Mirror syndrome associated with fetal cardiomyopathy.

Mirror syndrome is a rare condition of generalized maternal oedema caused by fetal hydrops. A 37-year-old patient was admitted to our hospital because of suspected mirror syndrome caused by fetal cardiomyopathy. At 26th week of gestation patient developed bilateral pulmonary oedema as her condition rapidly deteriorated. Consequently, preterm labor was induced, percutaneous evacuation of fetal ascites was performed, and the patient finally vaginally delivered stillborn fetus. Although the initial postpartum period was severely complicated by hemorrhage, the condition of the patient significantly improved later, and she was discharged seven days after delivery. We believe this case is worth presenting due to its rarity and significant perinatal and obstetric challenges in treatment of those patients. Furthermore, preimplantation genetic testing could be performed to prevent at least some of the cases.

MANAGEMENT OF RUPTURED CORPUS LUTEUM WITH HEMOPERITONEUM IN EARLY PREGNANCY - A CASE REPORT.

- Rupture of the corpus luteum is a frequent condition in women of reproductive age. Because of abdominal pain accompanied by hemoperitoneum, ruptured corpus luteum can easily be confused with ectopic pregnancy. The management of ruptured corpus luteum depends on the symptoms and laboratory findings, and can be just observation but laparoscopy or urgent laparotomy may also be needed. Although rare, hemoperitoneum following rupture of corpus luteum in early pregnancy should always be considered in the diagnostic process. We present a patient that was admitted to our department with amenorrhea, positive ßhCG and acute abdomen. Emergency laparoscopy was performed but no ectopic pregnancy was found, just blood, coagula and a ruptured corpus luteum. The day after the surgery, intrauterine pregnancy was found on ultrasound and the pregnancy ended with term delivery.

Ammonium-related metabolic changes affect somatic embryogenesis in pumpkin (Cucurbita pepo L.).

Somatic embryogenesis in pumpkin can be induced on auxin-containing medium and also on hormone-free medium containing 1mM ammonium (NH(4)(+)) as the sole source of nitrogen. Growth of NH(4)(+)-induced embryogenic tissue was slow and caused considerable acidification of the culture medium. Small spherical cells with dense cytoplasma formed proembryogenic cell clusters that could not develop into late stage embryos. Buffering of NH(4)(+) medium with 25mM 2-(N-morpholino)-ethane-sulfonic acid enhanced tissue proliferation, but no further differentiation was observed. Later stage embryos developed only after re-supply of nitrogen in form of nitrate or l-glutamine. Effects of nitrogen status and pH of culture media on ammonium assimilation were analyzed by following the activity of glutamine synthetase (GS) in relation to phenylalanine ammonia-lyase (PAL). Increased activity of GS and PAL in NH(4)(+) induced tissue coincided with significantly higher activity of stress-related enzymes superoxide dismutase (SOD) and soluble peroxidase (POD), indicating oxidative stress response of embryogenic tissue to NH(4)(+) as the sole source of nitrogen. In addition, considerable increase was observed in callose accumulation and esterase activity, the early markers of somatic embryogenesis. Activity of stress-related enzymes decreased after the re-supply of nitrate (20mM) or Gln (10mM) in combination with NH(4)(+) (1mM), which subsequently triggered globular embryo development. Together, these results suggest that stress responses, as affected by nitrogen supply, contribute to the regulation of embryogenic competence in pumpkin.

Nitrofurantoin-induced acute liver damage in pregnancy.

This article presents a rare case of acute toxic hepatitis in thirty-one-year old primigravida. In the 36th week of gestation, the patient was introduced nitrofurantoin 100 mg a day due to symptoms of dysuria and enterococcus isolated from urine culture. After induced delivery at term because of hypertension, repeated laboratory findings showed increased aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and negative hepatitis C and B markers. The patient was subicteric at the time. Coagulation and complete blood count values were within the normal range. Nitrofurantoin therapy was discontinued. Abdominal ultrasound was normal with the exception of a slight hepatomegaly without any lesions, focal or diffuse. Given that discontinuation of nitrofurantoin and introduction of methylprednisolon therapy significantly lowered liver enzyme levels, restoring most of them to normal, we concluded that this was probably the case of toxic liver damage caused by nitrofurantoin.

Clinical relevance of antibodies against myelin oligodendrocyte glycoprotein in different clinical types of multiple sclerosis.

OBJECTIVE: Myelin oligodendrocyte glycoprotein (MOG) is a highly immunogenic minor component on the outside surface of CNS myelin which is believed to be one of the autoantigens in multiple sclerosis. The aim of this study was to evaluate the diagnostic potential of anti-MOG IgG antibody levels in cerebrospinal fluid (CSF) and serum of patients with relapsing-remitting multiple sclerosis (RRMS), primary progressive multiple sclerosis (PPMS) and non-inflammatory neurological diseases (NIND) as markers for the different clinical types of multiple sclerosis. PATIENTS AND METHODS: Consecutive serum and cerebrospinal fluid samples were taken from 21 patients with RRMS, 7 patients with PPMS and 19 patients with NIND. The antibody responses to MOG were determined in paired samples of these different clinical groups by enzyme-linked immunoassay using a recombinant human MOG protein. RESULTS: The performed analysis indicated that the differences in levels of anti-MOG IgG antibody in serum and cerebrospinal fluid from the patients with RRMS, PPMS or NIND were not statistically significant. CONCLUSION: The assay is not sensitive or specific enough to be used as a differential diagnostic tool for the clinical types of MS, nor for MS itself.

Level of sFas/APO 1 in serum and cerebrospinal fluid in multiple sclerosis.

The aim of the study was to measure sFas/APO 1 serum and cerebrospinal fluid (CSF) levels in patients with relapsing-remitting multiple sclerosis (MS) during relapses, as an index of inhibition of apoptosis of activated lymphocytes in eight patients with clinically definite multiple sclerosis, and 12 healthy controls. The level of serum and CSF sFas/APO 1 was determined by commercially available enzyme-linked immunosorbent assay (ELISA) kits. No significant differences were detected in the sFas/APO 1 serum level between patients and controls, but the levels in CSF was lower in the former. Our results suggest the possibility of Fas mediated apoptosis as a contributing factor in the pathogenesis of multiple sclerosis.

Cerebrospinal fluid and serum protein levels of tumour necrosis factor-alpha (TNF-alpha) interleukin-6 (IL-6) and soluble interleukin-6 receptor (sIL-6R gp80) in multiple sclerosis patients.

The aim of this study was to evaluate soluble proteins of tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and IL-6 receptor subunit gp80 (sIL-6R gp80), as markers of multiple sclerosis (MS). Paired cerebrospinal fluid (CSF) and serum samples of 20 MS patients and 15 controls suffering from non-inflammatory neurological diseases have been assayed retrospectively using monoclonal antibodies-based ELISAs. While TNF-alpha could not be detected in CSF, it was measurable in 20% of total sera. Interleukin-6 was measurable in 5% of total CSF and in 10% of total sera only. However, soluble IL-6R gp80 protein subunit was readily measurable, showing sera concentration (pg/mL) about 34 times higher and specific content (pg/mg total protein) around five times lower than those in paired CSF, similarly for both group of patients. No significant difference of sIL-6R gp80 level, which could be disease-, gender- or age-related, and no correlation of CSF sIL-6R gp80 content with that of paired serum or with routine clinical data for CSF, have been observed. We have concluded that soluble proteins of TNF-alpha, IL-6 and sIL-6R gp80 assayed by monoclonal antibodies-based ELISAs could not serve as markers of the MS activity.