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Open access

Irena I. Gencheva-Angelova, Adelaida L. Ruseva and Juli I.Pastuhov

Summary

Significant losses of functional proteins such as hormones and hormone-binding proteins are seen in patients suffering from proteinuria. Studies have reported loss of thyroid hormones and thyroxine-binding globulin in the urine. There is evidence that subclinical hypothyroidism is six times more common in patients with proteinuria than in healthy people. The parameters of the effect of proteinuria on thyroid function have not been fully studiedyet.We investigated 74 patients with qualitatively established proteinuria, of whom 34 men and 40 women, without diagnosed thyroid disease. The average age of the patients was 60.9 years. We tested 20 free controls for free thyroxine (FT4), thyroid stimulating hormone (TSH), creatinine and albumin in serum, and the quantity of urine protein. The mean results found for TSH were higher in the patients with proteinuria than in those of the controls (2.719 mU/l vs 1.78 mU/l). For FT4, the mean result in the patients with proteinuria was 17.04 pmol/l vs 16.39 pmol/l. in the controls. A correlation was sought between TSH and FT4 levels and all the laboratory parameters we tested. Patients with proteinuria had higher TSH levels, probably due to the loss of thyroid hormones in the urine. However, these losses cannot lead to clinically proven hypothyroidism.

Open access

Petya P. Chaveeva, Slavcho T. Tomov and Atanas D. Shterev

Summary

A rare case is reported of twin-reversed arterial perfusion (TRAP) sequence in a triplet pregnancy, fetal intervention in the first trimester and pregnancy outcome. We report a case of TRAP sequence complication in dichorionic triamniotic triplet pregnancy, with a normally developing fetus and an acardiac fetus connected via arterio-arterial anastomoses in a monochorionic diamniotic twin pair and a separate fetus. TRAP sequence was diagnosed at 13 weeks in triplet pregnancy after in vitro fertilization (IVF) and embryo transfer of two blastocysts. Color Doppler assessment showed persistent arterial flow in the acardiac twin. Intrafetal laser coagulation was carried out at the time of the diagnosis, and the pregnancy outcome was two survivals at 36.4 weeks of gestation.

Open access

Dobromir Dimitrov

Open access

Regina S. Komsa-Penkova, Georgi M. Golemanov, Zdravka V. Radionova, Pencho T. Tonchev, Sergej D. Iliev and Veselin V. Penkov

Summary

Fetuin-A is a major plasma glycoprotein released mainly by the liver. Its functions include inhibition of the activity of insulin receptor, regulation of response to inflammation, inhibition of calcified matrix metabolism and ectopic mineralization, etc. Three major functional domains of fetuin-A have been identified: one similar to the Ca-binding domains, one inhibiting cysteine protease, and a domain with high affinity to insulin receptor. The fetuin-A molecule may be considered as a highly pleomorphic protein with an important impact in a variety of clinically expressed metabolic and pathological processes. It could be used as a marker in clinical practice in the future.

Open access

Ljubomir S. Kovachev, Pencho T. Tonchev and Kiril L. Nedialkov

Summary

Advanced information technologies have entered all spheres of human activities. In healthcare, this happens much too fast and encompasses all its branches. How does the Internet form the relationship between patients and medical staff? What information do patients seek and how do they get it? What problems arise during the communication process via new means? How can we describe an e-patient? How does the Internet model the doctor-patient relationship in case of cancer, one of the most dramatic diseases? Are students prepared to face an e-patient and how are they trained to do it? What is to be done to optimize internet communication between patients and health providers? This review analyzes information on these issues and outlines some opportunities for solving problems arising against the background of IT use in health care.

Open access

Władysław Lasoń, Joanna Ślusarczyk, Magdalena Regulska, Monika Leśkiewicz and Agnieszka Basta-Kaim

Summary

Introduction. An increasing body of evidence points to an important role of neuroinflammatory processes in the pathomechanism of epilepsy. This hypothesis is mainly supported by data showing an increase of pro-inflammatory cytokine levels and glia activation in animal models of epilepsy and in brain tissue of epileptic patients. On the other hand, less emphasis has been put on pharmacological verification of this hypothesis.

