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Biomedical subjects

G Landthaler

Publications and source records attributed to G Landthaler.

14 recordsLinked to original sources
PubMed1989

[Hereditary hyperoxaluria or oxalosis. Apropos of a case].

We report a case of primary oxalosis in a 12-year old girl. This unusual observation exemplifies two diagnostic pitfalls, i.e. false urinary tract infections and technical difficulties in accurately measuring oxalate urinary excretion. On the basis of this case and a review of the literature, we discuss diagnostic and therapeutic methods. Early diagnosis of the disease is important in order to monitor the patient and provide genetic counseling.

Child↗
PubMed1988

Acute pancreatitis in six non-transplanted uraemic children. A co-operative study from the French Society of Paediatric Nephrology.

Ten clinical episodes of acute pancreatitis (AP) occurred in six patients (mean age 10 years, range 3-15 years) with chronic renal failure (CRF) during a 9-year period (1977-1986). The underlying cause of CRF was vesicoureteral reflux (2); urethral valves (1); ureterohydronephrosis (1); nephronopthisis (1) and a haemolytic uraemic syndrome which occurred 12 years before (1). In all patients a diagnosis of AP was established both on clinical grounds and with a serum amylase level of greater than 600 IU/l. In 3 patients laparotomy was performed because of suspected appendicitis. All patients required exclusive parenteral feeding (mean duration 25 days) and 2 patients had a partial pancreatectomy. No patient developed pancreatic pseudocysts, 2 patients experienced one relapse (3 and 21 months later) and 1 patient had two relapses and died. Mean duration of follow up was 3 years (range 1-10 years). Possible aetiological factors were: choledochal cyst (1); parotitis without a rise in mumps antibodies (1); familial dyslipidaemia but without AP in other family members (1), and aluminium intoxication with hypercalcaemia and convulsive encephalopathy treated with valproic acid in 1 patient. Severe hyperparathyroidism with radiological signs was absent in all patients. Transplantation had been performed either before AP in 2 patients (1 and 3 years before AP) or had followed AP in 1 patient (7 years after) without occurrence or relapse of AP.

Acute Disease↗
PubMed1984

[Caffey's disease in a mother and her 2 children].

This case of familial infantile cortical hyperostosis is reported because of 2 special features: abnormal x-rays were available in the mother and one son; the mother presented with late manifestations. Literature data show the fairly high incidence of familial cases of Caffey disease; however, both particular features reported here were rarely mentioned.

Adult↗
PubMed1983

[Clinical tolerance of hemodialysis sessions in children. Comparison of bicarbonate and acetate baths].

Hemodialysis tolerance was studied in 3 children during periods of respectively 6, 7 and 9 months comparing bicarbonate (B) versus acetate (A) with equivalent number of sessions. Parameters used for tolerance in these three cases were: hypotensive bouts, solutes perfused during sessions, mean alimentary intake, vomiting, headache, abdominal pain and benzodiazepine prescriptions, taking account of ultrafiltration and dry weight variations during this periods. Results with bicarbonate are following: Obs. n degrees 1 (11 year old female, cystinosis, A: 38 sessions, B: 44 sessions): significant improvement of hypotension episodes and reduction of solutes perfused (p less than 0,05), of vomiting (p less than 0,001), and increase of mean alimentary intake (p less than 0,001). Obs. n degrees 2 (11 year old male, glomerular nephropathy, A: 25 sessions, B: 27 sessions): non significant improvement of hypotension episodes, but improvement for mean alimentary intake (p less than 0,01). Obs. n degrees 3 (4 year old male, uropathy with renal hypoplasia): no significant improvement, but for this child A hemodialysis tolerance was better than for both others. B hemodialysis seems a good alternative for children with A intolerance.

Acetates↗
PubMed1975

[Ataxia and deafness secondary to meningitis in children: the role of labyrinth diseases].

A study is made of post meningitic ataxia from 9 purulent meningitis observations in children. This ataxia is accompanied by a bilateral vestibular destruction syndrome in 6 of the 7 patients examined. The labyrinthic origin of the ataxia accounts for its pure static aspect, its regressive evolution and the frequency of associated deafness. The study of sightless walking on unstable ground (mattress) gives a clinical sight of the vestibular impairment long after the acute phase. In the same way, the study of post-meningitis deafness shows that, most of the time, it is accompanied by an impairment or the suppression of the vestibular reactions. The frequency of the inner ear impairment, after purulent meningitis is certainly underestimated for two reasons: on the one hand, the ataxia remains unknown most of the time because of the excellent vestibular compensation; on the other hand, the deafness can be slight or localized only on one side. Consequently it seems important to undertake in each purulent meningitis convalescent, a clinical examination of standing and walking positions, together with an examination of the hearing and vestibular functions, as soon as age allows it. Lastly, with regard to a pathogenic theory of purulent meningitis, the role of a possible viral component of the infection in the cochleo-vestibular impairment is called into question.

Ataxia↗
PubMedDate not supplied

Tubulointerstitial nephritis and uveitis syndrome (TINU syndrome) with unilateral neuroretinitis: a case report.

PURPOSE: To report a case of tubulointerstitial nephritis and uveitis syndrome (TINU syndrome) with unusual unilateral neuroretinitis. METHODS: An 11-year-old girl who developed anterior uveitis 3 months after acute tubulointerstitial nephritis, without any etiologic factors for either nephritis or uveitis, is presented. RESULTS: Several days after the anterior uveitis, the patient presented with unilateral optic disk edema associated with a serous retinal detachment of the posterior pole, never previously described in TINU syndrome, leading to the formation of perifoveal intraretinal exudates. CONCLUSIONS: In spite of these posterior lesions, clinical course confirmed the previously reported favorable visual outcome of TINU syndrome treated with corticosteroids. It appeared that ocular impairment in TINU syndrome could be more diffuse and more extensive than previously described. As well as the whole uveal tract, the retina and the optic nerve may also be the ocular targets of the idiopathic inflammatory response in TINU syndrome.

Child↗