18 research outputs found
ΠΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½Π°Ρ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠ° ΠΊΠ΅Π»ΠΎΠΈΠ΄Π½ΡΡ ΠΈ Π³ΠΈΠΏΠ΅ΡΡΡΠΎΡΠΈΡΠ΅ΡΠΊΠΈΡ ΡΡΠ±ΡΠΎΠ², ΠΎΡΠ½ΠΎΠ²Π°Π½Π½Π°Ρ Π½Π° ΡΠ°Π·Π»ΠΈΡΠΈΡΡ Π² ΠΊΠΎΠΆΠ½ΠΎΠΉ ΡΡΠ²ΡΡΠ²ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΠΈ
A study of different types of skin sensitivity in patients with keloid and hypertrophic scar tissues was conducted in order
to optimize clinical diagnostics of scar hypertrophy of the skin. A symmetrical area of unaffected skin was examined as
control. The revealed results suggest a sharp increase of deep skin sensitivity with simultaneous reduction of other types
of sensitivity, which was observed in 97% of subjects, as a new differential sign of keloid scar tissues.Π‘ ΡΠ΅Π»ΡΡ ΠΎΠΏΡΠΈΠΌΠΈΠ·Π°ΡΠΈΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ ΡΡΠ±ΡΠΎΠ²ΡΡ
Π³ΠΈΠΏΠ΅ΡΡΡΠΎΡΠΈΠΉ ΠΊΠΎΠΆΠΈ Π±ΡΠ»ΠΎ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΎ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅
ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
Π²ΠΈΠ΄ΠΎΠ² ΠΊΠΎΠΆΠ½ΠΎΠΉ ΡΡΠ²ΡΡΠ²ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΠΈ Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΊΠ΅Π»ΠΎΠΈΠ΄Π½ΡΠΌΠΈ ΠΈ Π³ΠΈΠΏΠ΅ΡΡΡΠΎΡΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΡΡΠ±ΡΠ°ΠΌΠΈ. Π ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅
ΠΊΠΎΠ½ΡΡΠΎΠ»Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π»ΠΈ ΡΠΈΠΌΠΌΠ΅ΡΡΠΈΡΠ½ΡΠΉ ΡΡΠ°ΡΡΠΎΠΊ Π½Π΅ΠΏΠΎΡΠ°ΠΆΠ΅Π½Π½ΠΎΠΉ ΠΊΠΎΠΆΠΈ. ΠΡΡΠ²Π»Π΅Π½Π½ΡΠ΅ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΡ ΠΏΠΎΠ·Π²ΠΎΠ»ΡΡΡ
ΠΏΡΠ΅Π΄Π»ΠΎΠΆΠΈΡΡ Π² ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅ Π½ΠΎΠ²ΠΎΠ³ΠΎ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΏΡΠΈΠ·Π½Π°ΠΊΠ° ΠΊΠ΅Π»ΠΎΠΈΠ΄Π½ΡΡ
ΡΡΠ±ΡΠΎΠ² ΡΠ΅Π·ΠΊΠΎΠ΅ ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠ΅ Π³Π»ΡΠ±ΠΎΠΊΠΎΠΉ
ΠΊΠΎΠΆΠ½ΠΎΠΉ ΡΡΠ²ΡΡΠ²ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΠΈ Π½Π° ΡΠΎΠ½Π΅ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΡ Π΄ΡΡΠ³ΠΈΡ
Π²ΠΈΠ΄ΠΎΠ² ΡΡΠ²ΡΡΠ²ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΠΈ, ΠΊΠΎΡΠΎΡΠΎΠ΅ Π½Π°Π±Π»ΡΠ΄Π°Π»ΠΎΡΡ Ρ 97%
ΠΎΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Π½ΡΡ
Π±ΠΎΠ»ΡΠ½ΡΡ
Diagnostic aspects of atopic dermatitis
Atopic dermatitis (AD) is a chronic recurrent inflammatory skin disease that is often familial. Atopic dermatitis leads among all dermatological diagnoses that pediatricians give their patients. There is a tendency to over diagnosis of this dermatosis, which, in turn, determines the vector of research aimed at developing more accurate algorithms for making the correct diagnosis. Currently, there are various diagnostic schemes based on the summation of major and minor AD criteria. If patients have major signs of the