cardiac function, ET-receptor blockade causes vasodilation and reduces systemic but not pulmonary vascular resistance and increases cardiac index and renal plasma flow.

Aged↗

Permanently reduced plasma ionized magnesium among renal transplant recipients on cyclosporine.

Hypomagnesemia is common after kidney transplantation. Until recently, only the determination of total plasma magnesium was possible, whereas the assessment of ionized magnesium has since become practicable. One hundred and nine renal transplant patients on cyclosporine with allografts functioning stably for more than 6 months and plasma creatinine levels of less than 200 micromol/l entered the study. Total and ionized circulating magnesium were assessed among these 109 patients, as well as among 15 renal transplant patients not on cyclosporine and 21 healthy volunteers. Cyclosporine patients showed significantly lower total and ionized circulating magnesium values than the two control groups. Plasma total and ionized magnesium levels were also significantly lower among cyclosporine patients treated concurrently with insulin or oral hypoglycemic agents than among those who were not. No correlation was noted between time after transplantation and plasma magnesium with respect to patients on cyclosporine. In conclusion, the study demonstrates that a large subset of renal transplant patients treated with cyclosporine have permanent deficiencies of ionized and total magnesium. The tendency towards hypomagnesemia is also more pronounced among patients with diabetes mellitus.

Adolescent↗

Precipitants in 42 cases of erythema multiforme.

UNLABELLED: A total of 42 children with erythema multiforme (aged 0.1 to 15.8 years, median 6.1 years) were treated between 1978 and 1997 at the Department of Paediatrics, University of Bern, Switzerland. Antecedent infections were noted in 30 cases: Mycoplasma pneumoniae infection (n = 14), acute upper respiratory tract disease (n = 10) and herpes simplex infection (n = 6). Four cases were associated with antecedent medication (n = 3) or immunization (n = 1). In 12 of the 30 patients in whom erythema multiforme followed an infectious disease, drugs described in the literature as inducers of erythema multiforme had been given for symptoms not suggestive of the condition. In the remaining eight children no precipitating agent could be detected. CONCLUSION: In this survey infections were found as a definite or at least presumptive trigger of erythema multiforme in 71% of cases. Drugs (including immunization) implicated as triggers of erythema multiforme played a definite causative role in 10% and a presumptive role in a further 29% of patients. In 19% of patients an associated condition was not diagnosed.

Acute Disease↗

Plasma ionized magnesium in tubular disorders with and without total hypomagnesemia.

Selective electrodes have been designed for determining plasma ionized magnesium. In kidney disease the relationship between ionized and total circulating magnesium is often altered. Hence plasma ionized magnesium (ETH 7025 membrane) was determined in 25 patients with primary renal tubular disorders; 6 patients had total hypomagnesemia. Total plasma magnesium was never reduced in the remaining 19 patients. Plasma ionized magnesium values were low in the 6 patients with total hypomagnesemia. In 18 of the 19 patients without total hypomagnesemia plasma ionized magnesium values were not reduced. Ionized hypomagnesemia was noted in a patient with normal total plasma magnesium in the context of hypercalciuric nephrocalcinosis of unknown origin. The study demonstrates an excellent concordance between plasma total and ionized magnesium in tubular disorders associated with total hypomagnesemia and a good concordance in tubular disorders that are not linked with total hypomagnesemia. The determination of circulating ionized magnesium is of little value in the diagnostic work-up of the vast majority of renal tubular disorders. The determination might perhaps disclose latent hypomagnesemia in nephrocalcinosis of unknown cause.

Adolescent↗

Magnesium supplementation in Gitelman syndrome.

The metabolism of potassium and magnesium are closely linked (in situations where potassium and magnesium depletion coexist, magnesium restoration alone is sufficient to correct hypokalemia). Moreover, magnesium deficiency blunts the interplay between circulating calcium and the calciotropic hormones. Renal magnesium wasting, hypokalemia, alkalosis, hypocalciuria, and a tendency towards hypocalcemia characterize Gitelman syndrome. Plasma or intracellular potassium, circulating calcium, and calciotropic hormones were therefore investigated in eight patients (4 females, 4 males, aged 9-20 years) with Gitelman syndrome before and during oral supplementation with magnesium pyrrolidone carboxylate 30 mmol daily for 4 weeks. Magnesium supplementation significantly increased plasma and intracellular magnesium and plasma calcium, but failed to completely restore magnesium deficiency. In contrast, blood levels of parathyroid hormone and calcitriol and plasma and intracellular potassium were not modified following magnesium administration.

Adolescent↗

[Arterial hypertension in childhood and adolescence].

