Neurological disorders in vitamin B12 deficiency.

The review discusses thesteps of vitamin B12 metabolism and its role in maintaining of neurological functions. The term "vitamin B12 (cobalamin)" refers to several substances (cobalamins) of a very similar structure. Cobalamin enters the body with animal products. On the peripherу cobalamin circulates only in binding with proteins transcobalamin I and II (complex cobalamin-transcobalamin II is designated as "holotranscobalamin"). Holotranscobalamin is absorbed by different cells, whereas transcobalamin I-binded vitamin B12 - only by liver and kidneys. Two forms of cobalamin were identified as coenzymes of cellular reactions which are methylcobalamin (in cytoplasm) and hydroxyadenosylcobalamin (in mitochondria). The main causes of cobalamin deficiency are related to inadequate intake of animal products, autoimmune gastritis, pancreatic insufficiency, terminal ileum disease, syndrome of intestinal bacterial overgrowth. Relative deficiency may be seen in excessive binding of vitamin B12 to transcobalamin I. Cobalamin deficiency most significantly affects functions of blood, nervous system and inflammatory response. Anemia occurs in 13-15% of cases; macrocytosis is an early sign. The average size of neutrophils and monocytes is the most sensitive marker of megaloblastic hematopoiesis. The demands in vitamin B12 are particularly high in nervous tissue. Hypovitaminosis is accompanied by pathological lesions both in white and gray brain matter. Several types of neurological manifestations are described: subacute combined degeneration of spinal cord (funicular myelinosis), sensomotor polyneuropathy, optic nerve neuropathy, cognitive disorders. The whole range of neuropsychiatric disorders with vitamin B12 deficiency has not been studied well enough. Due to certain diagnostic difficulties they are often regarded as "cryptogenic", "reactive", "vascular¼ origin. Normal or decreased total plasma cobalamin level could not a reliable marker of vitamin deficiency. In difficult cases the content of holotranscobalamin, methylmalonic acid / homocysteine, and folate in the blood serum should be investigated besides carefully analysis of clinical manifestations.

[Elastography in the diagnosis of portal hypertension in patients with liver cirrhosis]. / Elastometriya v diagnostike portal'noi gipertenzii u patsientov s tsirrozom pecheni.

AIM: To establish the diagnostic accuracy of liver and spleen density (LD and SD) measurements in patients with compensated alcoholic liver cirrhosis (LC) in the diagnosis of portal hypertension. SUBJECTS AND METHODS: The investigation enrolled 83 patients with compensated alcoholic and viral (hepatitis C virus) LC. All the patients underwent LD and SD determinations, abdominal ultrasonography, and endoscopy to detect esophageal varices (EV), as well as examination of blood indices. RESULTS: In viral LC, there were substantial LD differences in patients with and without EV. The patients with EV were ascertained to have higher LD [27.9 (21-45) kPa] than those without EV [19.5 (16-26.2) kPa]. SD was also significantly higher than that in the EV group than in the non-EV group (p<0.001). There were no statistically significant differences in SD and LD or in spleen size in patients with alcoholic LC in relation to the presence of EV. Comparison of patients with EV of different etiology revealed differences in platelet count and spleen size. Thrombocytopenia was more pronounced in HCV-related LC patients (p=0.04). The spleen size in patients with viral LC was higher than that in those with alcoholic LC. CONCLUSION: Elastography of the spleen and liver may be used to identify portal hypertension in patients with viral (HCV) LC (83% sensitivity, 75% specificity) with the following threshold values: LD=26 kPa and SD=50 kPa. The threshold LD and SD values obtained for viral LC do not make possible to diagnose clinically significant portal hypertension (EV) in patients with alcoholic LC. There is a need for further investigations to determine the optimal threshold values of LD and SD for the diagnosis of EV.

[Pharmacotherapy of portal hypertension and its complications: analysis of efficacy of preparations for clinical practice and discussion of promising methods of treatment].