disease, the diagnosis of AD does not cause any particular difficulties, however, current diagnostic trends are associated with focusing on minor criteria, that are especially important in subacute, chronic course and incomplete remission. This article presents relevant data on the role of genetic factors in AD development. It describes in detail the AD pathogenesis, where the main role is played by epidermal barrier lesion due to filaggrin protein mutation and body immune dysfunction, and, as a result, the predisposition of patients with AD to skin infection with pathogenic microorganisms. It gives a brief description of AD clinical picture depending on the age of the patient. Special attention is paid to various diagnostic algorithms for AD, among which the most recognized are J.M. Hanifin and G. Rajka diagnostic criteria (1980). All minor AD criteria from this algorithm are described in detail, authors also proposed additional signs of the disease that will help pediatricians to diagnose AD more accurately and select therapy for patients. Considering the fact that skin barrier dysfunction is the basis of this dermatosis, the article shows the high importance of emollients and regenerating agents, affecting the main pathogenesis links. Β© 2020, Pediatria Ltd.. All rights reserved
Π‘ΠΈΠ½Π΄ΡΠΎΠΌ Π ΠΎΡΡΠ»Π»Π° Π² Π΄Π΅ΡΠΌΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΏΡΠ°ΠΊΡΠΈΠΊΠ΅ (ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ΅ Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΠ΅)
Rowell syndrome is a rare cluster of symptoms characterized by clinical manifestation of lupus erythematosus and erythema multiforme (EM). About 100 cases of the syndrome have been reported in medical publications during the last 100 years. This may be related to misinterpretation of the symptoms and subsequent incorrect diagnosis due to its EM-like manifestations. Important clues for the diagnosis of Rowell syndrome are findings of positive rheumatoid factor, anti-nuclear antibodies and other erythematoid markers, as well as additional investigations, in particular, direct immunofluorescence technique. The paper describes a clinical case of Rowell syndrome in a 16-year old male patient. The diagnosis was challenging due to EM-like skin manifestations and required additional laboratory work-up, as well as the patient's follow-up. The diagnosis of Rowell syndrome was based on the clinical manifestations and on such diagnostic criteria as positive rheumatoid factor and anti-nuclear antibodies, as well as histological and laboratory abnormalities characteristic of the erythematosis. The patient was hospitalized and received the following treatment: prednisolone infusion (2.5 mg/kg/daily for 7 days), chloropyramine (1 mL i.m. twice daily for 5 