The importance of hypertension in the pediatric population is not as well-appreciated as in adults. This might well be related in part to the lower prevalence of high blood pressure in this age group. As with height and weight, blood pressure increases with age during childhood. 'High normal' blood pressure is a blood pressure above the 90th percentile and established hypertension a blood pressure above 95th percentile. The varying arm and thigh sizes of children and adolescents require blood pressure cuffs that are appropriately sized. A cuff that is too small will produce an artificially elevated blood pressure, while a cuff that is too large is not likely to obscure hypertensive levels of blood pressure. The use of an oscillometric device is more convenient for infants. The underlying causes of significant hypertension in the pediatric population differ considerably from those of adults: while the prevalence of hypertension in pediatrics is lower than in adults, clinically identifiable causes of hypertension account for a much higher proportion of hypertension in children. Children with chronic secondary hypertension will require drug therapy with converting-enzyme inhibitors, calcium-channel blockers, beta-blockers or diuretics. Therapy now tends to be initiated with converting-enzyme inhibitors because they are generally effective and have few side effects. Persistent cough sometimes develops on converting enzyme inhibitors. The term sartans denotes a new group of orally active antagonists of the angiotensin II receptor. Since sartans do not cause cough, these agents represent a promising treatment for patients who develop cough with converting enzyme inhibitors.

Adolescent↗

Circulating antineutrophil autoantibodies in a child with isolated central nervous system vasculitis.

An 8-year old girl with history of twisted neck and painful swelling on the left side of the neck was found to have malfunction of glossopharyngeal and hypoglossal nerves on the left side. Magnetic resonance angiography revealed a giant aneurysm of the internal carotid artery surrounded by a widespread inflammatory tumor. Cerebral angiography disclosed a large, false aneurysm with almost complete compression of the internal carotid artery. Circulating antineutrophil cytoplasmic autoantibodies (titer 1:2560) and high levels of antibodies against antiproteinase 3 were detectable. This observation indicates that these autoantibodies may be a diagnostic tool in children in whom an undiagnosed central nervous system inflammatory disease is present.

Angiography, Digital Subtraction↗

Abnormalities in insulin sensitivity, vascular resistance and erythrocyte cation transport are independent genetic traits in familial hypertension.

Several isolated abnormalities have been noted in normotensive members of hypertensive families, including exaggerated forearm vascular resistance (FVR), decreased insulin sensitivity and elevated sodium-lithium (Na/Li) countertransport. No family study has investigated the aforementioned abnormalities concurrently within the same hypertensive families. It is therefore unknown whether these disturbances reflect single or different genetic traits. Thus, we studied cardiovascular reactivity of the forearm vasculature, cellular sodium transport mechanisms and insulin sensitivity concomitantly in normotensive (n = 24) and borderline hypertensive (n = 16) members of hypertensive families, compared with normotensive members (n = 24) of normotensive families. At least one abnormality was noted in 27 (67%) out the 40 subjects with a positive family history of hypertension. Na/Li-countertransport was increased in 15 (37%), FVR was increased in 14 (35%) and insulin sensitivity was decreased in 9 (22%) subjects with familial hypertension. The concomitant occurrence of at least 2 out of the 3 abnormalities mentioned was noted in 9 (22%) out of the 40 subjects with family history of hypertension. Decreased insulin sensitivity, increased basal FVR and increased Na/Li countertransport were concurrently observed in two (5%) subjects. This investigation documents the frequent occurrence of abnormalities such as decreased insulin sensitivity, increased basal FVR and Na/Li-countertransport in subjects with family history of hypertension. The concomitant occurrence of at least two of the mentioned abnormalities being observed in less than one-quarter of the subjects with family history of essential hypertension, it is assumed that insulin sensitivity, basal FVR and Na/Li-countertransport reflect more than one genetic trait predisposing to hypertension.

Adolescent↗

Cisplatin therapy in childhood: renal follow up 3 years or more after treatment. Swiss Pediatric Oncology Group.

BACKGROUND: In childhood, cisplatin is an essential component of solid tumour therapy such as in neuroblastomas, germ cell tumours, bone tumours, liver tumours and brain tumours. The potential nephotoxicity of cisplatin is widely recognized, but little information is available on permanent sequelae. METHODS: Of the 500 children included in the Swiss Pediatric Oncology Group Late Effect Study, a group of 46 patients (27 males and 19 females) aged 5.7-28 years (median 14 years) surviving the above-mentioned solid tumours entered the present study. The patients were disease-free and off antineoplastic medication for at least 3 years. No recent gastrointestinal or urinary disturbances had occurred, and diets as well as appetites were normal. RESULTS: Blood pressure and plasma or urinary calcium and phosphate were similar in 17 patients treated with cisplatin (dose 142-717, median 400 mg/m2), in 19 patients without cisplatin and in 20 control subjects. A tendency (P<0.02) towards increased plasma creatinine (79 (69-89) micromol/l; median and interquartile range) and low plasma magnesium (0.80 (0.78-0.85) mmol/l) was noted in patients treated with cisplatin as compared with those without cisplatin (68 (58-80) micromol/l; 0.84 (0.79-0.90) mmol/l) and controls (71 (64 80) micromol/l; 0.83 (0.80-0.90) mmol/l). No correlation was noted between the dosage of cisplatin and circulating magnesium or creatinine. CONCLUSIONS: The study demonstrates that the permanent renal disturbances ((i) decreased renal function and (ii) hypomagnesaemia) noted after treatment with cisplatin during infancy or childhood are mild. Furthermore, the study does not demonstrate renal sequelae in patients with the same malignancies who had been treated without cisplatin.

Adolescent↗