May 18
Ο ψυχίατρος-ψυχοθεραπευτής, Γιάννης Αυγουστάτος, παρουσίασε στις 12 Μάη το νέο βιβλίο του διάσημου καθηγητή Μικροβιολογίας, Dr Sucharit Bhakdi και της Βιολόγου -Βιοχημικού, Dr Karina Reiss, «Corona Unmasked», («Ξεμασκαρεμένος Κορωνοϊός»), που αποκαλύπτει την ΕΜΒΟΛΙΑΣΤΙΚΗ ΤΡΕΛΑ της Νέας Παρανοϊκότητας.
Δείτε τι λέει στο βίντεο:
Τα σχόλια περιττά:
May 17
Ένα αντιικό φάρμακο κατά του κορωνοϊού, πέτυχε μείωση έως και 99.9% μείωση του ιικού φορτίου στους πνεύμονες των ποντικών.
Η θεραπεία εμποδίζει τον ιό να αναπαραχθεί επιτιθέμενη κατευθείαν στο γονιδίωμά του, ανέφεραν οι επιστήμονες του Ινστιτούτου Υγείας «Menzies» του πανεπιστημίου Γκρίφιθ της Αυστραλίας και του διάσημου ινστιτούτου City of Hope της Καλιφόρνια.
Σύμφωνα με τους Financial Times, το φάρμακο έχει σχεδιαστεί να αποδίδει τόσο ενάντια στην Sars-Cov-2 καθώς επίσης και έναντι κάθε νέας μετάλλαξης που μπορεί να προκύψει.
Ο κορωνοϊός, το φάρμακο και τα ποντίκια
Ο Νάϊτζελ ΜακΜίλαν, ένας από τους βασικούς ερευνητές του πρότζεκτ, ανέφερε ότι τα νανοσωματίδια που χρησιμοποιήθηκαν για να μεταφέρουν τη θεραπεία μέσα στο σώμα παραμένουν σταθερά στους 4 βαθμούς Κελσίου για 12 μήνες και σε θερμοκρασία δωματίου (παραμένουν σταθερά) για διάστημα άνω του μηνός, εννοώντας ότι το φάρμακο θα μπορούσε να χρησιμοποιηθεί για τη θεραπεία ασθενών χωρίς ιδιαίτερες ανάγκες αποθήκευσης και διανομής.
Μέχρι σήμερα, επιστήμονες από όλο τον κόσμο δεν έχουν καταφέρει να αναπτύξουν ένα αποτελεσματικό αντιϊκό φάρμακο κατά της Covid-19, παρότι κάποιοι από τους υποψήφιους είχαν φτάσει στο στάδιο των κλινικών δοκιμών.
Δύο υποψήφια σκευάσματα, το molnupiravir της εταιρείας Merck και το AT-527 των Roche και Atea, έχουν σημειώσει πρόοδο, με το πρώτο να εισέρχεται στη «φάση 3» και το δεύτερο, το οποίο έχει επιδείξει αντιϊκή δραστηριότητα σε ασθενείς με ηπατίτιδα C, να ακολουθεί σύντομα.
Μια μελέτη του Παγκόσμιου Οργανισμού Υγείας που είχε δημοσιευτεί τον περασμένο Νοέμβριο, πάντως, υποστήριζε ότι το φάρμακο redemsivir, το οποίο χρησιμοποιείται για θεραπεία ασθενών με κορωνοϊό στα νοσοκομεία Βρετανίας και ΗΠΑ, δεν έχει ουσιαστικό αντίκτυπο στις πιθανότητες επιβίωσής τους.
ΠΗΓΗ:https://www.ygeiamasnews.gr/astheneies/epidimies/54674/irthe-to-telos-tis-pandimias-farmako-eksafanise-ton-koronoio-sta-pontikia/
May 17
Στο έγκριτο περιοδικό Stroke δημοσιεύτηκε μία διεθνής, πολυκεντρική μελέτη παρατήρησης με στόχο την καταγραφή των κλινικών και απεικονιστικών χαρακτηριστικών των αγγειακών εγκεφαλικών επεισοδίων (ΑΕΕ) σε έδαφος λοίμωξης από τον ιό SARS-CoV-2.
Στη εκπόνηση της εργασίας αυτής συμμετείχε ο Γεώργιος Τσιβγούλης, Καθηγητής Νευρολογίας του ΕΚΠΑ.
Τη δημοσίευση αυτή σχολιάζουν ο Γεώργιος Τσιβγούλης, Καθηγητής Νευρολογίας του ΕΚΠΑ, ο Σωτήριος Γιαννόπουλος, Καθηγητής Νευρολογίας – Νευροψυχολογίας ΕΚΠΑ και η Νευρολόγος Λίνα Παλαιοδήμου.
Κατά τη διάρκεια της μελέτης ελέγχθηκαν 136 τεταρτοβάθμια κέντρα από 32 χώρες.
Από τους 432 ασθενείς συνολικά:
– οι 323 (74.8%) είχαν ισχαιμικό ΑΕΕ,
-οι 91 (21.1%) είχαν ενδοκράνια αιμορραγία, και,
-οι 18 (4.2%) είχαν θρόμβωση φλεβών, ή φλεβωδών κόλπων εγκεφάλου.
Συνολικά, 183 (42.4%) ασθενείς ήταν γυναίκες, και 104 (24.1%) είχαν ηλικία <55 ετών.
Θα πρέπει να τονιστεί επίσης ότι 105 (24.4%) ασθενείς δεν είχαν κανένα γνωστό αγγειακό παράγοντα κινδύνου.
Το διάμεσο σκορ βαρύτητας του ΑΕΕ, όπως αυτό μετρήθηκε με την κλίμακα NIHSS, ήταν 9 (με εύρος 4-17).
Σε σχέση με την αιτιοπαθογένεση του ΑΕΕ, μεταξύ των ασθενών με ισχαιμικό ΑΕΕ,
-το 44.5% (126 από 283) είχε απόφραξη μεγάλου αγγείου η οποία σχετιζόταν συχνότερα με αθηροθρομβωτικό, ή καρδιοεμβολικό ΑΕΕ, ενώ,
-μόνο το 10% είχε απόφραξη μικρού αγγείου και απεικονιστικά ευρήματα συμβατά με κενοχωριώδες έμφρακτο.
Μεταξύ 380 ασθενών για τους οποίους υπήρχαν αντίστοιχα δεδομένα, οι 144 (37.8%) είχαν ασυμπτωματική λοίμωξη από τον ιό SARS-CoV-2 στην εισαγωγή τους και το μόνο σύμπτωμά τους ήταν ουσιαστικά η εκδήλωση του ΑΕΕ.
Τέλος, η βαρύτητα του ΑΕΕ συσχετίσθηκε ανεξάρτητα με τον κίνδυνο μηχανικής υποστήριξης κατά τη διάρκεια της νοσηλείας των ασθενών με ΑΕΕ & νόσο COVID-19.