days), hydroxychloroquine (6.5 mg/kg daily for 5 days), magnesium asparaginate/potassium asparaginate (one tablet (166.3 mg/175 mg) 3 times daily for 7 days), topical methylprednisolone aceponate cream 1% (once daily for 7 days). The treatment resulted in positive changes in the skin lesion and improvement of his general state. This clinical observation gives an example of classic Rowell syndrome proven both by lab and clinical signs, taking into account skin symptoms of lupus erythematosus and EM-like rash.Π‘ΠΈΠ½Π΄ΡΠΎΠΌ Π ΠΎΡΡΠ»Π»Π° - ΡΠ΅Π΄ΠΊΠΎ Π²ΡΡΡΠ΅ΡΠ°ΡΡΠΈΠΉΡΡ ΡΠΈΠΌΠΏΡΠΎΠΌΠΎΠΊΠΎΠΌΠΏΠ»Π΅ΠΊΡ, Π΄Π»Ρ ΠΊΠΎΡΠΎΡΠΎΠ³ΠΎ Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠ½Ρ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΡ ΠΊΡΠ°ΡΠ½ΠΎΠΉ Π²ΠΎΠ»ΡΠ°Π½ΠΊΠΈ ΠΈ ΠΌΠ½ΠΎΠ³ΠΎΡΠΎΡΠΌΠ½ΠΎΠΉ ΡΠΊΡΡΡΠ΄Π°ΡΠΈΠ²Π½ΠΎΠΉ ΡΡΠΈΡΠ΅ΠΌΡ (ΠΠΠ). ΠΠ° ΠΏΠΎΡΠ»Π΅Π΄Π½ΠΈΠ΅ 100 Π»Π΅Ρ Π² Π½Π°ΡΡΠ½ΠΎΠΉ Π»ΠΈΡΠ΅ΡΠ°ΡΡΡΠ΅ ΠΎΠΏΠΈΡΠ°Π½ΠΎ ΠΎΠΊΠΎΠ»ΠΎ 100 ΡΠ»ΡΡΠ°Π΅Π² Π΄Π°Π½Π½ΠΎΠ³ΠΎ ΡΠΈΠ½Π΄ΡΠΎΠΌΠ°, ΡΡΠΎ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΡΠ²ΡΠ·Π°Π½ΠΎ Ρ ΠΎΡΠΈΠ±ΠΎΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΡΠΏΡΠ΅ΡΠ°ΡΠΈΠ΅ΠΉ ΡΠΈΠΌΠΏΡΠΎΠΌΠΎΠ² ΠΈ, ΠΊΠ°ΠΊ ΡΠ»Π΅Π΄ΡΡΠ²ΠΈΠ΅, Π½Π΅ΡΠΎΡΠ½ΠΎΠΉ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΎΠΉ ΠΏΠΎ ΠΏΡΠΈΡΠΈΠ½Π΅ Π΅Π³ΠΎ ΠΌΠ°Π½ΠΈΡΠ΅ΡΡΠ°ΡΠΈΠΈ Π²ΡΡΡΠΏΠ°Π½ΠΈΡΠΌΠΈ ΠΏΠΎ ΡΠΈΠΏΡ ΠΠΠ. ΠΠ°ΠΆΠ½ΠΎΠ΅ Π·Π½Π°ΡΠ΅Π½ΠΈΠ΅ Π² Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠ΅ ΡΠΈΠ½Π΄ΡΠΎΠΌΠ° Π ΠΎΡΡΠ»Π»Π° ΠΈΠΌΠ΅Π΅Ρ Π²ΡΡΠ²Π»Π΅Π½ΠΈΠ΅ ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ ΡΠ΅Π²ΠΌΠ°ΡΠΎΠΈΠ΄Π½ΠΎΠ³ΠΎ ΡΠ°ΠΊΡΠΎΡΠ°, Π°Π½ΡΠΈΡΠ΄Π΅ΡΠ½ΡΡ
Π°Π½ΡΠΈΡΠ΅Π» ΠΈ Π΄ΡΡΠ³ΠΈΡ
ΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ² ΡΡΠΈΡΠ΅ΠΌΠ°ΡΠΎΠ·Π°, Π° ΡΠ°ΠΊΠΆΠ΅ Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΡΠ΅ ΠΌΠ΅ΡΠΎΠ΄Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ, Π² ΡΠ°ΡΡΠ½ΠΎΡΡΠΈ ΠΏΡΡΠΌΠ°Ρ ΠΈΠΌΠΌΡΠ½ΠΎΡΠ»ΡΠΎΡΠ΅ΡΡΠ΅Π½ΡΠΈΡ. Π ΡΡΠ°ΡΡΠ΅ Π΄Π°Π½ΠΎ ΠΎΠΏΠΈΡΠ°Π½ΠΈΠ΅ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΡ ΡΠΈΠ½Π΄ΡΠΎΠΌΠ° Π ΠΎΡΡΠ»Π»Π° Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ° 16 Π»Π΅Ρ. Π£ΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½ΠΈΠ΅ Π΄ΠΈΠ°Π³Π½ΠΎΠ·Π° Π²ΡΠ·Π²Π°Π»ΠΎ Π·Π°ΡΡΡΠ΄Π½Π΅Π½ΠΈΡ ΠΏΠΎ ΠΏΡΠΈΡΠΈΠ½Π΅ ΠΌΠ°Π½ΠΈΡΠ΅ΡΡΠ°ΡΠΈΠΈ ΠΊΠΎΠΆΠ½ΡΡ
ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΠΉ ΠΏΠΎ ΡΠΈΠΏΡ ΠΠΠ ΠΈ ΠΏΠΎΡΡΠ΅Π±ΠΎΠ²Π°Π»ΠΎ Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΠΎΠΉ Π»Π°Π±ΠΎΡΠ°ΡΠΎΡΠ½ΠΎΠΉ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ, Π° ΡΠ°ΠΊΠΆΠ΅ Π΄ΠΈΠ½Π°ΠΌΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΡ. ΠΡΠΈ ΠΏΠΎΡΡΠ°Π½ΠΎΠ²ΠΊΠ΅ Π΄ΠΈΠ°Π³Π½ΠΎΠ·Π° ΡΠΈΠ½Π΄ΡΠΎΠΌΠ° Π ΠΎΡΡΠ»Π»Π° ΠΎΠΏΠΈΡΠ°Π»ΠΈΡΡ Π½Π° ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΡ, Π° ΡΠ°ΠΊΠΆΠ΅ Π½Π° ΡΠ°ΠΊΠΈΠ΅ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΊΡΠΈΡΠ΅ΡΠΈΠΈ, ΠΊΠ°ΠΊ ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½ΡΠ΅ ΠΏΡΠΎΠ±Ρ Π½Π° ΡΠ΅Π²ΠΌΠ°ΡΠΎΠΈΠ΄Π½ΡΠΉ ΡΠ°ΠΊΡΠΎΡ ΠΈ Π°Π½ΡΠΈΡΠ΄Π΅ΡΠ½ΡΠ΅ Π°Π½ΡΠΈΡΠ΅Π»Π°, Π³ΠΈΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈ Π»Π°Π±ΠΎΡΠ°ΡΠΎΡΠ½ΡΠ΅ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ, ΠΏΡΠΈΡΡΡΠΈΠ΅ ΡΡΠΈΡΠ΅ΠΌΠ°ΡΠΎΠ·Ρ. ΠΠ°ΡΠΈΠ΅Π½Ρ Π½Π°Ρ
