Ayhan Tastekin

Phototherapy causes a transient DNA damage in jaundiced newborns

In this study, we aimed to clarify the following questions: 1) Does phototherapy (PT) cause genotoxicity in full-term newborn babies undergoing PT as a result of neonatal jaundice?, 2) if genotoxic effect occurs, is there any relationship between the duration of PT and genotoxicity?, and 3) is genotoxic effect temporary or not? The frequency of sister chromatid exchange (SCE) was determined in jaundiced newborns before, during, and after phototherapy, then determined again in childhood (approximately 3.5 years old). Mean frequency of SCE of 22 full-term jaundiced babies significantly increased during the PT procedure and in every single day, compared to the previous day, in comparison to the pre-PT basal value (6.20 ± 0.57;); mean SCE frequencies at 24, 48, 72, and 96 hours were 7.75± 0.40, 8.16 ± 0.47, 8.50 ± 0.40, and 9.36 ± 0.55, respectively (all P-values <0.01). In childhood, no significant difference was found between the mean SCE value (4.9 ± 0.9) of 20 of 22 children, who received PT in the neonatal period, and the mean SCE value (4.7 ± 0.6) of 20 coevaluated healthy children (P = 0.40). This study demonstrates that the negative effect of PT on SCE is a temporary effect.

Pyridoxine may protect the cerebellar granular cells against glutamate-induced toxicity.

In the present study, the possible protective effect of the pyridoxine against glutamate-induced neurotoxicity in cerebellar granular cell culture of rat pups is investigated for its therapeutic potential. Glutamate (10(-7) M) was administered to cerebellar granular cell cultures that were prepared from one-day-old Sprague-Dawley rats. The neuroprotective effect of pyridoxine was examined. Pyridoxine at the doses of 10(-8), 10(-7), 10(-6), and 10(-5) M was introduced into the culture flasks before inclusion of glutamate. Pyridoxine at the doses of 10(-8) M and 10(-7) M significantly reduced glutamate cytotoxicity. A 10(-7) M dose of pyridoxine proved to be more effective than a 10(-8) M dose. The present study demonstrates that pyridoxine may protect glutamate-induced neurotoxicity. Neuroprotective effect of pyridoxine, at least in part, may result from its anti-glutamatergic activity. Pyridoxine merits further investigation as a therapeutic option in hypoxic-ischemic brain injury.

Prophylactic efficiency of 3-weekly benzathine penicillin G in rheumatic fever.

Benzathine penicillin G (BPG) is effective for secondary prophylaxis of rheumatic fever (RF). However, interval between injections a remains a controversial matter. In a study population of 74 patients, following the initial diagnosis of RF, 3-weekly BPG (1.2 million units) regimen was started. During the first three-week period, serum penicillin concentrations were examined on the 7th, 14th and 21st days and throat culture done for group-A b hemolytic streptococcal (GABHS) infection. Ten patients (13.5%) at 21st day of injection had low serum penicillin concentration after the first BPG. GABHS was isolated in 5 patients during this period. Although two of these 5 patients had symptoms of respiratory tract infection, according to laboratory data, the other three were accepted as carriers. All 74 patients were then followed-up for rheumatic recurrence (RR) during long-term period (6 to 60 months, mean 25 ± 5 months). There was no RR among regular (missing no more than one injection a year) group. We concluded that 3-weekly BPG regimen was satisfactory for secondary prophylaxis in RF, even though serum penicillin level was inadequate during the third week in some of the patients.

A preterm infant with intrauterine skin necrosis.