Σχετικά με τη διαχείριση των ασθενών με ΑΕΕ και μελετώντας επιπλέον την επίδραση των γεωγραφικών παραγόντων αλλά και του προϋπολογισμού των δαπανών της κάθε χώρας για την υγεία, φάνηκε ότι:
-Στις χώρες με υψηλότερες δαπάνες σε τομείς της υγείας οι ασθενείς είχαν χαμηλότερης βαρύτητας ΑΕΕ (όπως αυτή μετρήθηκε με την κλίμακα NIHSS), ενώ είχαν περισσότερες πιθανότητες να λάβουν μηχανική θρομβεκτομή στην οξεία φάση των ισχαιμικών ΑΕΕ, σε σύγκριση με τις χώρες με χαμηλότερες δαπάνες.
Συμπερασματικά, η εκδήλωση ΑΕΕ σε έδαφος λοίμωξης από τον ιό SARS-CoV-2 παρατηρείται σε σχετικά νεότερους ασθενείς και πιο συχνά σε άνδρες.
Το 1/3 των ασθενών δεν εμφανίζουν άλλα συμπτώματα χαρακτηριστικά για νόσο COVID-19, ενώ, οι περισσότεροι από τους ασθενείς με ισχαιμικό ΑΕΕ εμφανίζουν απόφραξη μεγάλου αγγείου και τυπικά βαρύτερη κλινική εικόνα.
Παρόλα αυτά, οι αυξημένες δαπάνες μιας χώρας και οι επενδύσεις της στον τομέα υγείας, ακόμα και κατά τη διάρκεια της πανδημίας, σχετίζεται με λιγότερο βαριά κλινική εικόνα των ασθενών και καλύτερη αντιμετώπιση στην οξεία φάση.
May 17
Γιατί μας δώσατε την ευκαιρία να θυμηθούμε μέρες από τα παλιά, Σεπτέμβρη του 2011 στη Γερμανία, που δεν θα ξανάρθουν ποτέ πια!
Είσαστε Il Volo αλησμόνητοι!… μια ονειρική μελωδία στην τραγωδία που ζούμε σήμερα…
May 17
Ο πατέρας Σάββας Αχιλλέως τα είχε προβλέψει και δεν τον πιστεύαμε. Δείτε τι σημαίνει αγιοπνευματικός φωτισμός:
May 16
Thrombotic Thrombocytopenia after ChAdOx1 nCov-19 Vaccination
List of authors.
Andreas Greinacher Awarded the Vox Sanguinis Best Paper
Abstract
Background
Several cases of unusual thrombotic events and thrombocytopenia have developed after vaccination with the recombinant adenoviral vector encoding the spike protein antigen of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (ChAdOx1 nCov-19, AstraZeneca). More data were needed on the pathogenesis of this unusual clotting disorder.
Methods
We assessed the clinical and laboratory features of 11 patients in Germany and Austria in whom thrombosis or thrombocytopenia had developed after vaccination with ChAdOx1 nCov-19. We used a standard enzyme-linked immunosorbent assay to detect platelet factor 4 (PF4)–heparin antibodies and a modified (PF4-enhanced) platelet-activation test to detect platelet-activating antibodies under various reaction conditions. Included in this testing were samples from patients who had blood samples referred for investigation of vaccine-associated thrombotic events, with 28 testing positive on a screening PF4–heparin immunoassay.
Results
Of the 11 original patients, 9 were women, with a median age of 36 years (range, 22 to 49). Beginning 5 to 16 days after vaccination, the patients presented with one or more thrombotic events, with the exception of 1 patient, who presented with fatal intracranial hemorrhage. Of the patients with one or more thrombotic events, 9 had cerebral venous thrombosis, 3 had splanchnic-vein thrombosis, 3 had pulmonary embolism, and 4 had other thromboses; of these patients, 6 died. Five patients had disseminated intravascular coagulation. None of the patients had received heparin before symptom onset. All 28 patients who tested positive for antibodies against PF4–heparin tested positive on the platelet-activation assay in the presence of PF4 independent of heparin. Platelet activation was inhibited by high levels of heparin, Fc receptor–blocking monoclonal antibody, and immune globulin (10 mg per milliliter). Additional studies with PF4 or PF4–heparin affinity purified antibodies in 2 patients confirmed PF4-dependent platelet activation.
Conclusions
Vaccination with ChAdOx1 nCov-19 can result in the rare development of immune thrombotic thrombocytopenia mediated by platelet-activating antibodies against PF4, which clinically mimics autoimmune heparin-induced thrombocytopenia. (Funded by the German Research Foundation.)
Vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are the most important countermeasure to fight the coronavirus 2019 (Covid-19) pandemic. From December 2020 through March 2021, the European Medicines Agency approved four vaccines on the basis of randomized, blinded, controlled trials: two messenger RNA–based vaccines — BNT162b2 (Pfizer–BioNTech) and mRNA-1273 (Moderna) — that encode the spike protein antigen of SARS-CoV-2, encapsulated in lipid nanoparticles; ChAdOx1 nCov-19 (AstraZeneca), a recombinant chimpanzee adenoviral vector encoding the spike glycoprotein of SARS-CoV-2; and Ad26.COV2.S (Johnson & Johnson/Janssen), a recombinant adenovirus type 26 vector encoding SARS-CoV-2 spike glycoprotein.
As of April 7, 2021, more than 82 million vaccine doses had been administered in the European Union; in Germany, approximately one quarter of vaccine recipients had received the ChAdOx1 nCov-19 vaccine.1 Beginning in late February 2021, several cases of unusual thrombotic events in combination with thrombocytopenia were observed in patients after vaccination with ChAdOx1 nCov-19.
Index Case
A previously healthy 49-year-old health care worker received her first dose of ChAdOx1 nCov-19 in mid-February 2021 (day 0). Over the next few days, she reported having minor symptoms (fatigue, myalgia, and headache). Beginning on day 5, she reported having chills, fever, nausea, and epigastric discomfort; she was admitted to a local hospital on day 10.
Table 1.
Laboratory Characteristics of the Index Patient.
Laboratory results are shown in Table 1. The platelet count was 18,000 per cubic millimeter, and the d-dimer level was 35 mg per liter (reference value, <0.5). The results of other blood tests were normal except for γ-glutamyltransferase and C-reactive protein levels, which were elevated. SARS-CoV-2 reverse-transcriptase–polymerase-chain-reaction assay of a nasopharyngeal swab was negative.