Bleeding from oesophageal varicose veins is the terminal stage of a sequence of complications of liver cirrhosis caused by progressive fibrosis, circulation blockade, and development of portal hypertension syndrome followed by collateral shunt. It leads to progressive vein dilation and their rupture. The main issue of today is to prevent the development of successive stages of portal hypertension, to search for therapeutic and surgical methods for marked reduction of pressure in the portal system, and to prevent the risk of hemorrhage from varicose veins. Another approach is to use local endoscopic treatment of varicose veins for prevention of their rupture. The authors analyse the efficacy of pharmacotherapy in patients with liver cirrhosis and portal hypertension and discuss the existing recommendations on the prevention of hemorrhage with special reference to the yet unsolved problems and prospects for the improvement of therapy.

[Serological tests of functional activity of the digestive system (gastrin, pepsinogen-I, trypsin), general IgE and serum cortisol levels in children with hepatitis A and B].

The mild form of hepatitis A and B with children is attended by a functional activity of pancreatic gland (tripsin), mucous coats of stomach and duodenum (gastrin) which permits to consider them as a factor of the risk of digestive organs combined pathology starting with the disease acuity. Differences in gastrin levels with children depending on hepatitis etiology were specified. Highest levels of gastrin were observed with persons suffering from hepatitis B.

[Portal hypertension as a clinical manifestation of hepatic lesions in sarcoidosis].

The paper is devoted to differential diagnostics of portal hypertension (PH) in view of frequent diagnostic mistakes (10-15%) associated with this pathology. PH syndrome is usually interpreted by practitioners as a clinical manifestation of liver cirrhosis even if it is not necessarily related to the involvement of this organ. In patients with hepatic pathology, PH is likely to develop not only in case of fibrotic transformation and false lobule formation but also in case of disturbed blood flow in the portal vein, e.g. when granulomatous lesion of parenchyma takes place. Pathophysiological mechanisms and clinical peculiarities of intra-, sub-, suprahepatic and mixed forms of this condition are discussed. Etiological factors leading to the development of PH syndrome are considered. An original observation is presented of a patient with generalized sarcoidosis and histologically confirmed thoracic lymph nodes, spleen, lungs, liver; moderate granulomatous hepatitis, septal fibrosis (Knodel histology activity index 1-1-3-3- (8 scores)), PH, grade 1 oesophageal varicosis, splenomegaly, splenorenal anastomoses. The involvement of liver in the pathological process did not exceed 20%. Clinical, laboratory and instrumental studies rarely reveal manifestations of these changes. The diagnosis is verified histologically (discovery of granulomas formed by epithelial and giant multinuclear cells without signs of caseous necrosis. The reported case is distinctive for the development of PH in association of multiple giant heatic granulomas preventing the normal blood flow.

[The prevalence of liver and gallbladder pathologies in overweight and obese patients].

This paper reports data on the prevalence of liver and gallbladder pathologies in ovenrweight and obese patients based on the examination of 1506 subjects (684 men, 820 women) aged 25-65 years. Changes in the liver and gall bladder constituted principal pathology of the gastrointestinal tract associated with excessive body mass and obesity. Body mass index (BMI) positively correlated with triglyceride, VLDLP and HDLP cholesterol levels (p = 0.001). 39.5% of the obese patients had elevated plasma triglyceride levels. Insulin resistance was diagnosed in 76% of the patients with morbid obesity (56.2% in grade II obesity and 51.4 in grade I obesity vs. 15.2% in controls). The occumrrence of insulin iresistance increased with BMI (p = 0.0001). Nonalcoholic fatty liver disease was diagnosed using hepatic elastography and senrum markers (FibroMax and SteatoScreen tests). Non-alcoholic steatohepatitis was foumnd in 6.74% of the overweight patients and in 13.1% of those with obesity The occurrence of this condition in obese patients increased with BMI (10.1, 14.3. 14.9% in grade I, II and III obesity respectively). 6.7% of the patients with excessive body mass and 11.6% with obesity had signs of cholelithiasis in their medical histories.

[Chronic hepatitis B, hemosiderosis, and hepatic fibrosis in a renal graft recipient].

