Diagnosis of chronic liver diseases in elderly patients has its own features due to polymorbidity, multiple organ failure, being subtle the course of the disease. The purpose of the study was to identify correlations of inflammation biochemical parameters and hepatocellular failure with histology in chronic hepatitis (CH) and liver cirrhosis (LC) in elderly patients. Materials and methods. The study included medical records of patients with chronic liver disease (CLD) who died in the Clinical Hospital for War Veterans of Saint Petersburg between 2009 and 2015 (with the average age of 81 year). The diagnosis of chronic hepatitis (45 cases) and chronic cirrhosis (54 cases) was confirmed by postmortem examination. Morphological changes in the liver were described according to Knodell creteria. The degree of inflammatory activity in the liver was evaluated in points (0.1 to 3.0) depending on the level of AST, ALT, -globulin, alkaline phosphatase, -GTP, bilirubin. For similar scoring severity hepatocellular insufficiency (0.13.0) considered total protein, albumin, prothrombin index, fibrinogen. For cirrhotic patients the Child-Pugh criteria were also used. Results. Chronic liver disease (CLD) hepatitis and cirrhosis of the elderly is detected in 1,5% of cases. In most cases, CLD develop secondary to diseases of the cardiovascular system, and are accompanied by subtle symptoms, which limits their life-time diagnosis. The integral evaluation of the process activity degree according to biochemical indices was significantly higher in the group of chronic hepatitis than in the group of liver cirrhosis. Correlations of the inflammation bichemical parameters (AST and / or ALT, -globulin, alkaline phosphatase, -GTP) having a degree of Knodell Histological Activity Group chronic hepatitis and cirrhosis have not been established. The study established correlation of histological activity with total bilirubin levels in both groups of CLD. Integral assessment of hepatocellular deficiency by biochemical indicators of liver cirrhosis group was higher than in the group of chronic hepatitis.

BACKGROUND: Actual mindset, concerning the pathogenesis of type 2 diabetes mellitus and its complications, is described in the glucocentric, lipocentric and lipokine theories. At the same time, it is known, that acute cerebrovascular disorder in type 2 diabetes mellitus can also develop with normoglycemia. The mechanism of association between obesity and type 2 diabetes mellitus in metabolic syndrome has not yet been studied, and 40% of diabetic patients are not obese. In the physiological state hyperglycemia is prevented by pancreatic regulatory oligopeptides rather than insulin, and protein glycation occurs before the development of diabetes symptoms. That facts indicate the need to continue investigation of the pathogenesis in general and diabetic encephalopathy in particular from the standpoint of metabology in order to substantiate the peptidergic theory of the diabetes mellitus and dyscirculatory encephalopathy pathogenesis. AIM: To consider little-known clinical, morphological and metabolic manifestations of diabetic encephalopathy from the standpoint of improving the disease diagnosis. MATHERIALS AND METHODS: Among 162 elderly and senile patients in the pre-stroke and stroke stages of diabetic encephalopathy, modern methods of radiological, laboratory, histological, psychometric and clinical analysis have been used: the relationship between low total cholesterol and disease progression has been determined according to Schulte and MMSE psychometric tests with the same hyperglycemia in different age groups sick; cases of amyloid angioencephalopathy on magnetic resonance imaging in the ultrasensitive weighted imaging mode and amyloidosis have been identified. Staining post-mortem ultrathin tissue biopsy sections with Congo red allowed to find amyloid deposition in 12% of autopsy cases in the absence of diagnosing amyloidosis during life; preparations, in which Congo red staining was positive for the presence of amyloid, were taken for inspection in polarizing light and typing of amyloid. Staining of histological preparations with hematoxylin-eosin and Van Gieson revealed a morphological characteristic of diabetic encephalopathy different from that of atherogenic and hypertensive dyscirculatory encephalopathy; using immunological studies, a statistically significant increased content of induced interleukin-1 production, a trigger for the serum amyloid analogue in the liver synthesis, was determined, and an experimental method for beta-amyloid peptide adhesion by monocytes and the density of amyloid expression on the surface of monocytes in patients with diabetic encephalopathy at senile age at 23 times higher than the density of the peptide in the elderly and in the patients with dyscirculatory encephalopathy of the same old age. RESULTS: It has been established that a fairly frequent and early manifestation of metabolic disorders in diabetic encephalopathy is a violation of protein metabolism with its final conformation into toxic amyloid tissue components. These observations indicate the multifactorial nature of diabetic encephalopathy. Literature data on the parametabolism of the serotonin mediator and tryptophan in the pathogenesis of diabetic encephalopathy are presented. CONCLUSIONS: Modern immunological, morphological, and histochemical capabilities make it possible to diagnose the conformation of the protein matrix and develop a protein-centric hypothesis of diabetic encephalopathy.

Basic clinical manifestations of diabetic encephalopathy in pre-stroke and stroke stages in the elderly are considered. Psychometrical tests (Shulte tables of and Mini Mental Score Examination scale) were used to reveal cognitive impairments, which are markers of diabetic encephalopathy progression. The case of intravital visualization of diabetic cerebral angiopathy using magnetic resonance imaging in susceptibility weighted imaging mode was described in detail. And the case of amyloidosis confirmed by kidney biopsy material coloring with Congo Red. The results of immunological examination are given, proving a high rate of Interleukin-1 production - initiator of serum amyloid A synthesis in liver (serum amyloid A). Histories of lethal cases and pathohystological analysis results of ultrathin sections, obtained by the means of cerebrum autopsy with Congo Red coloring, were investigated. Autopsy materials with positive qualitative reaction on amyloid were taken for further analyzing in polarizing light and amyloid typing. AA-amyloid was discovered in all cases. Morphologic characteristic of diabetic encephalopathy was revealed using coloring by hematoxylin, eosin and Van Gieson’s stain: angioedema, microhemorrhagia, leukoaraiosis, gliomatosis and atrophy of neurons. Case of genetic polyorganic AA- amyloidosis, not diagnosed intravital, was described in detail. It was established that impaired protein metabolism with its final conformation in toxic amyloid components of tissues is an early and fairly frequent manifestation of diabetic encephalopathy metabolic disorders. The substantiated opinion, implying the necessity of deep protein metabolism investigation in cases of diabetes complicated with encephalopathy and amyloidosis, is given. The term «diabetic amyloid encephalopathy» is offered to include in diabetic encephalopathy classification.