Computed tomography (CT) showed portal-vein thrombosis and peripheral pulmonary emboli. The patient received a platelet concentrate and was transferred to a tertiary hospital. On arrival, she had epigastric discomfort and nausea but was otherwise in good condition (blood pressure, 125/88 mm Hg; heart rate, 65 beats per minute; temperature, 36.5°C). The physical examination was unremarkable except for moderate epigastric pain on palpation. She received intravenous antibiotics, analgesia, and one 4000-unit dose of low-molecular-weight heparin (enoxaparin), given subcutaneously.
The following day, the platelet count and fibrinogen level remained low, and the d-dimer and aminotransferase levels increased. The abdominal pain worsened, and repeat CT imaging showed progression of portal-vein thrombosis to include the splenic and upper mesenteric veins; in addition, small thrombi were visualized in the infrarenal aorta and both iliac arteries. Low-dose intravenous unfractionated heparin (500 IU per hour) was initiated but was stopped shortly thereafter because of a sudden onset of tachycardia and concern for gastrointestinal bleeding. The lactate level was 3.7 mmol per liter, and the patient was transferred to the intensive care unit. Repeat CT imaging revealed diffuse gastrointestinal bleeding with reduced perfusion of the intestinal wall and pancreas by splanchnic-vein thrombosis, along with ascites. She received red-cell and platelet transfusions, prothrombin complex concentrates, and recombinant factor VIIa but died on day 11. In addition to the diagnosed medical findings, autopsy revealed cerebral venous thrombosis.
Case Series
Table 2. Clinical and Laboratory Summary of 11 Patients with Available Clinical Information.
By March 15, 2021, an additional 10 patients for whom clinical data were available were found to have one or more thrombotic complications beginning 5 to 16 days after vaccination with ChAdOx1 nCov-19. Characteristics of all 11 patients (including the index case) are presented in Table 2. Thrombotic events included cerebral venous thrombosis (in 9 patients), splanchnic-vein thrombosis (in 3 patients), pulmonary embolism (in 3 patients), and other types of thrombi (in 4 patients); 5 of 10 patients had more than one thrombotic event. Included in this analysis is one patient (Patient 11) who presented with fatal cerebral hemorrhage. The results of brain neuropathological analysis were pending at the time of this report, and cerebral venous thrombosis had not been ruled out; postmortem serum was available for testing for platelet-activating antibodies.
Among these patients, the median age was 36 years (range, 22 to 49); 9 of 11 were women. All the patients presented with concomitant thrombocytopenia (median nadir of platelet count, approximately 20,000 per cubic millimeter; range, 9000 to 107,000). One patient had preexisting von Willebrand disease, anticardiolipin antibodies, and factor V Leiden. None of the patients had received heparin before the onset of symptoms or the diagnosis of thrombosis. Given the striking clinical resemblance of this disorder to autoimmune heparin-induced thrombocytopenia (a prothrombotic thrombocytopenic disorder that can be triggered by heparin and certain other anions and that features heparin-independent platelet-activating properties), serum obtained from 4 of the 11 patients was referred for immediate investigation of platelet-activating antibodies directed against platelet factor 4 (PF4)–heparin. After characterizing the antibodies in serum obtained from Patients 1 through 4, we subsequently obtained serum from 5 of the 7 remaining patients. In addition, our reference laboratory received further serum samples from patients who were suspected of having prothrombotic thrombocytopenia related to ChAdOx1 nCov-19 vaccination. (No detailed clinical information regarding these patients was available at the time of this report.)
Methods
We purified platelets from whole blood (obtained from healthy volunteers) that had undergone anticoagulation with adenine citrate dextrose solution A. None of the volunteers had been taking antiplatelet drugs or had been vaccinated in the previous 10 days. We prepared platelets using methods that have been described previously.2,3 In a subgroup of experiments, platelets were preincubated in buffer with ChAdOx1 nCov-19 (1:2000 dilution) and washed before use. Washed platelets (75 microliters) were incubated with either buffer, a low-molecular-weight heparin (reviparin [Abbott]), or PF4 (Chromatec) in either the presence or absence of the FcγIIa receptor–blocking antibody IV.3. In some experiments, unfractionated heparin (100 IU per milliliter) was added to inhibit PF4-dependent reactions, or ChAdOx1 nCov-19 (1:50 dilution) was added per well. Serum was coincubated with PF4 and platelets in the presence of immune globulin (Privigen IVIG [CSL Behring]) at a concentration of 10 mg per milliliter. After establishing assay conditions using serum from the initial four patients, we investigated another 24 serum samples that tested positive on immunoassay to validate our findings. We refer to this modified platelet-activation test as the PF4-enhanced platelet-activation test.
To measure direct antibody binding, we used two immunoassays, a PF4–heparin enzyme-linked immunosorbent assay (ELISA) and a PF4 ELISA, with antibody binding measured by a secondary antihuman IgG, as described previously.4 In addition, antibodies from two serum samples were affinity purified by immobilized PF4–heparin and immobilized PF4, and the purified antibodies were tested in the assays. (Details about this method are provided in the Supplementary Appendix, available with the full text of this article at NEJM.org.)
We defined reactivity on ELISA according to the optical-density units as strong (≥2.00), intermediate (1.00 to 1.99), or weak (0.50 to 0.99). On the PF4-enhanced platelet-activation test, reactivity was graded according to the time that had elapsed until platelet aggregation,5 with shorter reaction times indicating stronger platelet activation (strong activation, 1 to 5 minutes; intermediate activation, >5 to 15 minutes; and weak activation, >15 to 30 minutes).
Results
All 11 patients in the initial analysis had moderate-to-severe thrombocytopenia and unusual thrombosis, particularly cerebral venous thrombosis and splanchnic-vein thrombosis (Table 2). We also found evidence of disseminated intravascular coagulation in 5 of the patients on the basis of the combination of greatly elevated d-dimer levels (>10.0 mg per liter) and one or more abnormalities in the international normalized ratio, partial thromboplastin time, or fibrinogen level. (Of the 6 patients with available fibrinogen levels, 4 had hypofibrinogenemia.)
Although evaluating the outcomes of different management strategies was not the goal of our study, we noted with interest the clinical course of Patient 2, who presented with pulmonary embolism and mild thrombocytopenia (platelet count, 107,000 per cubic millimeter), without disseminated intravascular coagulation. This patient received therapeutic-dose low-molecular-weight heparin for 3 days, with clinical improvement and an increase in the platelet count to 132,000; at that time, a positive result on PF4–heparin ELISA was obtained, and the patient was switched to oral apixaban, with continued clinical and laboratory recovery.
Figure 1. Reactivity of Patient Serum on Platelet-Activation Assays and Immunoassays.