ΠΎΠ΄ΠΈΠ»ΡΡ Π² ΡΡΠ°ΡΠΈΠΎΠ½Π°ΡΠ΅ ΠΈ ΠΏΠΎΠ»ΡΡΠ°Π» ΡΠ»Π΅Π΄ΡΡΡΠ΅Π΅ Π»Π΅ΡΠ΅Π½ΠΈΠ΅: ΠΈΠ½ΡΡΠ·ΠΈΠΎΠ½Π½Π°Ρ ΡΠ΅ΡΠ°ΠΏΠΈΡ (ΠΏΡΠ΅Π΄Π½ΠΈΠ·ΠΎΠ»ΠΎΠ½ 2,5 ΠΌΠ³/ΠΊΠ³/ΡΡΡ Π² ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ 7 Π΄Π½Π΅ΠΉ), Ρ
Π»ΠΎΡΠΎΠΏΠΈΡΠ°ΠΌΠΈΠ½ (1 ΠΌΠ» 2 ΡΠ°Π·Π° Π² Π΄Π΅Π½Ρ Π²Π½ΡΡΡΠΈΠΌΡΡΠ΅ΡΠ½ΠΎ Π² ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ 5 Π΄Π½Π΅ΠΉ), Π³ΠΈΠ΄ΡΠΎΠΊΡΠΈΡ
Π»ΠΎΡΠΎΡ
ΠΈΠ½ (ΡΡΡΠΎΡΠ½Π°Ρ Π΄ΠΎΠ·Π° 6,5 ΠΌΠ³/ΠΊΠ³, Π΄Π»ΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΡ - 5 Π΄Π½Π΅ΠΉ), ΠΌΠ°Π³Π½ΠΈΡ Π°ΡΠΏΠ°ΡΠ°Π³ΠΈΠ½Π°Ρ / ΠΊΠ°Π»ΠΈΡ Π°ΡΠΏΠ°ΡΠ°Π³ΠΈΠ½Π°Ρ (1 ΡΠ°Π±. (166,3 ΠΌΠ³/ 175 ΠΌΠ³) 3 ΡΠ°Π·Π° Π² Π΄Π΅Π½Ρ Π² ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ 7 Π΄Π½Π΅ΠΉ), Π½Π°ΡΡΠΆΠ½ΠΎ ΠΊΡΠ΅ΠΌ ΠΌΠ΅ΡΠΈΠ»ΠΏΡΠ΅Π΄Π½ΠΈΠ·ΠΎΠ»ΠΎΠ½Π° Π°ΡΠ΅ΠΏΠΎΠ½Π°Ρ 1% (1 ΡΠ°Π· Π² Π΄Π΅Π½Ρ Π² ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ 7 Π΄Π½Π΅ΠΉ). Π ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠ΅ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½Π½ΠΎΠ³ΠΎ Π»Π΅ΡΠ΅Π½ΠΈΡ Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ° ΠΎΡΠΌΠ΅ΡΠ΅Π½Π° ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½Π°Ρ Π΄ΠΈΠ½Π°ΠΌΠΈΠΊΠ° Π² ΡΠ΅ΡΠ΅Π½ΠΈΠΈ ΠΊΠΎΠΆΠ½ΠΎΠ³ΠΎ ΠΏΡΠΎΡΠ΅ΡΡΠ° ΠΈ ΡΠ»ΡΡΡΠ΅Π½ΠΈΠ΅ ΠΎΠ±ΡΠ΅Π³ΠΎ ΡΠΎΡΡΠΎΡΠ½ΠΈΡ. ΠΠ° ΠΏΡΠΈΠΌΠ΅ΡΠ΅ Π½Π°ΡΡΠΎΡΡΠ΅Π³ΠΎ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΡ ΠΏΠΎΠΊΠ°Π·Π°Π½ΠΎ ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΠ΅ ΡΠΈΠ½Π΄ΡΠΎΠΌΠ° Π ΠΎΡΡΠ»Π»Π°, ΠΈΠΌΠ΅ΡΡΠ΅Π΅ ΠΊΠ°ΠΊ Π»Π°Π±ΠΎΡΠ°ΡΠΎΡΠ½ΠΎΠ΅, ΡΠ°ΠΊ ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΠΎΠ±ΠΎΡΠ½ΠΎΠ²Π°Π½ΠΈΠ΅, ΡΡΠΈΡΡΠ²Π°Ρ Π½Π°Π»ΠΈΡΠΈΠ΅ ΠΊΠΎΠΆΠ½ΡΡ
ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΠΉ ΠΊΡΠ°ΡΠ½ΠΎΠΉ Π²ΠΎΠ»ΡΠ°Π½ΠΊΠΈ ΠΈ Π²ΡΡΡΠΏΠ°Π½ΠΈΠΉ ΠΏΠΎ ΡΠΈΠΏΡ ΠΠΠ
ΠΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΡ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ ΠΏΡΠΎΡΡΠΎΠ³ΠΎ Π³Π΅ΡΠΏΠ΅ΡΠ° Ρ Π΄Π΅ΡΠ΅ΠΉ, ΡΡΡΠ°Π΄Π°ΡΡΠΈΡ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΠΌ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠΎΠΌ
Atopic dermatitis is a disease of early childhood. Most children are infected with the herpes simplex virus at this age. The changes in the congenital and adaptive immunity in children with atopic dermatitis create precondition for the development of infectious complications, including those caused by herpes viruses. The authors of the article discuss details of various clinical manifestations of herpes infection in children with atopic dermatitis and they carry out differential diagnostics. Particular attention is paid to herpes eczema - the severe complication of atopic dermatitis in the course of disseminated herpes infection.ΠΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΠΉ Π΄Π΅ΡΠΌΠ°ΡΠΈΡ - Π±ΠΎΠ»Π΅Π·Π½Ρ ΡΠ°Π½Π½Π΅Π³ΠΎ Π΄Π΅ΡΡΠΊΠΎΠ³ΠΎ Π²ΠΎΠ·ΡΠ°ΡΡΠ°. Π ΡΡΠΎΠΌ Π²ΠΎΠ·ΡΠ°ΡΡΠ½ΠΎΠΌ ΠΏΠ΅ΡΠΈΠΎΠ΄Π΅ Π±ΠΎΠ»ΡΡΠΈΠ½ΡΡΠ²ΠΎ Π΄Π΅ΡΠ΅ΠΉ ΠΈΠ½ΡΠΈΡΠΈΡΡΡΡΡΡ Π²ΠΈΡΡΡΠΎΠΌ ΠΏΡΠΎΡΡΠΎΠ³ΠΎ Π³Π΅ΡΠΏΠ΅ΡΠ°. ΠΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ Π²ΡΠΎΠΆΠ΄Π΅Π½Π½ΠΎΠ³ΠΎ ΠΈ Π°Π΄Π°ΠΏΡΠΈΠ²Π½ΠΎΠ³ΠΎ ΠΈΠΌΠΌΡΠ½ΠΈΡΠ΅ΡΠ° ΠΏΡΠΈ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠΌ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ΅ ΡΠΎΠ·Π΄Π°ΡΡ ΠΏΡΠ΅Π΄ΠΏΠΎΡΡΠ»ΠΊΠΈ Π΄Π»Ρ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΎΠ½Π½ΡΡ
ΠΎΡΠ»ΠΎΠΆΠ½Π΅Π½ΠΈΠΉ, Π² ΡΠΎΠΌ ΡΠΈΡΠ»Π΅ ΠΎΠ±ΡΡΠ»ΠΎΠ²Π»Π΅Π½Π½ΡΡ
Π³Π΅ΡΠΏΠ΅ΡΠ²ΠΈΡΡΡΠ°ΠΌΠΈ. Π ΡΡΠ°ΡΡΠ΅ ΠΏΠΎΠ΄ΡΠΎΠ±Π½ΠΎ ΡΠ°ΡΡΠΌΠ°ΡΡΠΈΠ²Π°ΡΡΡΡ ΡΠ°Π·Π½ΠΎΠΎΠ±ΡΠ°Π·Π½ΡΠ΅ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΡ Π³Π΅ΡΠΏΠ΅ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ Ρ Π΄Π΅ΡΠ΅ΠΉ Ρ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΠΌ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠΎΠΌ, ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΡΡΡ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½Π°Ρ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠ°. ΠΡΠΎΠ±ΠΎΠ΅ Π²Π½ΠΈΠΌΠ°Π½ΠΈΠ΅ ΡΠ΄Π΅Π»Π΅Π½ΠΎ ΡΡΠΆΠ΅Π»ΠΎΠΌΡ ΠΎΡΠ»ΠΎΠΆΠ½Π΅Π½ΠΈΡ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠ° ΠΏΡΠΈ ΡΠ΅Π°Π»ΠΈΠ·Π°ΡΠΈΠΈ Π΄ΠΈΡΡΠ΅ΠΌΠΈΠ½ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ Π³Π΅ΡΠΏΠ΅ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ - Π³Π΅ΡΠΏΠ΅ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠΊΠ·Π΅ΠΌΠ΅
Herpetic eczema in children with atopic dermatitis: Prognosis, clinical and immunological diagnostics and management tactics
Herpetic eczema (HE), being a manifestation of disseminated herpetic infection, mainly complicates the course of atopic dermatitis (AtD). This is a potentially life-threatening infection for children, the mortality of which, according to the literature, reaches 9%. Early diagnosis of HE helps to reduce the incidence of adverse outcomes and improve treatment quality for these patients. The goal is to improve the management tactics of children with herpetic eczema based on the patient-oriented algorithm for monitoring children with AtD risk groups, taking into account the predictors complex of disease development and severity. Material and methods: the single-center prospective observational study included 150 children aged from 4 months to 18 years with AtD. The main group consisted of 113 children with HE caused by AtD, the comparison group β 37 children with AtD in the exacerbation period not combined with HE. HSV infection is confirmed by determining the virus DNA in blood by