389 Gas chromatography/mass spectrometry was conducted for the qualitative investigation. In the gas chromatogram, an abnormally large peak was also recognized and identified as homogentisic acid by comparing the mass spectrum with that of the authentic compound. The HPLC screening system for neuroblastoma can detect homogentisic acid and may also be useful for screening for alkaptonuria.
B 19-virus suppresses fetal erythropoiesis [2]. It is not clear why a fetal infection at a practically identical gestational age as shown in the above two patients - sometimes causes anaemia. In cases of maternal infectious erythema the fetus should be closely monitored by sonography. If fetal hydrops develops intrauterine blood exchange appears to be the therapy of choice.
References References
1. Bessho F, HashizumeK, Nakajo T, KamoshitaS (1991) Mass screening in Japan increasedthe detection of infantswith neuroblastomawithout a decrease in causes in older children. J Pediatr 119 :237-241 2. Hanai J, KawaiT, TakasugiN, NishiM, Takeda T (1987) Simpleliquidchromatographic measurementof vanillyl-mandelicacid and homovanillic acid in urine on filter paper for mass screeningof neuroblastomain infants. Clin Chem 33 : 2043-2046 3. NyhanWL (1984)Alkaptonuria. In: Abnormalitiesin aminoacid metabolism in clinicalmedicine. Norwalk, Appleton-Century-Crofts,pp 170177
1. Anderson MJ, Khousam MN, MaxwellDJ, Gould SJ, Happerfield IC, Smith WJ (1988) Human parvovirus B 19 and hydrops fetalis. Lancet I:535 2. Ozawa K, Kurtzman G, Young N (1986) Replicationof B 19 parvovirus in human bone marrow cell cultures. Science233 :883-886
Megadose methylprednisolone for diffuse infantile haemangiomatosis ~. 0 z s o y l u
Parvovirus B 19 infection during pregnancy an ongoing prognostic challenge
Hacettepe UniversityFacultyof Medicine,Department of Paediatrics, HaematologyUnit and Hacettepe Children'sHospital, Ankara 06100, Turkey
W. Sterniste 1 and A . Rosen z
Received July 10, 1991 / Accepted November 19, 1991
aChildren'sHospital Glanzing,Glanzinggasse37, A-1190Vienna, Austria 2Department of Obstetrics, Hanusch-Hospital,Vienna, Austria Received January 31, 1991 / Accepted October 29, 1991
Sir: Maternal infection with human pathogenetic parvovirus B 19 during pregnancy may induce fetal hydrops [1], but the question remains whether there is a gestational phase associated with an elevated fetal risk. We would like to address this question by presenting two case reports with almost identical history although different clinical courses. The first patient was a 27-year-old primigravida who had an outbreak of infectious erythema in the 28th gestational week. In the 29th week fetal hydrops was diagnosed by sonography. The patient delivered spontaneously in the 30th week (birth weight 1780 g, height 39 cm, placenta 700 g). The premature baby girl had a generalised hydrops and died on the 3rd day post delivery despite intensive therapeutic measures. IgM and IgG parovirus B 19 antibodies were determined with the ELISA test in blood and ascites of the newborn as well as in the maternal serum in the 28th and 30th gestational week, respectively. The optical density ratio in the serum of the newborn was IgM > 2 and IgG 0.383; in the maternal serum IgM 0.865 and IgG 1,880 (the cutoff value of IgM was 0.323 and of IgG was 0.325). The second patient was a 30-year-old primigravida with an outbreak of infectious erythema in the 26th gestational week. By repeated sonographic examination no fetal impairment was noted. Fetal blood was not obtained. A healthy baby was delivered at term (birth weight 3610g, height 50cm, placenta 760 g). The postnatal course of the newborn girl (birth weight 3610 g, height 50 cm, placenta 760 g) was uneventful. B 19 antibodies of the groups IgM and IgG were found in maternal serum in the 26th and 30th gestational weeks, respectively. In the neonate, specific parvovirus B 19 antibodies of the groups IgM and IgG were found in serum.
Sir: Byard et al. [1] stated that "the importance of prompt treatment can not be overemphasized" in their recent paper on diffuse infantile haemangiomatosis, but failed to mention megadose methylprednisolone [2] among the therapeutic modalities. Although they mentioned "maximal medical therapy with steroids and inotropes", it should be emphasized that megadose methylprednisolone administration is a quite different approach than conventional corticosteroids (2 mg/kg, given usually in four divided doses). This difference is well demonstrated in the treatment of acute childhood idiopathic thrombocytopenic purpura [3] and suggestive findings are observed in different haematological disorders [4].
References
1. Byard RW, Burrows PE, IzakawaT, SilverMM (1991) Diffuse infantile haemangiomatosis: clinicopathologicalfeatures and managementproblems in five fatal cases. Eur J Pediatr 150:224-227 2. Ozsoylu ~, Irken G, Gt~rgeyA (1989) High dose intravenous methylprednisolone for Kasabach-Merritt syndrome. Eur J Pediatr 148:403405 3. CIzsoylu~, Irken G, Karabent A (1989) High dose intravenousmethylprednisolonefor acute childhoodidiopathicthrombocytopenicpurpura. Eur J Haemato142:431-435 4. Ozsoylu ~ (1990) High dose intravenousmethylprednisolone(HIVMP) in haematologicdesorders. Hematol Rev 4:197-207
B 19-virus suppresses fetal erythropoiesis [2]. It is not clear why a fetal infection at a practically identical gestational age as shown in the above two patients - sometimes causes anaemia. In cases of maternal infectious erythema the fetus should be closely monitored by sonography. If fetal hydrops develops intrauterine blood exchange appears to be the therapy of choice.
