暂无摘要。

Összefoglaló. Bevezetés: Egy új, számítógép által segített betegminta-asszociációs analízis eredménye szerint a COVID-19 tüneteinek kialakításában kiemelt tényezőként jelenik meg a bradikinin. Eszerint a bradikinin lebontása lelassul az angiotenzinkonvertáló enzim aktivitásának csökkenése miatt, ami jelentősen megemelkedő bradikininszinthez vezet a tüdőben. Nem merült fel azonban a véralvadási faktorok lehetséges szerepe a \"bradikininviharban\", annak ellenére, hogy az idősebb cardiovascularis betegekben aktiválódó XII-es faktor és a C1-észteráz-inhibitor (C1INH) alacsony szintje nagy mennyiségű bradikinin képződéséhez vezethet. Módszer: Átfogó irodalmi áttekintés. Eredmények: 1) A vírus által fertőzött, sérült endotheliumsejtek felülete az a hely, amellyel érintkezve elindulhat a XII-es véralvadási faktor aktivációja - ez serkenti a prekallikrein/kallikrein/kinin rendszert, és bradikininképződést okoz. Ez a folyamat megtörténik a súlyos vese- és tüdőkárosodást okozó hantavírus-fertőzésekben. 2) Idős betegekben az atherosclerosis miatt többszörösen sérült, merev, \"stiff\" erek endotheliumfelszínein jóval magasabb lehet a XII-es faktor kontakt úton történő aktivációja, mint a fiatal egyének ereiben. Ez a tény egyik oka lehet az idős, cardiovascularis betegek körében tapasztalt magasabb halálozásnak. Következtetés: Az aktivált XII-es véralvadási faktor célzott gátlása újabb gyógyítási lehetőség lehet a SARS-CoV-2-fertőzött idős betegekben. Jelenleg már hatásosnak bizonyult a bradikininképzést gátló C1INH-nak, továbbá a bradikininreceptor-gátlóknak az adása is. Orv Hetil. 2020; 161(50): 2099-2103.

Bradykinin was implicated in a new complex model of pathomechanism leading to the symptoms of COVID-19 created by a computer-assisted association analysis. According to this model, the decrease in angiotensin-converting enzyme expression leads to impaired bradykinin elimination and subsequent enrichment in the lungs. However, there is no mentioning of the importance of blood coagulation factor XII in increased bradykinin production, in spite of its age-dependent activation and the lower level of C1-esterase inhibitor (C1INH). Activated factor XII may be an important contributor to the \"bradykinin storm\" in elder cardiovascular patients.
Literature review.
1) Activation of the coagulation factor XII on the surface of SARS-CoV-2 infected endothelial cells may trigger the prekallikrein/kallikrein/kinin system producing bradykinin. Such process is taking place in hantavirus infections causing severe lung and kidney damages. 2) The endothelial system is dysregulated in elderly patients, resulting in potentially higher factor XII activities on the surface of damaged endothelial cells in the stiffened arteries. This can contribute to the higher mortality rates in the elderly.
The targeted inhibition of activated blood coagulation factor XII may represent a new therapeutic target for COVID-19, especially for elder patients. Recently, beneficial results have already been observed by the clinical applications of recombinant C1INH and bradykinin receptor antagonists. Orv Hetil. 2020; 161(50): 2099-2103.

OBJECTIVE: Angioedema (AE) caused by angiotensin-converting enzyme inhibitors (ACEIs) requires prompt and appropriate management, but current treatment options are limited to symptomatic treatment. Icatibant is a bradykinin receptor antagonist approved for hereditary AE treatment. Some recent studies showed a potential role for icatibant on ACEI-induced AE while others have shown no promising effect. This meta-analysis of randomized controlled trials (RCTs) was conducted to provide evidence for the use of icatibant in the treatment of ACEI-induced AE.
METHODS: Relevant RCTs that examined the effects of icatibant for ACEI-induced AE were retrieved from EMBASE, PubMed and Cochrane Library (Central). Included articles for the meta-analysis were assessed using the Cochrane risk of bias tool. For meta-analysis, the pooled mean differences (MD) with 95% CIs and the pooled relative risk (RR) with 95% CIs were calculated using RevMan 5.3. The systematic review was performed in accordance with the PRISMA statement.
CONCLUSIONS: A total of 234 records were identified after searching the databases. In total, three RCTs involving 179 patients were included in the meta-analysis. The three RCTs had a low risk of bias and the characteristics of the participants and the outcome measures were similar among the RCTs. Treatment with icatibant shortened the time to achieve complete resolution of ACEI-induced AE symptoms compared to placebo or conventional treatments. However, the difference was not statistically significant (MD: -7.77 hours; 95% CI: -25.18-9.63 hours). There were no differences between groups in terms of drug-related adverse effects, apart from the reactions at the site of injection (RR: 1.35; 95% CI: 0.53-3.45).
CONCLUSIONS: This meta-analysis evaluated the effectiveness and tolerability of icatibant therapy for ACEI-induced AE, but the benefit of icatibant therapy over placebo or conventional treatment strategies could not be shown.

Early identification of patients at risk of a severe course of hantaviral disease and lack of effective medication represent a global challenge in the treatment of this emerging infection. We describe a 67-year-old female patient with a history of chronic lymphoproliferative disease involving the spleen and an extremely severe acute Puumala hantavirus infection. She was treated with the bradykinin receptor antagonist icatibant and recovered. She is the second patient with a spleen abnormality and severe Puumala infection treated with icatibant in our hospital. We suggest that patients with spleen abnormalities may be more susceptible to severe hantavirus disease. The activation of the kinin-kallikrein system and the formation of bradykinin in hantavirus-infected endothelial cells indicate that the role of bradykinin receptor antagonist icatibant in the treatment of hantavirus disease is worth studying.