the method of polymerase chain reaction. The diagnosis of AtD in children was verified according to the criteria proposed by J. Hanifin and G. Rajka. The severity of AtD at the time of inspection was assessed according to the SCORAD scale. Results: the main predictors of HE development in patients with AtD are: age up to 1 year (increase in relative risk (IRR) 2,86, 95% confidence interval (CI) 7,91/0,68, p<0,001), autumn-winter period (IRR 1,68, 95% CI 5,3/0,15, p=0,018), close relatives with combination of pollinosis and asthma (IRR 2,56, 95% CI β 9,95/β0,16, p<0,001), moderate or severe form of AtD (IRR 0,91, 95% CI β 2,11/β0,17, p<0,001). Laboratory immunological signs of HE developing risk in children with AtD include eosinophilia more than 3β’109/l (p<0,001); an increased level of IL8 more than 2 times the norm value (p<0,001); prediction of a severe course of the disease β an increase in total IgE level to 850 kE/l (p<0,017) and an increase TNFΞ± serum concentration above 2 pg/ml (p<0,001). Conclusion: the combination of at least 3 risk factors allows to classify a patient with AtD as a high risk group for HE development with recommendations for nonspecific prophylaxis, namely: separation from patients with manifest HSV infection. If a child has a high risk of HE adverse course, differentiated therapy is necessary, Ρonsidering the possible accession of a secondary infection and the exacerbation of AtD after HE regression. Β© 2019, Pediatria Ltd.. All rights reserved
Modern aspects of rendu-osler-weber disease
Rendu-Osler-Weber disease (hereditary hemorrhagic telangiectasia) is a rare hereditary disease that develops in childhood, characterized by vascular dysplasias, multiple telangiectasias of the skin and mucous membranes, and hemorrhagic syndrome of different localization. One of the first and most noticeable signs of the disease is spider veins on the skin and nasal mucous membranes. With lesions of nasal mucosa and gastrointestinal tract, the disease proceeds with frequently recurring bleeding. In chronic blood loss, iron deficiency anemia develops, and in acute cases, a fatal outcome is possible. The article provides a brief historical summary of Rendu-Osler-Weber disease description, etiopathogenetic mechanisms of the disease development, clinical picture with the most typical manifestations, as well as modern diagnostic and treatment criteria. Particular attention is paid to the early diagnosis of the disease. In conclusion, the authors cite their own observation of an 11-year-old patient with Rendu-Osler-Weber disease. Β© 2019, Pediatria Ltd. All right reserved
Peutz-Jeghers' syndrome in pediatric dermatological practice [Π‘ΠΈΠ½Π΄ΡΠΎΠΌ ΠΠ΅ΠΉΡΡΠ°-ΠΠ³Π΅ΡΡΠ° Π² Π΄Π΅ΡΡΠΊΠΎΠΉ Π΄Π΅ΡΠΌΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΏΡΠ°ΠΊΡΠΈΠΊΠ΅]