References References
1. Bessho F, HashizumeK, Nakajo T, KamoshitaS (1991) Mass screening in Japan increasedthe detection of infantswith neuroblastomawithout a decrease in causes in older children. J Pediatr 119 :237-241 2. Hanai J, KawaiT, TakasugiN, NishiM, Takeda T (1987) Simpleliquidchromatographic measurementof vanillyl-mandelicacid and homovanillic acid in urine on filter paper for mass screeningof neuroblastomain infants. Clin Chem 33 : 2043-2046 3. NyhanWL (1984)Alkaptonuria. In: Abnormalitiesin aminoacid metabolism in clinicalmedicine. Norwalk, Appleton-Century-Crofts,pp 170177
1. Anderson MJ, Khousam MN, MaxwellDJ, Gould SJ, Happerfield IC, Smith WJ (1988) Human parvovirus B 19 and hydrops fetalis. Lancet I:535 2. Ozawa K, Kurtzman G, Young N (1986) Replicationof B 19 parvovirus in human bone marrow cell cultures. Science233 :883-886
Megadose methylprednisolone for diffuse infantile haemangiomatosis ~. 0 z s o y l u
Parvovirus B 19 infection during pregnancy an ongoing prognostic challenge
Hacettepe UniversityFacultyof Medicine,Department of Paediatrics, HaematologyUnit and Hacettepe Children'sHospital, Ankara 06100, Turkey
W. Sterniste 1 and A . Rosen z
Received July 10, 1991 / Accepted November 19, 1991
aChildren'sHospital Glanzing,Glanzinggasse37, A-1190Vienna, Austria 2Department of Obstetrics, Hanusch-Hospital,Vienna, Austria Received January 31, 1991 / Accepted October 29, 1991
Sir: Maternal infection with human pathogenetic parvovirus B 19 during pregnancy may induce fetal hydrops [1], but the question remains whether there is a gestational phase associated with an elevated fetal risk. We would like to address this question by presenting two case reports with almost identical history although different clinical courses. The first patient was a 27-year-old primigravida who had an outbreak of infectious erythema in the 28th gestational week. In the 29th week fetal hydrops was diagnosed by sonography. The patient delivered spontaneously in the 30th week (birth weight 1780 g, height 39 cm, placenta 700 g). The premature baby girl had a generalised hydrops and died on the 3rd day post delivery despite intensive therapeutic measures. IgM and IgG parovirus B 19 antibodies were determined with the ELISA test in blood and ascites of the newborn as well as in the maternal serum in the 28th and 30th gestational week, respectively. The optical density ratio in the serum of the newborn was IgM > 2 and IgG 0.383; in the maternal serum IgM 0.865 and IgG 1,880 (the cutoff value of IgM was 0.323 and of IgG was 0.325). The second patient was a 30-year-old primigravida with an outbreak of infectious erythema in the 26th gestational week. By repeated sonographic examination no fetal impairment was noted. Fetal blood was not obtained. A healthy baby was delivered at term (birth weight 3610g, height 50cm, placenta 760 g). The postnatal course of the newborn girl (birth weight 3610 g, height 50 cm, placenta 760 g) was uneventful. B 19 antibodies of the groups IgM and IgG were found in maternal serum in the 26th and 30th gestational weeks, respectively. In the neonate, specific parvovirus B 19 antibodies of the groups IgM and IgG were found in serum.
Sir: Byard et al. [1] stated that "the importance of prompt treatment can not be overemphasized" in their recent paper on diffuse infantile haemangiomatosis, but failed to mention megadose methylprednisolone [2] among the therapeutic modalities. Although they mentioned "maximal medical therapy with steroids and inotropes", it should be emphasized that megadose methylprednisolone administration is a quite different approach than conventional corticosteroids (2 mg/kg, given usually in four divided doses). This difference is well demonstrated in the treatment of acute childhood idiopathic thrombocytopenic purpura [3] and suggestive findings are observed in different haematological disorders [4].
References
1. Byard RW, Burrows PE, IzakawaT, SilverMM (1991) Diffuse infantile haemangiomatosis: clinicopathologicalfeatures and managementproblems in five fatal cases. Eur J Pediatr 150:224-227 2. Ozsoylu ~, Irken G, Gt~rgeyA (1989) High dose intravenous methylprednisolone for Kasabach-Merritt syndrome. Eur J Pediatr 148:403405 3. CIzsoylu~, Irken G, Karabent A (1989) High dose intravenousmethylprednisolonefor acute childhoodidiopathicthrombocytopenicpurpura. Eur J Haemato142:431-435 4. Ozsoylu ~ (1990) High dose intravenousmethylprednisolone(HIVMP) in haematologicdesorders. Hematol Rev 4:197-207
