Publications by authors named "L V Tikhonova"

103 Publications

[Diagnostic nomograms for the treatment of urogenital fistula].

Urologiia 2021 Mar(1):13-20

Department of Urology of A. I. Evdokimov Moscow State University of Medicine and Dentistry.

Aim: Studies on non-obstetric urogenital fistula provide limited information on predictive factors. The aim of our study was to specify and to analyze the predictors for long-term anatomical and functional results in women with non-obstetric urogenital fistula.

Materials And Methods: A cross-section study of surgical repair for non-obstetric urogenital fistula repairs was carried out. From 2012 to 2018, a total of 446 patients with urogenital fistulas were treated in two tertiary centers. Patients with vesicovaginal and urethrovaginal fistulas with at least 12 months of follow-up were identified and contacted by phone and/or examined in the clinic. Anatomical outcome was assessed by resolution of symptoms and/or results of clinical examination. Urinary distress inventory (UDI-6) was used for the measurement of functional outcomes. The nomogram is based on a multiple regression equation, the solution of which is performed using a computer. The nomogram is presented as a set of scales, each of which corresponds to a certain variable. The baseline parameter is assigned certain points, depending on its value, then the sum of all parameters is calculated. As a result, it is possible to determine the risk using a couple or three scales.

Results: Overall, 169 patients were studied (mean age of 49.2, mean follow-up of 34 months). The most common cause of fistulas included hysterectomy (69.4%), followed by pelvic radiotherapy (18.9%). Only 64% of cases were primary fistula. Closure rate was 90.7% (98/108). Anatomical success depended on the surgical approach. For transvesical procedure, success rate was 89.4% (42/47), compared to 84% (89/106) and 87.5% (14/16), respectively for transvaginal and transabdominal success rate. According to Clavien-Dindo, complications were grade 1 (11.8%) and grade 2 (4.7%). As UDI-6 showed, the most common symptoms were frequency (62%), urgency (50%), incontinence (73%), pain (55%) and voiding symptoms (27%). Fistula size > 3.0 cm, pelvic radiation, and previous vaginal surgeries were associated with a higher risk of failure or more severe lower urinary tract symptoms. A high number of re-do cases and complex fistulas could be a limitation of this study. Factors for successful non-obstetric urogenital fistula closure were fistula size less than 3.0 cm, absence of pelvic radiation, and previous vaginal surgeries.

Conclusion: According to our results, only fistula size > 3 cm, previous vaginal procedures and pelvis irradiation were unfavorable predictors for anatomic success of fistula repair. In addition, our results allow to determine the predictors for successful repair and risk of recurrence lower urinary tract symptoms postoperatively.
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March 2021

[Systematic review of current russian-language literature on urogenital fistulas in women].

Urologiia 2020 12(6):137-141

AO European Medical Center, Moscow, Russia.

Urogenital fistulas in women are an urgent problem in modern urology, gynecology and surgery. Several decades earlier, iatrogenic damage was the main reason for their development. The aim of this review was to analyze the etiology, characteristics and results of treatment of fistulas in women in Russia and the CIS countries. A systematic analysis of the articles in the PubMed and eLibrary databases dedicated to etiology, treatment technique and postoperative results of treatment of urogenital fistulas in women was carried out. The results were compared with European data. A total of 16 articles were selected over a 20-year period that met the inclusion criteria. Iatrogenic injury resulted in the fistula formation in 40.54% (373/920) of cases. The majority of fistulas were caused by radiation therapy (58.91%, 542/920). According to the results, 84.02% (773/920) of fistulas were successfully healed. Cure rate of patients with post-radiation fistulas was 75.83% (411/542). Comparison of surgical techniques was difficult, since in most cases the preference of the surgeon was main determinant factor.
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December 2020

A Look into Liver Mitochondrial Dysfunction as a Hallmark in Progression of Brain Energy Crisis and Development of Neurologic Symptoms in Hepatic Encephalopathy.

J Clin Med 2020 Jul 16;9(7). Epub 2020 Jul 16.

Hospital Clinico Research Foundation, INCLIVA Health Research Institute, 46010 Valencia, Spain.

Background: The relationship between liver disease and neuropathology in hepatic encephalopathy is well known, but the genesis of encephalopathy in liver failure is yet to be elucidated. Conceptually, the main cause of hepatic encephalopathy is the accumulation of brain ammonia due to impaired liver detoxification function or occurrence of portosystemic shunt. Yet, as well as taking up toxic ammonia, the liver also produces vital metabolites that ensure normal cerebral function. Given this, for insight into how perturbations in the metabolic capacity of the liver may be related to brain pathology, it is crucial to understand the extent of ammonia-related changes in the hepatic metabolism that provides respiratory fuel for the brain, a deficiency of which can give rise to encephalopathy.

