Role of Cord Blood Carboxyhemoglobin in Detecting Significant Hyperbilirubinemia in Term Neonates with ABO Alloimmunization.

OBJECTIVE: This study aimed to assess whether cord blood carboxyhemoglobin (COHb) levels in jaundiced term neonates with and without a positive direct Coombs test (DCT) and in healthy controls could be used as a predictor of severe hyperbilirubinemia. The percentage of cord blood COHb should be higher among neonates with Coombs-positive ABO hemolytic disease than among those with Coombs-negative ABO incompatibility and higher than that of ABO-compatible control neonates. STUDY DESIGN: This cross-sectional descriptive study of 198 term neonates comprised three subgroups: group I featured 68 DCT-positive ABO-incompatible neonates (ABO + DCT), group II featured 60 DCT-negative ABO-incompatible neonates with hyperbilirubinemia (ABO-DCT), and group III featured 70 healthy controls. COHb was determined by an OSM3 hemoximeter. RESULTS: Group I differed from groups II and III for cord blood bilirubin, cord blood hemoglobin, and cord blood hematocrit. Groups I and II had higher mean total serum bilirubin (TSB) levels than group III, while there was no difference in the mean TSB levels between groups I and II. There was no significant difference between the COHb group means for groups I, II, and III (p = 0.98). The area under the receiver operating characteristic curve calculated for group I/group III and group II/group III were found to be 0.62 and 0.54, respectively. CONCLUSION: COHb levels did not prove to be superior to the DCT for predicting the risk of developing severe hyperbilirubinemia in term neonates. KEY POINTS: · COHb levels do not predict the risk of developing severe hyperbilirubinemia in term neonates.. · COHb levels may predict that ABO incompatibility in early life.. · COHb levels did not prove to be superior to the direct coombs test..

A Case of Homocystinuria Misdiagnosed as Moyamoya Disease: A Case Report.

INTRODUCTION: Homocystinuria is a hereditary disease caused by a defect in the enzymes involved in metabolizing methionine. Homocystinuria can influence many systems and may be mistaken for other diseases, including Moyamoya disease. Here, we report the case of a 10-year-old male patient with a diagnosis of Moyamoya disease who had been monitored for that for an extended period. The patient's diagnosis was changed to homocystinuria as a result of lens subluxation and cataract findings. CASE PRESENTATION: A 10-year-old male patient presented with vomiting, headache, lethargy, muscular weakness, and eye redness. The patient was mentally retarded, his right pupil was hyperemic, and he had muscle weakness on his left side. In addition, his blood pressure was high. The patient's history included a diagnosis of Moyamoya. A neck and cranial computed tomography (CT) angiography showed no flow bilaterally past the bifurcation of the carotid artery. The patient's bilateral internal carotid arteries were determined to be occluded. It was considered that his eye findings could be compatible with a metabolic disease. On metabolic screening, the patient's homocysteine level was very high. In addition, a heterozygous A1298C mutation was identified in MTHFR. Therefore, the patient was started on a diet free from homocysteine and methionine. In addition, his treatment regimen included vitamins B12 and B6. With these treatments, the patient's complications regressed. CONCLUSIONS: In cases of unusual vascular lesions, metabolic diseases must be considered. In homocystinuria, early diagnosis and treatment are important. Blood homocysteine levels can be returned to normal, and some complications can be prevented.