Chronic hepatitis B is a frequent concomitant disease in recipients of a renal graft that worsens results of kidney transplantation due to renal and extrarenal complications. Much rarer hemochromatosis either has genetic roots (hereditary hemochromatosis) or results from multiple blood transfusions and hemolysis during treatment by hemodialysis (secondary hemochromatosis). Combination of chronic hepatitis B and hemochromatosis increases the risk of chronic liver disease leading to cirrhosis and hepatocellular carcinoma. Success of antiviral therapy combined with massive phlebotomy is illustrated by a case of kidney transplantation to a patient with chronic hepatitis B of large duration and iron overload syndrome.

[The scope of clinical applications of noninvasive methods for the assessment of liver fibrosis results of orginial studies in a multi-field hospital].

Potential and limitations of non-invasive methods for the evaluation of hepatic fibrosis are discussed (hepatic elastography, fibrotest, ultrasound dopplerography of portal vessels). Each non-invasive method was assessed in terms of threshold values it provides for the characteristic of successive stages ofhepatic fibrosis. The data obtained were used to develop the optimal algorithm for the diagnosis of hepatic fibrosis in patients with chronic viral liver infection.

[The place of the biopsy and morphological study of hepatic tissue in children and adults in the clinician's practice].

The authors analyze their own (more than 2500 manipulations in children and adults) and foreign experience in hepatic biopsy, and describe the most wide-spread techniques of puncture biopsy, paying special attention to complications of the manipulation and ways of their prevention. Indications and contra-indications to biopsy in children and adults are defined; the role of morphological studies in diagnostics of chronic hepatic diseases is discussed.

[Methods of early diagnostics of hepatic fibrosis and cirrhosis].

The article covers the functional and clinical importance of hepatic fibrosis. Contemporary principles of invasive and non-invasive diagnostics of fibrotic changes are described. The article deals with the main types of fibrosis, chronic hepatic diseases in which they develop, and the most wide-spread systems of semiquantitative evaluation of fibrotic process' morphologic signs.

[Current methods of early diagnosis of hepatic fibrosis].

The article covers the functional and clinical significance of hepatic fibrosis. Contemporary principles of invasive and non-invasive methods of diagnostics of fibrotic alterations are described. The article also covers the main forms of fibrosis, chronic hepatic diseases in which they are found, and the most wide-spread systems of half-quantitative evaluation of morphological signs of the fibrotic process.

[Spontaneous bacterial peritonitis: a clinical variant of ascites-peritonitis: diagnosis and treatment]. / Spontannyi bakterial'nyi peritonit -- klinicheskii variant astsit-peritonita: diagnostika i lechenie.

The lecture deals with diagnosis, prevention and treatment of spontaneous bacterial peritonitis (SBP). The choice of treatment groups is described according to recommendations of the International Ascitis Club (IAC). Algorithm of SBP examination for different SBP forms, the disease course characteristics and factors of prognosis are provided.

[Hematological syndromes in patients with chronic hepatitis C]. / Gematologicheskie sindromy u bol'nykh khronicheskim gepatitom C.

AIM: To examine hemopoiesis and to estimate proinflammatory cytokines in blood serum from 42 patients with chronic viral hepatitis (CVH) associated with 1-3 lineage cytopenia in the blood. MATERIAL AND METHODS: 42 patients with diagnostically complicated hematological picture suggestive of hemoblastosis were examined using standard tests, bone marrow puncture and trepanobiopsy, laparoscopy with biopsy of the liver and spleen, transcutaneous puncture biopsy of the liver under ultrasonic control, explorative laparotomy with splenectomy and liver biopsy and, on demand, laboratory tests for hemolysis, presence of antithrombocytic and antileukocytic antibodies, iron metabolism, karyological analysis of bone marrow cells was also made. RESULTS: The majority of the patients were diagnosed to have chronic hepatitis C with low activity of hepatic inflammation and frequent (55%) absence of the diagnostic antibodies to hepatitis C virus in the serum. In 86% of cases blood cytopenia reflected uneffective hemopoiesis and in 14% of cases hemopoiesis hypoplasia was found. CONCLUSION: Uneffective hemopoiesis, high content of immune response cells-effectors in the bone marrow and high concentration of TNF in the serum indirectly evidence for a pathogenetic relationship of chronic HCV infection with cytopenic hematological syndromes.