Methods: Hepatic encephalopathy was induced in starved rats by injection of ammonium acetate. Ammonia-induced toxicity was evaluated by plasma and freeze-clamped liver and brain energy metabolites, and mitochondrial, cytoplasmic, and microsomal gluconeogenic enzymes, including mitochondrial ketogenic enzymes. Parameters of oxidative phosphorylation were recorded polarographically with a Clark-type electrode, while other measures were determined with standard fluorometric enzymatic methods.

Results: Progressive impairment of liver mitochondrial respiration in the initial stage of ammonia-induced hepatotoxicity and the subsequent energy crisis due to decreased ATP synthesis lead to cessation of gluconeogenesis and ketogenesis. Reduction in glucose and ketone body supply to the brain is a terminal event in liver toxicity, preceding the development of coma.

Conclusions: Our study provides a framework to further explore the relationship between hepatic dysfunction and progression of brain energy crisis in hepatic encephalopathy.
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http://dx.doi.org/10.3390/jcm9072259DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7408643PMC
July 2020

The Erythrocytic Hypothesis of Brain Energy Crisis in Sporadic Alzheimer Disease: Possible Consequences and Supporting Evidence.

J Clin Med 2020 Jan 12;9(1). Epub 2020 Jan 12.

Hospital Clinico Research Foundation, INCLIVA Health Research Institute, 46010 Valencia, Spain.

Alzheimer's disease (AD) is a fatal form of dementia of unknown etiology. Although amyloid plaque accumulation in the brain has been the subject of intensive research in disease pathogenesis and anti-amyloid drug development; the continued failures of the clinical trials suggest that amyloids are not a key cause of AD and new approaches to AD investigation and treatment are needed. We propose a new hypothesis of AD development based on metabolic abnormalities in circulating red blood cells (RBCs) that slow down oxygen release from RBCs into brain tissue which in turn leads to hypoxia-induced brain energy crisis; loss of neurons; and progressive atrophy preceding cognitive dysfunction. This review summarizes current evidence for the erythrocytic hypothesis of AD development and provides new insights into the causes of neurodegeneration offering an innovative way to diagnose and treat this systemic disease.
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http://dx.doi.org/10.3390/jcm9010206DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7019250PMC
January 2020

Metabolic Abnormalities of Erythrocytes as a Risk Factor for Alzheimer's Disease.

Front Neurosci 2017 5;11:728. Epub 2018 Jan 5.

Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Russia.

Alzheimer's disease (AD) is a slowly progressive, neurodegenerative disorder of uncertain etiology. According to the amyloid cascade hypothesis, accumulation of non-soluble amyloid β peptides (Aβ) in the Central Nervous System (CNS) is the primary cause initiating a pathogenic cascade leading to the complex multilayered pathology and clinical manifestation of the disease. It is, therefore, not surprising that the search for mechanisms underlying cognitive changes observed in AD has focused exclusively on the brain and Aβ-inducing synaptic and dendritic loss, oxidative stress, and neuronal death. However, since Aβ depositions were found in normal non-demented elderly people and in many other pathological conditions, the amyloid cascade hypothesis was modified to claim that intraneuronal accumulation of soluble Aβ oligomers, rather than monomer or insoluble amyloid fibrils, is the first step of a fatal cascade in AD. Since a characteristic reduction of cerebral perfusion and energy metabolism occurs in patients with AD it is suggested that capillary distortions commonly found in AD brain elicit hemodynamic changes that alter the delivery and transport of essential nutrients, particularly glucose and oxygen to neuronal and glial cells. Another important factor in tissue oxygenation is the ability of erythrocytes (red blood cells, RBC) to transport and deliver oxygen to tissues, which are first of all dependent on the RBC antioxidant and energy metabolism, which finally regulates the oxygen affinity of hemoglobin. In the present review, we consider the possibility that metabolic and antioxidant defense alterations in the circulating erythrocyte population can influence oxygen delivery to the brain, and that these changes might be a primary mechanism triggering the glucose metabolism disturbance resulting in neurobiological changes observed in the AD brain, possibly related to impaired cognitive function. We also discuss the possibility of using erythrocyte biochemical aberrations as potential tools that will help identify a risk factor for AD.
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http://dx.doi.org/10.3389/fnins.2017.00728DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5760569PMC
January 2018
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