Aim. The aim of this review is to summarize current knowledge on potential usefulness of microglia regulators and anti-inflammatory agents in designing antiepileptic/antiepileptogenic drugs, with the primary mechanism of action based on the inhibition of neuroinflammation.

Methods. We reviewed PubMed and MEDLINE databases to select publications in the topic: epilepsy, neuroinflammation, microglia and microglia regulators with antiepileptic properties. We searched the databases up to April 2017 with no date restrictions.

Review and Discussion. In the present paper, we will discuss new concepts of epileptogenesis which focus not only on changes in neurons but also take into consideration the role of activation of glial cells: microglia and astrocytes. Neuroinflammation, mainly through increased production of pro-inflammatory factors such as cytokines or chemokines, may play an important role in the development of epilepsy. Drugs regulating glial cells activation and consequently inflammatory status in the central nervous system have beneficial effects in different animal models of epilepsy as well as in clinical study in patients. The most promising compound seems to be minocycline which in some studies has been shown to possess antiepileptogenetic action. On the other hand, some antiepileptic drugs exhibit marked anti-inflammatory potency.

Conclusions. There are much data to suggest that there is significant opportunity for designing new antiepileptic drugs whose primary mechanism of action entails the inhibition of neuroinflammatory processes.

Open access

Matthias Wittstock, Uwe Walter, Daniela Schirrmeister, Kyrylo Kurtieiev, Jan Klinke, Annette Grossmann and Johannes Rösche

Summary

Introduction. The differentiation between the clinical and electroencephalographic changes in nonconvulsive status epilepticus (NCSE) and those in sporadic Creutzfeldt-Jakob disease (sCJD) is a crucial question.

Case report. A 77-year old woman was admitted because of fluctuating behavioural chancaseges, adynamia and apraxia since several months for diagnostic. The diagnosis of sCJD was suggested. Subsequently, she had a generalized tonic clonic seizure (GTCS) and the EEG revealed periodic lateralized epileptiform discharges and NCSE was considered.

Discussion. The presented case illustrates the dilemma in the differential diagnosis of sCJD and (symptomatic) NCSE in the light of the recently published new Salzburg consensus criteria and unified EEG terminology. Concerning these criteria, the patient showed after an initial generalized seizure and substantial clinical improvement after administration of antiepileptic drugs, persisting epileptic discharges and only subtle clinical ictal phenomena during the EEG patterns with typical spatiotemporal evolution as a correlate of a symptomatic NCSE. During the further course of the disease in the presented patient the picture changed into an encephalopathic pattern.

Conclusion. EEG criteria for the diagnosis of NCSE are complex. In our case the EEG resembled the pattern of NCSE in the postictal phase of a GTCS according to a classification of NCSE in use at this time. After initial responsiveness to antiepileptic medication the patient lost responsiveness to therapy displaying the typical encephalopathic EEG findings in sCJD. These findings may support the hypothesis of initial NCSE and transformation into prion protein induced encephalopathic EEG and demonstrated clinical usefulness of the Salzburg consensus criteria for NCSE.

Open access

Duncan Palka, Mahinda Yogarajah, Hannah R. Cock and Marco Mula

Summary

Background. Epilepsy is among the most frequent neurological conditions and it is estimated that approximately 8% of the population experience a seizure at some time in their lives.

Aim. To examine the characteristics of patients referred to a First Seizure Clinic (FSC) at a University Hospital in South-West London.

Methods. All subjects referred to the FSC at St George’s University Hospitals between January and December 2015 were included in this audit.

Results. From a total of 257 patients, males 49.5%, age range 16–90, 30% referred by General Practices (GPs), 59.1% by the Accident & Emergency Department (A&E) and 10.9% by other hospital wards, 24.5% did not attend (DNA) the clinical appointment. Females who did not attend were significantly older than males (49.8 years old vs 39.7; p = 0.007). Among those who attended the clinical appointment, 17% were diagnosed first unprovoked seizure, 12.4% acute symptomatic seizure and 28.9% epilepsy. These patients were referred mainly by A&E while GPs referred seizure mimics especially non-epileptic attack disorder (NEAD) and syncope. Patients with NEAD were significantly younger than those with seizures (29.4 years old vs 44.2; p < 0.001) and had a previous psychiatric history (72.7% vs 16.8%; p < 0.001). The proportion of seizure mimics was similar in the older sample group (> 65 years). Regarding acute symptomatic seizures, 33.3% were alcohol-related, 20.8% acute brain insults and 12.5% drug-related (always overdose).