Table 2 also shows results of the PF4–heparin ELISA, including for the first 4 patients in whom detailed laboratory studies were performed. Serum obtained from these patients showed strong reactivity on PF4–heparin ELISA, with optical densities of more than 3.00 units (reference value, <0.50); all reactivity reactions were inhibited to less than 0.50 units by the addition of heparin (100 IU per milliliter). Figure 1 shows the serologic profile of the 4 initial patients, as assessed by means of the platelet-activation assay. Three of the four serum samples showed weak-to-moderate reactivity at buffer control, which was inhibited by low-molecular-weight heparin. In three of the samples, PF4 (10 μg per milliliter) greatly enhanced reactivity; serum from Patient 2 subsequently showed strong platelet activation in the presence of PF4 when retested along with platelets from other volunteers. All reactions were blocked by monoclonal antibody IV.3 and immune globulin at a dose of 10 mg per milliliter, which indicated that platelet activation had occurred through platelet Fcγ receptors (Figure 1A). None of the controls showed platelet activation (data not shown).
Platelet activation was enhanced when platelets were pelleted from platelet-rich plasma, resuspended in washing buffer, preincubated (1:2000) with ChAdOx1 nCov-19, centrifuged, and resuspended in the final suspension buffer or when they were coincubated in the suspension buffer with ChAdOx1 nCov-19 (1:50). The monoclonal antibody IV.3 blocked PF4-dependent platelet activation in all 7 samples that were tested.
Figure 1B shows the results of platelet activation in serum samples obtained from 24 patients with clinically suspected vaccine-induced immune thrombotic thrombocytopenia who tested positive on the screening PF4–heparin ELISA. Whereas approximately half the serum samples (13 of 24) showed platelet activation at buffer control, most samples (19 of 24) were inhibited by low-molecular-weight heparin; almost all samples (22 of 24) showed platelet activation by the addition of PF4. All but one serum sample was inhibited by a high dose of heparin.
Figure 1C shows strong reactivity of the serum samples obtained from all 28 patients (including Patients 1, 2, 3, 4, 5, 8, 9, 10, and 11) in results on both PF4–heparin and PF4 ELISA, with inhibition by high heparin doses. Antibodies that were affinity purified with the use of either immobilized PF4 or immobilized PF4–heparin showed the same reactivity pattern as the original serum — in other words, they strongly activated platelets in the presence of 10 μg per milliliter of PF4, an effect that was completely inhibited by a high concentration of heparin.
Discussion
The clinical picture of moderate-to-severe thrombocytopenia and thrombotic complications at unusual sites beginning approximately 1 to 2 weeks after vaccination against SARS-CoV-2 with ChAdOx1 nCov-19 suggests a disorder that clinically resembles severe heparin-induced thrombocytopenia, a well-known prothrombotic disorder caused by platelet-activating antibodies that recognize multimolecular complexes between cationic PF4 and anionic heparin.6 However, unlike the usual situation in heparin-induced thrombocytopenia, these vaccinated patients did not receive any heparin to explain the subsequent occurrence of thrombosis and thrombocytopenia.
In recent years, it has been recognized that triggers other than heparin can cause a prothrombotic disorder that strongly resembles heparin-induced thrombocytopenia on both clinical and serologic grounds, including certain polyanionic drugs (e.g., pentosan polysulfate,7 antiangiogenic agent PI-88,8 and hypersulfated chondroitin sulfate8). Such a prothrombotic syndrome has also been observed in the absence of preceding exposure to any polyanionic medication, such as after both viral and bacterial infections9,10 and knee-replacement surgery.11,12 These various clinical scenarios with apparent nonpharmacologic triggers have been classified under the term autoimmune heparin-induced thrombocytopenia.13 Unlike patients with classic heparin-induced thrombocytopenia, patients with autoimmune heparin-induced thrombocytopenia have unusually severe thrombocytopenia, an increased frequency of disseminated intravascular coagulation, and atypical thrombotic events. Serum from these patients strongly activate platelets in the presence of heparin (0.1 to 1.0 IU per milliliter) but also in the absence of heparin (heparin-independent platelet activation). When these unusual antibodies are observed in patients who have thrombocytopenia without preceding heparin exposure, the term “spontaneous” heparin-induced thrombocytopenia syndrome13,14 has been used. Sometimes, patients in whom heparin-induced thrombocytopenia develops after exposure to heparin present with atypical clinical features, such as an onset of thrombocytopenia beginning several days after stopping heparin (delayed-onset heparin-induced thrombocytopenia15,16) or thrombocytopenia that persists for several weeks despite the discontinuation of heparin (persisting or refractory heparin-induced thrombocytopenia17,18). Serum from these patients also shows the phenomenon of heparin-independent platelet-activating properties.
These clinical features that resemble those of autoimmune heparin-induced thrombocytopenia were observed in the patients with vaccine-induced immune thrombotic thrombocytopenia. The serum usually showed strong reactivity on the PF4–heparin ELISA. Moreover, serum showed variable degrees of platelet activation in the presence of buffer that was in most cases greatly enhanced in the presence of PF4 (Figure 1A and 1B). More strikingly, most serum showed inhibition, rather than increased activation, in the presence of low-dose low-molecular-weight heparin (0.2 U per milliliter of anti–factor Xa). In addition, antibodies from two patients, which were affinity purified on either immobilized PF4 or immobilized PF4–heparin, strongly activated platelets but only in the presence of PF4. Enhancement of platelet activation by PF4 is also a feature of heparin-induced thrombocytopenia19,20 and has been used to enhance detection of platelet-activating antibodies in diagnostic testing for this adverse drug reaction.21 Whether these antibodies are autoantibodies against PF4 induced by the strong inflammatory stimulus of vaccination or antibodies induced by the vaccine that cross-react with PF4 and platelets requires further study.
Although we found enhanced reactivity of patient serum with platelets in the presence of ChAdOx1 nCov-19, this is likely to be an in vitro artifact. It is well known that adenovirus binds to platelets22 and causes platelet activation.22,23 Furthermore, the amount of adenovirus in a 500-microliter vaccine injection administered 1 or 2 weeks earlier would seem unlikely to contribute to subsequent platelet activation observed in these patients. However, interactions between the vaccine and platelets or between the vaccine and PF4 could play a role in pathogenesis. One possible trigger of these PF4-reactive antibodies could be free DNA in the vaccine. We have previously shown that DNA and RNA form multimolecular complexes with PF4, which bind antibodies from patients with heparin-induced thrombocytopenia and also induce antibodies against PF4–heparin in a murine model.24 Unfortunately, other Covid-19 vaccines were not available to us for testing.
Our findings have several important clinical implications. First, clinicians should be aware that in some patients, venous or arterial thrombosis can develop at unusual sites such as the brain or abdomen, which becomes clinically apparent approximately 5 to 20 days after vaccination. If such a reaction is accompanied by thrombocytopenia, it can represent an adverse effect of the preceding Covid-19 vaccination. To date, this reaction has been reported only with the ChAdOx1 nCov-19 vaccine, which has been used in approximately 25% of vaccine recipients in Germany and in 30% of those in Austria.