Peutz-Jeghers' syndrome is a rare hereditary disease inherited by an autosomal dominant type, manifested by a characteristic clinical picture of skin lesions and hamartomas of the gastrointestinal tract. Complications of the disease include bleeding from polyps, anemia, intussusception and intestinal necrosis, as well as a high likelihood of developing malignant tumors. For the first time the syndrome was described at the beginning of the last century, and it is of interest to dermatologists, gastroenterologists, oncologists and surgeons due to the clinical heterogeneity of intestinal and skin manifestations. The article describes a clinical case of a 5-year-old girl with the Peutz-Jaegers syndrome. The patient complained of periodic dull abdominal pain that worsened after eating solid food. During the examination of the skin and mucous membranes the doctors discovered rashes on the face: perioral area, on the red border of the lips and on the mucous membrane of the lips, inside the cheeks, hard palate. Esophagogastroduodenoscopy (EGDS) revealed a polyp on a pedicle in the prepyloric part - it was removed during repeated EGDS under endotracheal anesthesia. Fibrocolonoscopy revealed hyperpigmentation of the dome of the cecum. To confirm the diagnosis, the doctors carried out DNA testing which found a mutation of the STK11 gene. Pigmentation of the perioral area is an early symptom of Peutz-Jeghers' syndrome suggesting optimal examination. Early recognition of the syndrome in children is important in the context of reducing the risk of developing intestinal obstruction, bleeding, and cancer complications in the future. Β© 2021 National Academy of Pediatric Science and Innovation. All rights reserved
Clinical manifestations of herpes simplex virus infection in children with atopic dermatitis [ΠΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΡ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ ΠΏΡΠΎΡΡΠΎΠ³ΠΎ Π³Π΅ΡΠΏΠ΅ΡΠ° Ρ Π΄Π΅ΡΠ΅ΠΉ, ΡΡΡΠ°Π΄Π°ΡΡΠΈΡ Π°ΡΠΎΠΏΠΈΡΠ΅ΡΠΊΠΈΠΌ Π΄Π΅ΡΠΌΠ°ΡΠΈΡΠΎΠΌ]
Atopic dermatitis is a disease of early childhood. Most children are infected with the herpes simplex virus at this age. The changes in the congenital and adaptive immunity in children with atopic dermatitis create precondition for the development of infectious complications, including those caused by herpes viruses. The authors of the article discuss details of various clinical manifestations of herpes infection in children with atopic dermatitis and they carry out differential diagnostics. Particular attention is paid to herpes eczema β the severe complication of atopic dermatitis in the course of disseminated herpes infection. Β© 2018 National Academy of Pediatric Science and Innovation. All rights reserved