To the Editor: Newborns have a physiological tendency to hypercoagulation. When hereditary thrombophilic risk factors contribute to that physiological status, the development of the thromboembolic events in these patients becomes easier.1,2 We present a case of a preterm female infant with intrauterine growth retardation, and heterozygous prothrombin G20210A and homozygous methylenetetrahydrofolate reductase C677T mutations, who was born at 32 weeks of gestation with extensive skin necrosis. The patient was referred to our hospital because of multiple bruises on the skin at birth. Her mother suffered from placental abruption and vaginal bleeding during pregnancy; however, there was no thrombosis in family history. She had the body weight, height, and head circumference below 10 percentile. Physical examination revealed skin necroses located on the lateral surface of the right thigh (4 6 cm), lateral surface of the left lower extremity (1 1 cm), right inguinal region 1 1cm), left antecubital area (1 1cm), and left lower quadrant of the abdomen (4 6 cm) (Fig. 1). On laboratory examination carried out on first day of life, hemoglobin of 22 g/dL, platelet count of 165,000/ mm, and white blood cell count of 21,500/mm were detected. Blood urea nitrogen, creatinine, and liver function tests were within normal limits. Coagulation studies were as follows: prothrombin time 17 seconds (N: 10.6–16.2 s), activated partial thromboplastin time over 2 minutes (N: 27.5 to 79.4 s), international normalized ratio 2.5 (N: 0.53 to 1.62), D-dimer 8.6mg/L (N: 0.1 to 0.5mg/L), protein C 34 % (N: 35%±0.09%), protein S 13 % (N: 36%±12%), and antithrombin-III 35 % (N: 70% to 120%). Plasma homocysteine level was 36.6 mmol/L (N: 4.14 to 15 mmol/L) and methionine level was 3.38 mmol/L (N: 3.7 to 10.3 mmol/L). After vitamin K administration, activated partial thromboplastin time and international normalized ratio values returned to normal ranges. Genetic studies revealed homozygous MTHFR C677T and heterozygous prothrombin G20210A mutations in the patient; heterozygous MTHFR C677T, heterozygous PM G20210A, and heterozygous factor V Leiden mutations in her mother and heterozygous MTHFR C677T mutation in her father. The patient required mechanical ventilation because of respiratory distress syndrome. She was started on subcutaneous low-molecular weight heparin (150U/kg twice a day) and other medications including folic acid (1mg/d), acetylsalicylic acid (50mg/d), betaine (50mg/kg/d), and vitamin B12 (500mg/d). She was detached from mechanical ventilation on the seventh day of life; however, she needed mechanical ventilation again on day 15. Despite all supportive efforts, the patient died because of nosocomial sepsis on day 22. During the follow-up, the number and the size of the skin necroses were stable. Maternal and fetal factor V Leiden mutation is the most common mutation that is known to cause tendency for thrombosis.3,4 Genetic prothrombotic risk factors, especially when they exist in combination, play an important role in abdominal venous thrombosis seen in neonatal period and in infants.5 Thornburg et al6 reported on a full-term infant presenting at 7 days of life with HSV pneumonitis, a tricuspid valve thrombus, and a subsequent pulmonary embolus. The infant was found to be heterozygous for the prothrombin G20210A mutation and homozygous for the methylenetetrahydrofolate reductase C667T mutation and was treated with lowmolecular weight heparin. Our patient, who carried homozygous MTHFR C677T and heterozygous prothrombin G20210A mutations, presented with a rare symptoms such as intrauterine skin lesions. In conclusion, skin bruising and necrosis during delivery, which is mostly attributed to birth trauma, may be the sign of underlying inherited thrombophilia.

Early abdomino-perineal pull-through vaginoplasty

Vaginal agenesis is known as one of the Mόllerian anomalies. Mόllerian anomalies occur during gonadal development and differentiation, and may lead to complex outcomes. McKusick-Kaufman syndrome (MKS) is an autosomal recessive multiple malformation syndrome characterized by Mόllerian anomalies with hydrometrocolpos (HMC) and postaxial polydactyly (PAP). We report a case of a female newborn that developed hydronephrosis and respiratory distress due to compression of the cystic mass and underwent surgery on postpartum day 3. Pull-through vaginoplasty was performed with an abdomino-perineal approach. We report the unique treatment approach in this case.

Perinatal Suçiçeği (Varisella Zoster Virüs) Enfeksiyonu

Chickenpox is due to infection with the varicella zoster virus (VZV), a human alphaherpervirus found worldwide. Classically, the cinical disease is a febrile illness with a pruritic vesicular rash. Maternal chickenpox between 5 days before delivery to 2 days after delivery (perinatal varicella) can cause severe and even fatal illness in the newborn. A 7-day old girl baby presented on day 4 of postnatal with the complaints of widespread vesicular rash and non-suckling. Mother of the baby also had a similar eruption four day prior to delivery, which was clinically characteristic of varicella. Considering history and clinical presentation, a diagnosis of perinatal chickenpox was considered and the baby was treated with acyclovir which she responded and recovered. Herein, the clinical feasures and treatment of chickenpox infection in the perinatal period have been emphasized with this case report.