Anaphylactic reactions after COVID-19 vaccination in Germany.

. For the COVID-19 vaccines used in Germany, severe allergic (anaphylactic) reactions after vaccination have been reported in very rare cases. While Comirnaty and Spikevax are mRNA vaccines, Vaxzevria and Jcovden comprise vector vaccines, and Nuvaxovid a recombinant spike protein vaccine. The reporting rate of anaphylaxis after mRNA vaccination was higher in females receiving their first vaccination dose, with 0.97 and 1.12 reports per 100,000 vaccinations for Comirnaty and Spikevax, respectively, compared with vaccinated males and subsequent vaccinations. The Paul-Ehrlich-Institut (PEI) investigated 106 responses of 321 cases of confirmed anaphylactic reactions concerning subsequent allergy testing and revaccination with a COVID-19 vaccine. The collected data indicate that only a small proportion of cases (22%) were IgE-mediated reactions. A large proportion (73%) of patients could be revaccinated under precautionary measures without recurrence of anaphylaxis. The pathomechanism of the majority of anaphylactic reactions remains unclear and should be investigated in further studies.

Lung T cell response in COVID-19.

The COVID-19 pandemic has shown the potentially devastating impact of novel respiratory infections worldwide. Insightful data obtained in the last years have shed light on the pathophysiology of SARS-CoV-2 infection and the role of the inflammatory response in driving both the resolution of the disease and uncontrolled deleterious inflammatory status in severe cases. In this mini-review, we cover some important aspects of the role of T cells in COVID-19 with a special focus on the local response in the lung. We focus on the reported T cell phenotypes in mild, moderate, and severe COVID-19, focusing on lung inflammation and on both the protective and damaging roles of the T cell response, also highlighting the open questions in the field.

Unusual Presentation of COVID-19 Headache and Its Possible Pathomechanism.

Headache was the most common neurological symptom during the H1N1 pandemic in 2009 and the most recrudescing symptom of human coronavirus (hCoV) in 2016. Even in this prevailing global coronavirus disease 2019 (COVID-19) pandemic, the main neurological symptom is found to be a headache. Headache phenotypes identified with COVID-19 are largely migraine, tension-type headache, or cough headache located in the frontotemporal or occipital region with wavering intensity and essentially of acute onset. We present two cases of unusual headache phenotypes with COVID-19 infection and attempt to shed light on their pathomechanism. Trigeminal autonomic cephalgia may be a possibility in our case, triggered by the virus itself, either directly or through an indirect path elaborated well in the pathomechanism segment. Severe acute respiratory syndrome coronavirus 2 (SARs-CoV-2) binds to angiotensin-converting enzyme 2 (ACE2) located in the peripheral nerve and intracranial vascular endothelium, sensitizing the trigeminovascular system by further interacting with higher cortical pain centers via the thalamic and hypothalamic nuclei, producing pain. CSF analysis along with opening pressure measurement in Case 2 may portray a comprehensive understanding of our patient's headache. Coupling with the dorsal pons and trigeminal nucleus caudalis (TNC), the hypothalamus could be the supreme generator for an attack. Hypothalamic perturbance could be a possible phenomenon for abnormal headache experiences and requires further validation. The possible COVID-19 pain pathway pathomechanism engaging interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF) alpha aided with a cortical spreading depression disturbing the hypothalamus is also described in this study. Undoubtedly, this pandemic could prove to be a guiding tool for mankind, for a comprehensive understanding of the enigmatic concepts of headaches.

Pathomechanisms and Treatment Implications for Stroke in COVID-19: A Review of the Literature.

Stroke in patients with COVID-19 has received increasing attention throughout the global COVID-19 pandemic, perhaps due to the substantial disability and mortality that can result when the two conditions co-occur. We reviewed the existing literature and found that the proposed pathomechanism underlying COVID-19-associated ischemic stroke is broadly divided into the following three categories: vasculitis, endothelialitis, and endothelial dysfunction; hypercoagulable state; and cardioembolism secondary to cardiac dysfunction. There has been substantial debate as to whether there is a causal link between stroke and COVID-19. However, the distinct phenotype of COVID-19-associated strokes, with multivessel territory infarcts, higher proportion of large vessel occlusions, and cryptogenic stroke mechanism, that emerged in pooled analytic comparisons with non-COVID-19 strokes is compelling. Further, in this article, we review the various treatment approaches that have emerged as they relate to the proposed pathomechanisms. Finally, we briefly cover the logistical challenges, such as delays in treatment, faced by providers and health systems; the innovative approaches utilized, including the role of tele-stroke; and the future directions in COVID-19-associated stroke research and healthcare delivery.