Second, ELISA to detect PF4–heparin antibodies in patients with heparin-induced thrombocytopenia is widely available and can be used to investigate patients for potential postvaccination thrombocytopenia or thrombosis associated with antibodies against PF4.25 A strongly positive ELISA result that is obtained in a patient who has not been recently exposed to heparin would be a striking abnormality.
Third, we have shown that these antibodies recognize PF4 and that the addition of PF4 greatly enhances their detectability in a platelet-activation assay. Since vaccination of millions of persons will be complicated by a background of thrombotic events unrelated to vaccination, a PF4-dependent ELISA or a PF4-enhanced platelet-activation assay may be used to confirm the diagnosis of vaccine-induced immune thrombotic thrombocytopenia through this novel mechanism of postvaccination formation of platelet-activating antibodies against PF4. Although treatment decisions such as administering intravenous immune globulin and starting anticoagulation do not need to await laboratory diagnosis, detection of these unusual platelet-activating antibodies will be highly relevant for case identification and future risk–benefit assessment of this and other vaccines.
Figure 2.
Potential Diagnostic and Therapeutic Strategies for Management of Suspected Vaccine-Induced Immune Thrombotic Thrombocytopenia.
Figure 2 shows a potential diagnostic and therapeutic strategy for managing this novel prothrombotic thrombocytopenic disorder. One consideration is to administer high-dose intravenous immune globulin to inhibit Fcγ receptor–mediated platelet activation. This recommendation parallels emerging experience in the treatment of severe autoimmune heparin-induced thrombocytopenia in which high-dose intravenous immune globulin has resulted in rapid increases in platelet count and de-escalation of hypercoagulability.12,26 We found that the addition of immune globulin in doses that are readily achieved clinically was effective in inhibiting platelet activation by patients’ antibodies. Clinician reluctance to start anticoagulation may be tempered by administering high-dose intravenous immune globulin to raise the platelet count, especially when a patient presents with severe thrombocytopenia and thrombosis, such as cerebral venous thrombosis.
Given the parallels with autoimmune heparin-induced thrombocytopenia, anticoagulant options should include nonheparin anticoagulants used for the management of heparin-induced thrombocytopenia,27 unless a functional test has excluded heparin-dependent enhancement of platelet activation. Finally, we suggest naming this novel entity vaccine-induced immune thrombotic thrombocytopenia (VITT) to avoid confusion with heparin-induced thrombocytopenia.
Supported by a grant (374031971–TRR 240) from the German Research Foundation.
Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.
Drs. Greinacher and Thiele contributed equally to this article.
This article was published on April 9, 2021, at NEJM.org.
We thank the colleagues who provided serum samples for this study, including Dr. Michael Hirschl of Landesklinikum Zwettl, Austria; Dr. Johannes Thaler of the Medical University of Vienna; Dr. Brigitte Keller-Stanislawski, Dr. Dirk Mentzer, and Prof. Dr. Klaus Cichutek of the Paul-Ehrlich-Institut, Langen, Germany; and Prof. Dr. Hans-Georg Bone, Dr. Juliane Alfes, and Dr. Hans-Christian Atzpodien of Klinikum Vest, Recklinghausen; technologists Ulrike Strobel, Carmen Freyer, Katrin Stein, Ines Warnig, and Ricarda Raschke of Transfusion Medicine Greifswald; and the members of the council of the Gesellschaft für Thrombose und Hämostaseforschung (Prof. Dr. Johannes Oldenburg, Dr. Robert Klamroth, Prof. Dr. Florian Langer, and Prof. Dr. Bernd Pötzsch) for their support.
Author Affiliations
From Institut für Immunologie und Transfusionsmedizin, Universitätsmedizin Greifswald, Greifswald (A.G., T.T.), and the Division of Safety of Medicinal Products and Medical Devices, Paul-Ehrlich-Institut (Federal Institute for Vaccines and Biomedicines), Langen (K.W.) — both in Germany; the Departments of Pathology and Molecular Medicine and of Medicine, McMaster University, Hamilton, ON, Canada (T.E.W.); and the Department of Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Vienna (P.A.K., S.E.).
Address reprint requests to Dr. Greinacher at Institut für Immunologie und Transfusionsmedizin, Abteilung Transfusionsmedizin, Sauerbruchstrasse, 17487 Greifswald, Germany.
https://www.nejm.org/doi/10.1056/NEJMoa2104840
NEJ means New England Journal of Medicine
May 16
https://www.youtube.com/watch?v=HQdZfzcTWyk
Ασφαλώς και το έκοψαν οι φασίστες του Youtube.
May 15
ΔΙΕΘΝΗ. ΥΓΕΙΑ. – 16 Μαΐ 2021 – 8:57
Ο Γερμανός ερευνητής, Andreas Greinacher, υποστηρίζει ότι ανακάλυψε το αίτιο της σπάνιας πρόκλησης θρόμβων από το εμβόλιο κατά του Covid-19 της AstraZeneca.
Ο Andreas Greinacher του University of Greifswald ισχυρίζεται ότι ένα συντηρητικό και κάποιες πρωτεΐνες που εντόπισε στο εμβόλιο προκαλούν μια αυτοάνοση αντίδραση του οργανισμού, η οποία οδηγεί στη δημιουργία θρόμβων.
Ο Greinacher και οι συνεργάτες του, σύμφωνα με τη «Wall Street Journal», μόλις άρχισε να αναλύει το εμβόλιο της Johnson & Johnson, ωστόσο έχει ολοκληρώσει την μελέτη του εμβολίου της AstraZeneca.
Η ερευνητική ομάδα υποστηρίζει ότι μέσα από πειράματα σε ποντικούς κατέληξε στο συμπέρασμα ότι σπανίως η ουσία EDTA έχει ως αποτέλεσμα να διαχυθούν ανεξέλεγκτα στην κυκλοφορία του αίματος οι 1.000 πρωτεΐνες, που ενώνονται με τα αιμοπετάλια.
Αυτό έχει ως συνέπεια να ενεργοποιείται το ανοσοποιητικό σύστημα, το οποίο απελευθερώνει την πρωτεΐνη PL4 και αντισώματα για να «καθαρίσει» τα αιμοπετάλια.
