12 research outputs found
ΠΠ»ΠΈΠ½ΠΈΠΊΠΎ-ΡΠΏΠΈΠ΄Π΅ΠΌΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠ°Ρ Ρ Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΡΡΠΈΠΊΠ° Π³Π΅ΠΏΠ°ΡΠΈΡΠΎΠ² Π ΠΈ Π΄Π΅Π»ΡΡΠ° Π² Π Π΅ΡΠΏΡΠ±Π»ΠΈΠΊΠ΅ ΠΠ°Π³Π΅ΡΡΠ°Π½
Aim: The analysis of the incidence of hepatitis B in the Republic of Dagestan (RD) and clinical and epidemiological characteristics of HBV/HDV coinfection in the region.Materials and Methods. The dynamics of the hepatitis B incidence rates and the coverage of vaccination against this infection in the RD in 2008-2022 were analyzed based on the data from of the statistical forms of Rospotrebnadzor. The clinical and epidemiological characteristics of delta hepatitis were analyzed in 371 patients under dispensary observation at the Republican Center for Infectious Diseases named after S.-Π.Π. Magomedov.Results. Over the past 10 years, the incidence of CHB in the RD has increased more than 4.5 times, from 1.4 per 100 thousand population in 2008 to 6.7 per 100 thousand population in 2022. A decrease in the rates of hepatitis B child immunization in the RD is observed since 2009. Hepatitis B vaccination coverage rates in adult population fell sharply after 2010, both in the RD and in the Russian FederationΒ on average. The frequency of HDV co-infection in persons infected with HBV in the RD is 13.8%, but reaches 15% in some regions of the republic, indicating the moderate levelΒ Β of endemicity. Patients with HBV/HDV coinfection are predominantly males aged 25β45 years with advanced fibrosis or cirrhosis. All cases of HDV infection in the RD are caused by viral genotype 1.Conclusions. The obtained results testify to the significance of the problem of hepatitis B and delta in the RD. The number of identified patients and, accordingly, the rate of co-infection, apparently, will increase with the expansion of screening for markers of HDV infection, when patients who were registered as HBsAg carriers will be examined according to the patient routing guidelines. The late diagnosis of delta hepatitis in RD and the limited possibilities of antiviral therapy are another significant issues.