Conclusions. 1 in 4 patients referred to a FSC does not attend the clinical appointment, especially older females. More than 1 in 3 cases represent seizure mimics and are referred mainly by GPs.

Open access

Aleksandar A. Todorov, Petranka G. Chumpalova-Tumbeva, Maya Y. Stoimenova-Popova, Vanya S. Popova, Doroteya K. Todorieva-Todorova, Nikolai T. Tzvetkov, Ivailo G. Hristov, Georgi K. Georgiev, Valentin I. Valtchev, Niya A. Krasteva, Ralitza G. Ilieva, Emiliya M. Dimitrova, Ljudmil Z. Tumbev and Adelaida L. Ruseva

Summary

Affective disorders, including depression, are of great social importance and lead to serious everyday life infringement and disability. Affective disorders are one of the main causes of suicide causes. Anxiety disorders represent a variety of psychic disorders that often lead to disability. Anxiety and depression syndromes together are often seen in patients. Vitamin B12 (cobalamin) is the only vitamin containing cobalt. Our aim was to investigate, evaluate and compare depression and increased anxiety and serum Vitamin B12 level in patients with depression, in patients with Vitamin B12 deficiency anemia and healthy controls. We investigated 74 subjects – 38 patients and 36 healthy controls. Serum Vitamin B12 level was measured in all participants. It is assumed that normal ranges of Vitamin B12 level vary. The most recently accepted ones are 200 to 900 pg/ml. In cases of levels below 200 pg/ml, a therapy with vitamin B12 should be applied. On the other hand, the level necessary for normal biochemical processes is higher – 250 pg/ml. In our study, serum Vitamin B12 level in more than 50% of patients with depression/anxiety was below 200 pg/ml, and in more than 60% of these patients it was below 250 pg/ml.

Open access

Elena Belousova, Vladimir Sukhorukov, Marina Dorofeeva, Lev Shagam and Dmitrii V. Vlodavetz

Summary

Introduction. There are some genetic disorders with combination of mental retardation, epilepsy and autism in which the abnormal mammalian Target of Rapamycin (m-TOR) signaling is implicated. The most important of them is tuberous sclerosis complex (TSC), but the disturbances of the m-TOR pathway can also be detected in Rett syndrome (RS), Fragile X syndrome and Down syndrome. We describe the rare case of co-occurrence of TSC and RS.

Case study. The female child was born at term by normal delivery after a non-complicated pregnancy. Family history was negative for epilepsy and mental retardation. The neonatal period was uneventful and psychomotor development was normal before the child became 1.5 years old. At the age of 18 months the girl developed hand-wringing stereotypes, facial hypotonia, ataxia and gait apraxia. She lost eye-to-eye contact and verbal contact with relatives, and became indifferent to the surrounding environment. When she was 2 years old, focal adversive seizures started which were readily controlled with carbamazepine. Cerebral cortical and subcortical tubers, cerebral white-matter radial migration lines and subependymal nodules on brain MRI together with hypomelanotic macules suggested the presence of TSC. Diagnosis was confirmed at age of 3 years by a heterozygous mutation c.5161-2A>G in TSC2 gene on chromosome 16p13. But the rude regression of psychomotor development and speech, autistic features alongside with characteristic hand-wringing stereotypes were unexplained until at age of 4.5 years RS was diagnosed by finding a heterozygous missense mutation in exon 4 of the MECP2 gene c.455C>T, resulting in a P152R substitution in the methyl-binding domain of the protein. At age of 5 the patient is not able to walk independently and has no expressive speech, she is autistic, has ataxia, limb rigidity, hyperreflexia, lack of purposeful hand movements, verbal and motor stereotypies.

Discussion. The presence of two mutations (one characteristic for TSC2 and one – characteristic for RS) significantly worsened the developmental and motor delay and autistic features in our patient. Dysregulation of m-TOR way is well established in TSC and recently described in RS, Down syndrome and Fragile X syndrome.