Ωστόσο η PL4 προκαλεί την ένωση των αιμοπεταλίων που είναι συνδεδεμένα με τις πρωτεΐνες, με τα αντισώματα και την έναρξη της δημιουργίας θρόμβων. Για να τους καταστρέψει το ανοσοποιητικό σύστημα, στέλνει άλλα αντισώματα, με αποτέλεσμα ο θρόμβος να μεγαλώνει.
pronews.gr and https://www.triklopodia.gr/%ce%b5%ce%bc%ce%b2%cf%8c%ce%bb%ce%b9%ce%bf-astrazeneca-%ce%b3%ce%b5%cf%81%ce%bc%ce%b1%ce%bd%cf%8c%cf%82-%ce%b5%cf%80%ce%b9%cf%83%cf%84%ce%ae%ce%bc%ce%bf%ce%bd%ce%b1%cf%82-%cf%85%cf%80%ce%bf%cf%83/
May 14
Coping with Mental Health Challenges During COVID-19
Chapter
First Online: 30 April 2020
Part of the Medical Virology: From Pathogenesis to Disease Control book series (MVPDC)
Abstract
The ongoing pandemic of COVID-19 is a global challenge which resulted in significant morbidity and mortality worldwide. It has also adversely affected the economy and social integrity. There is rising concern about the mental health challenges of the general population, COVID-19-infected patients, close contacts, elderly, children and health professionals. This chapter focusses on various mental health challenges during the COVID-19 pandemic.
Keywords
COVID-19 Mental health Coping Pandemic
Sujita Kumar Kar and Shailendra K. Saxena contributed equally as first author.
Download chapter PDF
16.1 Introduction
There is a major health crisis going on in the world currently. A newly emerged zoonotic viral infection known as novel coronavirus disease (COVID-19) is affecting people, globally taking the form of a pandemic. Over the past few months, there is a significant increase in mortality and morbidity due to this pandemic. Till date (29 March 2020), there are more than 680,000 total cases with 31,920 deaths, 146,396 recovered over 202 countries (COVID-19 Coronavirus Pandemic 2020). As per the situation report of the World Health Organization (WHO), by the end of 28 March 2020, more than half of the global deaths and infected cases were from the European region (World Health Organization 2020a). As the disease is spreading in a rapid pace, most of the affected countries are not able to meet the demands of the personal protective equipment (PPE) and infrastructure requirement (World Health Organization 2020a). At the current stage, the major objectives laid by the WHO are prevention of human-to-human transmission, limiting the spread of infection to close contacts and medical professionals, preventing the development of complications in infected persons, isolation and quarantine facility provision, availing diagnostic and laboratory facility, research to produce specific treatment and vaccine and minimizing the socioeconomic impact on the community (World Health Organization 2020a). It has been noticed over the past few months that during this outbreak of COVID-19 infection, there are increasing mental health issues among the general population, elderly, children, migrant workers and healthcare professionals other than the patients with COVID-19 infection (Duan and Zhu 2020; Chen et al. 2020; Liem et al. 2020; Yang et al. 2020a, b). To date there are no specific recommendations from international bodies regarding addressing the mental health issues during this COVID-19 pandemic.
16.2 Impact of COVID-19 in Society
The global impact of COVID-19 has been profound, and the public health threat due to this is the most serious seen since the 1918 H1N1 influenza pandemic. The overall case fatality rate of COVISD-19 was 2.3% in China and could be variable in different countries (Novel Coronavirus Pneumonia Emergency Response Epidemiology Team 2020; Livingston and Bucher 2020). A nationwide analysis done in China showed that comorbidities are present in around one-fourth of patients with COVID-19 and predispose to poorer clinical outcomes (Novel Coronavirus Pneumonia Emergency Response Epidemiology Team 2020). The impact of the disease is beyond mortality, and morbidity has become apparent since the outbreak of the pandemic. A large population throughout the world is certain to have a massive psychological impact as evidenced by a preliminary report from China where among 1210 respondents more than half of the respondents rated the psychological impact as moderate-to-severe and about one-third reported moderate-to-severe anxiety (Wang et al. 2020a). Studies post-SARS pandemic or post-Ebola indicate that even after recovering physically from the disease, individuals suffered from social and psychological problems and similar could be the impact with this pandemic (Bobdey and Ray 2020). Evidence suggests that vulnerable groups who are confined to their homes during a pandemic can have negative health outcomes. Children especially become physically less active and have much longer screen time, irregular sleep patterns and less favourable diets, resulting in weight gain and a loss of cardiorespiratory fitness (Wang et al. 2020b). Also, there are other direct and indirect implications of the closure of schools like unintended childcare obligations, which are particularly large in healthcare occupations (Bayham and Fenichel 2020). This could be related to the current situation in most of the countries throughout the world not only in child care but also in the adult and geriatric population (Heckman et al. 2020).
COVID-19 is a supply shock and a demand shock. Both the aspects will impact on aggregate trade flow (Baldwin and Tomiura 2020). It has both direct and indirect economic implications. The stocks and flow of physical and financial assets are interrupted. An increase in health budget and a lowering of overall GDP is sure to impact the whole world (McKibbin and Fernando 2020). Another area of impact would be travel and tourism. In the current scenario, the travel of any citizen of any country has been virtually been stopped. Also, even once the pandemic is over, it is almost certain to take a long time before people become confident of travel (Anzai et al. 2020; Dinarto et al. 2020).
Stigma and fear are other aspects of the outbreak of a pandemic. It can present major barriers against healthcare seeking, social marginalization, distrust in health authorities and distortion of public perceptions of risk, resulting in mass panic among citizens and the disproportionate allocation of healthcare resources by politicians and health professionals (Barrett and Brown 2008).
Impact on the sports and other mass gatherings throughout the world cannot be ignored (Gallego et al. 2020). Within weeks of the emergence of this pandemic in China, there have been circulation of misinformation, misleading rumours and conspiracy theories about the origin paired with fear mongering, racism and compulsive buying and stocking of goods and face masks. This can be attributed to impact the social media has created (Depoux et al. 2020). Over all the pandemic will have impact in all domains of the current world starting from health, society and economy and would also impact the future policy making at global, regional and country level (Djalante et al. 2020).
16.3 Emerging Mental Health Issues in COVID-19 Pandemic
The COVID-19 pandemic is a global emergency situation while the diagnosis of specific disorders needs a specific time period which is a major constraint to quantify the mental health issues. Moreover, many of the survivors may develop mental disorders long after the event. Therefore, multiple and complex confounding variables makes the issue hazy. Fortunately, studies evaluating the mental health issue have been coming out gradually which needs more time certainly to get replicable findings.
16.3.1 Among General Population
As the COVID-19 pandemic has been spreading rapidly across the globe, the foremost mental health issue has raised the level of stress or anxiety expressed in public mental health term (Dong and Bouey 2020). Inadequate knowledge regarding the incubation period of the virus, route of transmission, treatment and safety measures cause fear and anxiety (Li et al. 2020; Ho et al. 2020; Goyal et al. 2020). The locked-down state bounds residents to become homebound which causes negative mental health outcomes like anxiety states and insecurity regarding the future (Li et al. 2020). The citizens also feel monotony, disappointment and irritability under the locked-down state (Ho et al. 2020). One study reported severe and wide spectrum mental health impacts of the pandemic (Goyal et al. 2020). The event can precipitate new mental disorders and exacerbate the previously present disorders (Goyal et al. 2020). The general population can experience fear and anxiety of being sick or dying, helplessness, blame the people who are already affected and precipitate the mental breakdown (Goyal et al. 2020). A wide range of psychiatric disorders can be found such as depressive disorders, anxiety disorders, panic disorder, somatic symptoms, self-blame, guilt, posttraumatic stress disorder (PTSD), delirium, psychosis and even suicide (Goyal et al. 2020; Yi et al. 2020).