Π¦Π΅Π»Ρ: Π°Π½Π°Π»ΠΈΠ· Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π΅ΠΌΠΎΡΡΠΈ Π³Π΅ΠΏΠ°ΡΠΈΡΠΎΠΌ Π Π² Π Π΅ΡΠΏΡΠ±Π»ΠΈΠΊΠ΅ ΠΠ°Π³Π΅ΡΡΠ°Π½ ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΠΊΠΎ-ΡΠΏΠΈΠ΄Π΅ΠΌΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠ°Ρ Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΡΡΠΈΠΊΠ° ΠΊΠΎ-ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ HBV/HDV Π² ΡΠ΅Π³ΠΈΠΎΠ½Π΅.ΠΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ: ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ Π°Π½Π°Π»ΠΈΠ· Π΄ΠΈΠ½Π°ΠΌΠΈΠΊΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π΅ΠΌΠΎΡΡΠΈ Π³Π΅ΠΏΠ°ΡΠΈΡΠΎΠΌ Π ΠΈ ΠΎΡ
Π²Π°ΡΠ° Π²Π°ΠΊΡΠΈΠ½Π°ΡΠΈΠ΅ΠΉ ΠΏΡΠΎΡΠΈΠ² ΡΡΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ Π² Π Π΅ΡΠΏΡΠ±Π»ΠΈΠΊΠ΅ ΠΠ°Π³Π΅ΡΡΠ°Π½ Π² 2008β2022 Π³Π³. ΠΏΠΎ ΠΌΠ°ΡΠ΅ΡΠΈΠ°Π»Π°ΠΌ ΡΠΎΡΠΌ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΡΡΠ΅ΡΠ° Π ΠΎΡΠΏΠΎΡΡΠ΅Π±Π½Π°Π΄Π·ΠΎΡΠ°. ΠΡΠΎΠ°Π½Π°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π½Ρ ΠΊΠ»ΠΈΠ½ΠΈΠΊΠΎ-ΡΠΏΠΈΠ΄Π΅ΠΌΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅Β Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΡΡΠΈΠΊΠΈΒ Π³Π΅ΠΏΠ°ΡΠΈΡΠ°Β Β Π΄Π΅Π»ΡΡΠ°Β Ρ 371 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ°, Π½Π°Ρ
ΠΎΠ΄ΡΡΠΈΡ
ΡΡ Π½Π° Π΄ΠΈΡΠΏΠ°Π½ΡΠ΅ΡΠ½ΠΎΠΌ Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΠΈ Π² Π Π΅ΡΠΏΡΠ±Π»ΠΈΠΊΠ°Π½ΡΠΊΠΎΠΌ ΡΠ΅Π½ΡΡΠ΅ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΎΠ½Π½ΡΡ
Π±ΠΎΠ»Π΅Π·Π½Π΅ΠΉ ΠΈΠΌ. Π‘.-Π.Π. ΠΠ°Π³ΠΎΠΌΠ΅Π΄ΠΎΠ²Π°.Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ: Π·Π° ΠΏΠΎΡΠ»Π΅Π΄Π½ΠΈΠ΅ 14 Π»Π΅Ρ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π΅ΠΌΠΎΡΡΡ Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΌ Π³Π΅ΠΏΠ°ΡΠΈΡΠΎΠΌ Π Π² Π Π΅ΡΠΏΡΠ±Π»ΠΈΠΊΠ΅ ΠΠ°Π³Π΅ΡΡΠ°Π½ ΡΠ²Π΅Π»ΠΈΡΠΈΠ»Π°ΡΡ Π±ΠΎΠ»Π΅Π΅ ΡΠ΅ΠΌ Π² 4,5 ΡΠ°Π·Π°, Ρ 1,4 Π½Π° 100 ΡΡΡ. Π½Π°ΡΠ΅Π»Π΅Π½ΠΈΡ Π² 2008 Π³. Π΄ΠΎ 6,7 Π½Π° 100 ΡΡΡ. Π½Π°ΡΠ΅Π»Π΅Π½ΠΈΡ Π² 2022 Π³. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ Π°Π½Π°Π»ΠΈΠ·Π° ΠΎΡ
Π²Π°ΡΠ° Π²Π°ΠΊΡΠΈΠ½Π°ΡΠΈΠ΅ΠΉ ΠΏΡΠΎΡΠΈΠ² Π³Π΅ΠΏΠ°ΡΠΈΡΠ° Π ΡΠ²ΠΈΠ΄Π΅ΡΠ΅Π»ΡΡΡΠ²ΡΡΡ ΠΎ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠΈ ΡΡΠΎΠ²Π½Ρ ΠΈΠΌΠΌΡΠ½ΠΈΠ·Π°ΡΠΈΠΈ Π΄Π΅ΡΡΠΊΠΎΠ³ΠΎ Π½Π°ΡΠ΅Π»Π΅Π½ΠΈΡ Π² Π Π΅ΡΠΏΡΠ±Π»ΠΈΠΊΠ΅ ΠΠ°Π³Π΅ΡΡΠ°Π½ ΠΏΠΎΡΠ»Π΅ 2009 Π³. ΠΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΠΈ ΠΎΡ
