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  • 1
    Electronic Resource
    Electronic Resource
    Prenatal allergen contact with milk proteins (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 27 (1997), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Cellular proliferation to various allergens (Dermatophagoides pleronyssinus, β-lactoglobulin, bovine serum albumin, ovalbumin) has been found in cord blood cells. Whether this reflects a sensitization during foetal life is uncertain.Objective We studied the cellular reactivity and cytokine production of cord blood cells in response to cow's milk proteins in a randomely selected group of newborns. The delineation of possible in utero allergen contact was attempted.Objective Cord blood mononuclear cells from 39 neonates were incubated with cow's milk proteins (α-lactalbumin, β-lactoglobulin, casein, α-casein, β-casein, k-casein, bovine serum albumin) for 7 days, and proliferation was assessed by incorporation of [3H]thymidine. Cord blood cell-derived interferon-γ (IFNγ) and interleukin-4 (IL-4) secretion was evaluated in response to allergen or phytohaemagglutinin (PHA) stimulation.Results A pronounced proliferation of cells stimulated with α-lactalbumin (ALA; mean stimulation index 8.0, 95% confidence interval 5.2–10.8), β-lactoglobulin (BLG; mean stimulation index 5.9, 95% confidence interval 3.2–8.6) and α-casein (2.6, 95% confidence interval 2.9–9.1), as opposed to unstimulated cells in medium, was found. No correlation was found between cellular proliferation to milk proteins and parental atopy, maternal total IgE or cord blood IgE. IFNγ production (but not IL-4) was inducible by PHA (range 429–1810 pg/ml), but only in one individual upon stimulation with BLG. Preferentially, reduced IFNγ levels were found in individuals with positive parental allergic history.Conclusion The recognition of allergen by cord blood cells indicates that allergen priming must occur prenatally. The relevance for subsequent sensitization is unclear.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1997.tb00669.x
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  • 2
    Electronic Resource
    Electronic Resource
    Follow-Up of Infants with Congenital Toxoplasmosis Detected by Polymerase Chain Reaction Analysis of Amniotic Fluid (1998)
    Springer
    European journal of clinical microbiology & infectious diseases 17 (1998), S. 853-858 
    Details
    ISSN: 1435-4373
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  This study was conducted to assess the validity of performing the polymerase chain reaction (PCR) on amniotic fluid for detecting fetal Toxoplasma infection. The primary endpoint was the outcome of the infant at 1 year of age. A prospective, consecutive study was performed in 49 infants born to mothers with primary Toxoplasma infection during pregnancy. PCR determinations of Toxoplasma gondii DNA in amniotic fluid were carried out as part of their prenatal management. Infants were examined at birth, and at 1, 3, 6, 9, and 12 months of age. Nine of 11 infants from pregnancies with positive PCR results proved to be infected based on follow-up serological investigations conducted during the first year of life. Two fetal deaths occurred. All 38 infants with negative PCR results remained uninfected at 1 year of age, irrespective of whether their mothers had received treatment with sulfadiazine/pyrimethamine or spiramycin alone. Psychomotor development was normal in all infants. This follow-up study confirms that PCR performed on amniotic fluid is a useful method for identification or exclusion of fetal Toxoplasma infection. Treatment of infected pregnant women and – in the event of a positive PCR result – subsequent treatment of their infants is associated with a favorable outcome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s100960050206
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  • 3
    Electronic Resource
    Electronic Resource
    Tyrosinämie Typ I Klinische und biochemische Symptome bei 3 Säuglingen (2000)
    Springer
    Monatsschrift Kinderheilkunde 148 (2000), S. 1001-1005 
    Details
    ISSN: 1433-0474
    Keywords: Schlüsselwörter Hepatopathie ; Tubulopathie ; Anämie ; Succinylacetoaceton ; Neugeborenenscreening ; NTBC ; Keywords Hepatopathy ; Tubulopathy ; Anemia ; Succinylacetoacetone ; Newborn screening ; NTBC
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract Background. Tyrosinemia type I is an autosomal recessively inherited deficiency of fumarylacetoacetate hydrolase resulting in accumulation of tyrosin and its degradation products (succinylacetoacetone mainly). Typical clinical features include liver and kidney failure as well as central nervous system involvement. There are three main forms of the disease: the acute form with manifestation in newborn infants and the subacute and the chronic form in children older than one year of age. Case reports. We report on three infants with acute tyrosinemia type 1. In two patients impaired liver function with coagulopathy, hypalbuminemia and low cholinesterase as well as renal tubulopathy with urinary phosphate loss led to the diagnosis. In one patient high galactose and phenylalanine levels at routine neonatal screening gave the hint for further investigations. All patients had anemia and thrombocytopenia. Diagnosis was established by measurement of urinary succinylacetoacetone at mean age of 54.6 days. Treatment. Treatment with 2-(nitro-4-trifluoromethylbenzoyl)-1–3-cyclohexanedione (NTBC) and a diet low in tyrosine, and phenylalanine was started. Clinical improvement and normalization of laboratory findings were noted in all patients. Discussion. Tyrosinemia type I must be considered in newborns and infants with impaired hepatic synthesis of coagulation parameters, albumin and cholinesterase and with additional signs of renal tubulopathy (hypophosphatemia and rickets mainly). For diagnosis measurements of urinary succinylacetoaceton is essential.
    Notes: Zusammenfassung Hintergrund. Die Tyrosinämie Typ I ist durch einen autosomal-rezessiv vererbten Defekt der Fumarylazetoazetathydrolase bedingt, der biochemisch zu einer Akkumulation von Tyrosin und dessen Abbauprodukten (hauptsächlich Succinylacetoaceton) führt. Typische klinische Zeichen sind Lebersynthesestörung, Nephropathie und Affektion des zentralen Nervensystems. Akute Verlaufsformen treten im Säuglingsalter auf, die seltenere chronische Form wird nach dem ersten Lebensjahr beobachtet. Fallbeispiele. Wir berichten über 3 an Tyrosinämie Typ I erkrankte Säuglinge. Durch eine massive Lebersynthesestörung mit schlechter Gerinnung, Hypalbuminämie und erniedrigter Cholinesterase sowie durch eine Tubulopathie mit renalem Phosphatverlust fielen 2 Patienten auf. Beim 3. Patienten waren hohe Phenylalanin- und Galaktosewerte im allgemeinen Neugeborenenscreening die ersten unspezifischen Hinweise für die Erkrankung. Alle Patienten wiesen auch eine Anämie und eine Thrombozytopenie auf. Durch den Nachweis von Succinylacetoaceton im Urin wurde die Diagnose belegt. Therapie. Nach Einleiten einer Therapie mit 2-(Nitro-4-Trifluoromethylbenzoyl)-1,3-Cyclohexamedion (NTBC) und einer phenylalanin- und tyrosinarmen Diät im Durchschnittsalter von 54,6 Tagen kam es bei allen 3 Säuglingen zu einer raschen klinischen Besserung und Normalisierung der Laborwerte. Diskussion. Bei Neugeborenen mit Lebersynthesestörungen und renalem Phosphatverlust sollte an die Tyrosinämie Typ I gedacht werden und diagnostisch das Succinylacetoaceton im Harn bestimmt werden.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001120050683
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