16.3.2 Among COVID-19 Cases
The suspected and/or confirmed COVID-19 persons largely experience fear regarding the high contagiousness and fatality (Wang et al. 2020a; Li et al. 2020). The quarantined people feel boredom, loneliness, anger, depression, anxiety, denial, despair, insomnia, harmful substance use, self-harm and suicidality (Wang et al. 2020a; Dong and Bouey 2020; Li et al. 2020; Yi et al. 2020). The survivors are the high-risk people to develop a wide range of mental disorders such as depression, anxiety and PTSD (World Health Organization 2020a). As a continuation of safety behaviours, patients may develop obsessive-compulsive disorder (OCD) (Li et al. 2020). Moreover, physical symptoms of COVID-19 such as fever, hypoxia and cough along with adverse effects of prescribed medications (corticosteroids) may cause more anxiety and mental distress (Wang et al. 2020a). A recent study of 1210 participants from 194 cities in China reported that 53.8% had a moderate or severe psychological impact, 31.3% had some sort of depression, 36.4% had some sort of anxiety and 32.4% had some sort of stress (Liu et al. 2020). Poor or very poor self-rated health status was significantly associated with a greater psychological impact of the COVID-19 (Liu et al. 2020).
16.3.3 Among Family Members and Close Contacts
Along with the persons with COVID-19, the family members and close contacts face psychological problems as they have been traced, isolated or quarantined which makes people anxious and guilty regarding the aftermath of the contagion, quarantine and stigma on their family members and friends (Wang et al. 2020a). The family members who lose their loved ones from the pandemic results in anger and resentment (Goyal et al. 2020). Furthermore, they also feel shame, guilt or stigma for those family members who are sick and/or quarantined, and some studies reported PTSD and depression among the family members and close contacts (Goyal et al. 2020). On the other hand, the children who have been isolated or quarantined during the pandemic have higher chances to develop acute stress disorder, adjustment disorder and grief (Shah et al. 2020). PTSD was reported among 30% of the children and early loss of or separation from parents during childhood also has long-term adverse effects on mental health, including higher chances of developing mood disorders, psychosis and suicidality (Shah et al. 2020).
16.3.4 Among Healthcare Workers
As pandemics are the global public mental health emergency, healthcare services demand increases sharply. Furthermore, many countries do not have adequate manpower as well as resources to cope with COVID-19. Thus, healthcare providers have to face an increased workload with the fear of being infected. Many times, they have been quarantined frequently when they contact COVID-19-confirmed persons.
Increased workload, isolation and discrimination are common which result in physical exhaustion, fear, emotional disturbance and sleep disorders (Ho et al. 2020). A recent study involving 1563 health professionals reported that more than half (50.7%) of the participants reported depressive symptoms, 44.7% anxiety and 36.1% sleep disturbance (Ho et al. 2020). Moreover, there are not adequate services to provide counselling and psychiatric screening services for anxiety, depression and suicidality for physicians who have been dealing with infected persons (World Health Organization 2020b). It is also meaningful to postulate that many physicians develop PTSD, depression, anxiety and burnout after the cessation of the pandemic (World Health Organization 2020b). Along with the physicians, the frontline healthcare providers (FHCP) can develop mental disorders such as depression, anxiety and PTSD (Li et al. 2020). Previous articles reported that FHCP (paramedics, ambulance personnel and healthcare workers) have also shown heightened stress and emotional disturbances and have higher levels of depression and anxiety (Goyal et al. 2020).
This is estimated as the chances of getting infected is much higher with the risk of exposure which creates a fear of transmission to their loved ones and children. Furthermore, the conflict professionalism and personal fear for oneself causes burnouts and physical and mental symptoms (Goyal et al. 2020).
16.3.5 Among Special Population (Old Age and Co-morbidities)
As this pandemic has been spreading rapidly across the world, it is bringing a considerable degree of fear, worry and concern among few certain groups particularly, in older adults and people with underlying comorbid disorders (Dong and Bouey 2020). It has a potential impact on the existing diseases, and the affected persons may lead to psychiatric symptoms which possibly related to the interplay of mental disorders and immunity (World Health Organization 2020b). The symptoms of COVID-19 can also worsen cognitive distress and anxiety among people who have poor mental capabilities previously (World Health Organization 2020b).
Patients with pre-existing severe mental illness (SMI) have been inevitably affected by the pandemic (Ho et al. 2020). In-patients, especially those requiring long-term hospitalization in closed wards, pose a high risk of cluster contagion. Due to traffic restrictions and isolation measures, outpatients with SMI are facing difficulties to receive maintenance treatment and may thus end up with mental relapse and uncontrollable situations (Ho et al. 2020). Patients with chronic physical illness (e.g., chronic renal failure, diabetes mellitus and cardio-cerebrovascular diseases) also need regular follow-up in hospitals which become problematic and raise the chances of deterioration.
16.4 Coping with Mental Health Issues During COVID-19 Pandemic
While the healthcare sector and government officials from all over the world is focusing on the control of the pandemic adopting various preventive strategies, there is little attention provided to the mental health status of the isolated, panicked and house-arrested people. Due to lack of regular social activities and staying at home for a longer time will impact their emotional well-being. Research has also shown that sudden outbreak can worsen the mental health conditions of those with pre-existing mental health illness (Ho et al. 2020).
To avoid a distressing situation, individuals should not get exposed to media coverage too much, to maintain a healthy relationship, get in touch with friends and family members on a regular interval using social media and start thinking positively (CDC 2020). If coronavirus anxiety shows up, try to share the fear with others, which will calm the fear, and also try to increase self-awareness by getting adequate sleep, exercising regularly and employing different relaxation techniques (Kecmanovic 2020). As recommended by Ho et al. (2020) in this era of technology, healthcare services can introduce providing online psychological support services for those individuals who lost their close relatives due to COVID-19 (Ho et al. 2020). To support the morale and mental health of the frontline healthcare professionals, healthcare organizations should introduce shorter working periods, regular breaks and rotating shifts (Ho et al. 2020). People can cope with the mental health challenges by adopting various lifestyle-related measures (Figs. 16.1 and 16.2).