Π²Π°ΡΠ° Π²Π°ΠΊΡΠΈΠ½Π°ΡΠΈΠ΅ΠΉ ΠΏΡΠΎΡΠΈΠ² Π³Π΅ΠΏΠ°ΡΠΈΡΠ° Π Π²Π·ΡΠΎΡΠ»ΠΎΠ³ΠΎ Π½Π°ΡΠ΅Π»Π΅Π½ΠΈΡ ΡΠ΅Π·ΠΊΠΎ ΡΠΏΠ°Π»ΠΈ ΠΏΠΎΡΠ»Π΅ 2010 Π³., ΠΊΠ°ΠΊ Π² Π Π΅ΡΠΏΡΠ±Π»ΠΈΠΊΠ΅ ΠΠ°Π³Π΅ΡΡΠ°Π½, ΡΠ°ΠΊ ΠΈ Π² Π ΠΎΡΡΠΈΠΉΡΠΊΠΎΠΉ Π€Π΅Π΄Π΅ΡΠ°ΡΠΈΠΈ Π² ΡΡΠ΅Π΄Π½Π΅ΠΌ. Π§Π°ΡΡΠΎΡΠ° ΠΊΠΎ-ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ HDV Ρ Π»ΠΈΡ, ΠΈΠ½ΡΠΈΡΠΈΡΠΎΠ²Π°Π½Π½ΡΡ
HBV, Π² Π Π΅ΡΠΏΡΠ±Π»ΠΈΠΊΠ΅ ΠΠ°Π³Π΅ΡΡΠ°Π½ ΡΠΎΡΡΠ°Π²Π»ΡΠ΅Ρ 13,8%, Π½ΠΎ Π΄ΠΎΡΡΠΈΠ³Π°Π΅Ρ 15% Π² ΠΎΡΠ΄Π΅Π»ΡΠ½ΡΡ
ΡΠ°ΠΉΠΎΠ½Π°Ρ
ΡΠ΅ΡΠΏΡΠ±Π»ΠΈΠΊΠΈ, ΡΡΠΎ ΠΏΠΎΠ·Π²ΠΎΠ»ΡΠ΅Ρ ΠΎΡΠ½Π΅ΡΡΠΈ Π΅Π΅ ΠΊ ΡΠ΅Π³ΠΈΠΎΠ½Π°ΠΌ Ρ ΡΠΌΠ΅ΡΠ΅Π½Π½ΠΎΠΉ ΡΠ½Π΄Π΅ΠΌΠΈΡΠ½ΠΎΡΡΡΡ. Π‘ΡΠ΅Π΄ΠΈ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΊΠΎ-ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠ΅ΠΉ HBV/HDV ΠΏΡΠ΅ΠΎΠ±Π»Π°Π΄Π°ΡΡ ΠΌΡΠΆΡΠΈΠ½Ρ Π² Π²ΠΎΠ·ΡΠ°ΡΡΠ΅ 25β45 Π»Π΅Ρ, Ρ ΠΏΡΠΎΠ΄Π²ΠΈΠ½ΡΡΡΠΌΠΈ ΡΡΠ°Π΄ΠΈΡΠΌΠΈ ΡΠΈΠ±ΡΠΎΠ·Π° ΠΈΠ»ΠΈ ΡΠΈΡΡΠΎΠ·ΠΎΠΌ. ΠΠΎ Π²ΡΠ΅Ρ
ΡΠ»ΡΡΠ°ΡΡ
HDV-ΠΈΠ½ΡΠ΅ΠΊΡΠΈΡ Π±ΡΠ»Π° Π²ΡΠ·Π²Π°Π½Π° 1 Π³Π΅Π½ΠΎΡΠΈΠΏΠΎΠΌ Π²ΠΈΡΡΡΠ°.ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅:Β ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΠ΅Β ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΡΒ ΡΠ²ΠΈΠ΄Π΅ΡΠ΅Π»ΡΡΡΠ²ΡΡΡ ΠΎ Π·Π½Π°ΡΠΈΠΌΠΎΡΡΠΈ ΠΏΡΠΎΠ±Π»Π΅ΠΌΡ Π³Π΅ΠΏΠ°ΡΠΈΡΠΎΠ² Π ΠΈ Π΄Π΅Π»ΡΡΠ° Π² Π Π΅ΡΠΏΡΠ±Π»ΠΈΠΊΠ΅ ΠΠ°Π³Π΅ΡΡΠ°Π½. ΠΠΎΠ»ΠΈΡΠ΅ΡΡΠ²ΠΎ Π²ΡΡΠ²Π»Π΅Π½Π½ΡΡ
Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΈ, ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²Π΅Π½Π½ΠΎ, ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»Ρ ΡΠ°ΡΡΠΎΡΡ ΠΊΠΎ-ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ, ΠΏΠΎΠ²ΠΈΠ΄ΠΈΠΌΠΎΠΌΡ, Π±ΡΠ΄ΡΡ ΡΠ²Π΅Π»ΠΈΡΠΈΠ²Π°ΡΡΡΡ ΠΏΡΠΈ ΡΠ°ΡΡΠΈΡΠ΅Π½ΠΈΠΈ ΡΠΊΡΠΈΠ½ΠΈΠ½Π³Π° Π½Π° ΠΌΠ°ΡΠΊΠ΅ΡΡ HDV-ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ, ΠΊΠΎΠ³Π΄Π° ΠΏΠ°ΡΠΈΠ΅Π½ΡΡ, Π½Π°Ρ
ΠΎΠ΄ΠΈΠ²ΡΠΈΠ΅ΡΡ Π½Π° Π΄ΠΈΡΠΏΠ°Π½ΡΠ΅ΡΠ½ΠΎΠΌ ΡΡΠ΅ΡΠ΅ ΠΊΠ°ΠΊ Π½ΠΎΡΠΈΡΠ΅Π»ΠΈ HΠsAg, Π±ΡΠ΄ΡΡ ΠΎΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Ρ ΠΏΠΎ Π°Π»Π³ΠΎΡΠΈΡΠΌΡ ΡΠΎΠ³Π»Π°ΡΠ½ΠΎ ΠΏΡΠΈΠΊΠ°Π·Ρ ΠΎ ΠΌΠ°ΡΡΡΡΡΠΈΠ·Π°ΡΠΈΠΈ. ΠΠ΅ ΠΌΠ΅Π½ΡΡΠ΅ΠΉ ΠΏΡΠΎΠ±Π»Π΅ΠΌΠΎΠΉ ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΏΠΎΠ·Π΄Π½ΡΡ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠ° Π³Π΅ΠΏΠ°ΡΠΈΡΠ° Π΄Π΅Π»ΡΡΠ° Π² Π Π΅ΡΠΏΡΠ±Π»ΠΈΠΊΠ΅ ΠΠ°Π³Π΅ΡΡΠ°Π½ ΠΈ ΠΎΠ³ΡΠ°Π½ΠΈΡΠ΅Π½Π½ΡΠ΅ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΠΈ ΠΏΡΠΎΡΠΈΠ²ΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ
Immune-mediated epilepsies in children
The paper reviews the current literature on immune-mediated pediatric epilepsies. It describes the clinical picture, laboratory diagnosis, and treatment of autoimmune encephalitides (limbic encephalitis and anti-NMDA-receptor antibody encephalitis), Hashimoto's encephalopathy, opsoclonus-myoclonus-syndrome, and Rasmussen's syndrome, as well as groups of acute encephalopathies with immune-mediated status epilepticus (FIRES-, DESK-, HHE- syndrome). A clinical case of Hashimoto's encephalopathy is described. Emphasis is laid on a close relationship between epilepsy and inflammation, including the development of an autoimmune process due to recurrent epileptic seizures
Clinical significance of FLG gene mutations in children with atopic dermatitis
Skin barrier dysfunction due to deficiency of the skin protein filaggrin is one of the factors involved in the pathogenesis of atopicΒ dermatitis. Objective: to determine the clinical significance of 2282 del CAGT, R501X, R2447X, and S3247X mutations in the FLGΒ gene in children with atopic dermatitis. The investigation included 58 children with atopic dermatitis. A molecular genetic analysis ofΒ the four mutations in the FLG gene was done in all the children. In the patients with FLG gene mutations, there was a tendency towardsΒ a higher frequency of sensitization to house dust allergens, significantly more often sensitization to cat epidermal allergen, andΒ significantly higher levels of specific IgE to the cat epidermis. Conclusion. Mutations in the FLG gene encoding the protein filaggrinΒ raise the risk for sensitization to domestic and epidermal allergens and, in case of already existing sensitization to the cat epidermis,Β the patients are found with a high degree of probability to have the high concentration of specific IgE to this allergen. The above factΒ justifies the need to place special emphasis on measures to eliminate house dust allergens, and cat epidermis allergen in particular,Β and to personalize approaches to therapy and prevention of atopic dermatitis in children