[COVID-19: neurological manifestations-update : What we know so far]. / COVID-19: neurologische Manifestationen ­ Update : Was wir bisher wissen.

Beyond pulmonary presentation, COVID-19 infection can manifest with a variety of both acute and chronic neurologic and neuropsychiatric (concomitant) symptoms and diseases. Nonspecific symptoms such as headache, fatigue, olfactory and gustatory disturbance have been reported more frequently, and severe disease such as encephalopathy, encephalitis, and cerebrovascular events have been reported relatively rarely. The heterogeneity of neurologic and neuropsychiatric presentations is large, as well as the range of recorded prevalences. Older patients, pre-existing neurologic and non neurologic comorbidities and severe COVID-19 disease were associated with increased risk of severe neurologic complications and higher in-hospital mortality. Probable neurotropic pathomechanisms of SARS-CoV­2 have been discussed, but a multifactorial genesis of neurologic/neuropsychiatric symptoms and disease beyond these is likely.

Making a complex dental care tailored to the person: population health in focus of predictive, preventive and personalised (3P) medical approach.

An evident underestimation of the targeted prevention of dental diseases is strongly supported by alarming epidemiologic statistics globally. For example, epidemiologists demonstrated 100% prevalence of dental caries in the Russian population followed by clinical manifestation of periodontal diseases. Inadequately provided oral health services in populations are caused by multi-factorial deficits including but not limited to low socio-economic status of affected individuals, lack of insurance in sub-populations, insufficient density of dedicated medical units. Another important aspect is the "participatory" medicine based on the active participation of population in maintaining oral health: healthcare will remain insufficient as long as the patient is not motivated and does not feel responsible for their oral health. To this end, nearly half of chronically diseased people do not comply with adequate medical services suffering from severely progressing pathologies. Noteworthy, the prominent risk factors and comorbidities linked to the severe disease course and poor outcomes in COVID-19-infected individuals, such as elderly, diabetes mellitus, hypertension and cardiovascular disease, are frequently associated with significantly altered oral microbiome profiles, systemic inflammatory processes and poor oral health. Suggested pathomechanisms consider potential preferences in the interaction between the viral particles and the host microbiota including oral cavity, the respiratory and gastrointestinal tracts. Since an aspiration of periodontopathic bacteria induces the expression of angiotensin-converting enzyme 2, the receptor for SARS-CoV-2, and production of inflammatory cytokines in the lower respiratory tract, poor oral hygiene and periodontal disease have been proposed as leading to COVID-19 aggravation. Consequently, the issue-dedicated expert recommendations are focused on the optimal oral hygiene as being crucial for improved individual outcomes and reduced morbidity under the COVID-19 pandemic condition. Current study demonstrated that age, gender, socio-economic status, quality of environment and life-style, oral hygiene quality, regularity of dental services requested, level of motivation and responsibility for own health status and corresponding behavioural patterns are the key parameters for the patient stratification considering person-tailored approach in a complex dental care in the population. Consequently, innovative screening programmes and adapted treatment schemes are crucial for the complex person-tailored dental care to improve individual outcomes and healthcare provided to the population.

Silent hypoxia in COVID-19: pathomechanism and possible management strategy.

The novel coronavirus disease 2019 (COVID-19) has become a severe health issue, especially to the patients who develop silent hypoxia condition after SARS-CoV-2 infection. Due to the lack of dyspnoea and extremely low oxygen saturation level, these patients are at exceptionally higher risk. Although the prevalence of silent hypoxia in COVID-19 patients has been evident in several cases, the underlying pathomechanism behind this condition is still unclear. Silent hypoxia in SARS-CoV-2 infected patients can be diagnosed with the help of a pulse oximeter, blood gas levels, and a 6-min walking test. While the clinicians and researchers figure out the exact reason for this phenomenon, the patients must be under strict day-to-day monitoring. In this article, we aim to provide comprehensive insights into the underlying symptoms, mechanism, and possible factors behind the occurrence of silent hypoxia among COVID-19 patients.