Fig. 16.1
Summary of coping measures during COVID-19 pandemic
Fig. 16.2
Tips for positive mental health during COVID-19 pandemic
16.5 Myths and Facts About COVID-19
During a new infectious disease outbreak, a great deal of uncertainty remains from the pattern of transferring, risk factors involved and prevention and treatment (Schuchat et al. 2011). Rumours and myths create more panic among the general public as they are malevolent in nature and can alter people’s observations towards the disease. The world is witnessing the same for the new public health crises with the emergence and spread of 2019 novel coronavirus. When the disease originated from Wuhan city of China, it was declared as a second-class infectious disease, but most of the areas of the country adopted the first level of response measure to control, and the measures were taken has no scientific basis and no effective outcomes were recorded after applying those measures by the China government (Xiao and Torok 2020).
The virus cannot be killed by cold and snow, and it can be transmitted in areas with hot and humid climate (WHO 2020). People of all age groups are susceptible to get infected with COVID-19. Elderly people with underlying health conditions such as diabetes, heart disease and asthma are more vulnerable (Fong 2020). Although there is no significant number of paediatric cases so far, children are vulnerable to the infection (Hong et al. 2020), and to date, there is no evidence of vertical transmission of this infection (Baud et al. 2020).
Several national and international newspapers, tabloids and media channels all over the world are reporting that the smokers are prone to catch coronavirus infection due to weakened lungs and will put the smokers at risk (Mullin 2020). However, a recent systematic review finding revealed that no significant association is found between active smoking and the severity of COVID 19 (Lippi and Henry 2020).
There are reports of using oseltamivir, lopinavir/ritonavir, prednisone, antibiotics, and traditional Chinese medicine for the treatment of patients with COVID-19. Again, there is no scientific evidence to support that they will be effective against COVID-19 apart from scrupulous personal care such as the use of personal protection precaution to reduce the risk of transmission, early diagnosis, isolation and supportive treatments for affected patients (Xiao and Torok 2020; Wang et al. 2020c).
There is also some misconception among the general people that by taking hot bath, people will not get infected with the infection or spraying alcohol or chlorine all over the body can kill the infection (WHO 2020). Proper public health information should be provided, based on scientific research to general people to reduce stress and anxiety, otherwise it will be difficult to implement control measures.
16.6 Precautionary Measures and Recommendations
No definite treatment is available for the treatment of the COVID-19 infection. Prevention is the best strategy to combat the COVID-19 pandemic. Prevention is not a difficult task as it is commonly thought to be. For the effective prevention of COVID-19, broadly two types of precautionary measures to be taken, as mentioned below:
General precautionary measures (Fig. 16.3): It is meant for everybody in the community.
Specific precautionary measures (Fig. 16.4): It is meant for persons who are sick, close contacts of COVID-19, travellers and healthcare workers.
Fig. 16.3
General precautionary measures during COVID-19 pandemic. (Source: Adapted from Centre for Disease Control and Prevention, USA)
Fig. 16.4
Specific precautionary measures during COVID-19 pandemic. (Source: Adapted from Centre for Disease Control and Prevention USA)
Broadly, there are three groups of population as mentioned below:
General population
COVID-19 cases and close contacts
Healthcare workers
The precautions and recommendations are targeted to address the needs of the above three groups of the population. Prevailing myths and unawareness about precautionary measures may cause distress among people. There is a need to follow certain recommendations for effective coping with mental health challenges (Table 16.1).
Table 16.1
Recommendations for effective coping with mental health challenges
| 1. Adequate awareness about the COVID-19 and regular updates (as understanding about COVID-19 changing day by day) about appropriate precautionary measures |
| 2. Developing preparedness to meet the challenges like scarcity of resources |
| 3. Ignoring fake news and social media posts that spreads panic |
| 4. Regular scheduling of the daily activities |
| 5. Inclusion of indoor recreational activities and relaxation exercises to daily practice |
| 6. Approaching (rather than avoiding) healthcare system, if any symptoms develop |
| 7. Positive thinking and installation of hope |
Individuals who experience psychological distress must report or inform their difficulties, rather than hiding them. Individuals who experience persistence distress may seek help from the mental health professionals through helplines available or in hospitals in cases of emergency situations. Figures 16.5 and 16.6 summarize the recommendations according the risk severity and management approach to mental health difficulties during COVID-19 pandemic, respectively.
Fig. 16.5
Recommendations according the COVID-19 risk severity
Fig. 16.6
Management approach to mental health difficulties during COVID-19 pandemic
16.7 Conclusions
COVID-19 carries significant mental health hazards. There is a paucity of research addressing the mental health issues during the COVID-19 pandemic. As the mortality and morbidity statistics are reaching new peaks every day, isolation and lockdown states are getting prolonged, recreational opportunities for people are lessened and the financial crisis is building in, mental health issues are likely to grow exponentially. There is a need to understand the mental perspectives of COVID-19 and possible measures to cope with the pandemic for their effective management.
16.8 Future Perspectives
The mental health issues associated with the COVID-19 pandemic can be immediate (short-term) or remote (long-term). Existing literature addresses the immediate mental health concerns only. It is important to see the long-term mental health sequels of COVID-19 infection. Earlier pieces of evidence suggest that maternal exposure to influenza infection during the epidemic of influenza in Europe increased the risk of schizophrenia in offspring, possibly by altering the neurodevelopmental process (Mednick et al. 1988; Murray et al. 1992). Similarly, childhood exposure to measles may later result in the development of subacute sclerosing panencephalitis (SSPE) (Campbell et al. 2007). Nothing is known about the after-effects of novel coronavirus infection; hence, there is a need for extensive research in terms of its impact on various groups of populations (pregnant, young children, adults and other vulnerable populations).
Similarly, it is required to understand the mental healthcare needs of patients with COVID-19, close contacts, health professionals dealing with COVID-19 patients and the general population. Future research should also consider the feasibility and efficacy of various online psychotherapeutic interventions during the COVID-19 pandemic, globally with a specific focus in the low- and middle-income countries (LMICs). As there is a concern about contacting infection during direct contact with patients, online consultation can be a potential mode of delivering therapy (Greenhalgh et al. 2020).
Executive Summary
References
May 14
Αργότερα αφέθηκε ελεύθερος με προφορική εντολή εισαγγελέα. Τι είπε ο δικηγόρος του καθηγητή
Καθηγητής γυμνασίου συνελήφθη ύστερα από μήνυση που υπέβαλε εις βάρος του η διευθύντρια του σχολείου, επειδή πήγε να διδάξει χωρίς να έχει υποβληθεί προηγουμένως σε self test, ενώ αρνήθηκε και να φύγει.
Το περιστατικό συνέβη το πρωί σε σχολική μονάδα της Θέρμης, όπου κλήθηκε η αστυνομία μετά την υποβολή της μήνυσης.
Ο 50χρονος καθηγητής συνελήφθη και εις βάρος του σχηματίστηκε δικογραφία για διατάραξη λειτουργίας δημόσιας υπηρεσίας.
Λίγο αργότερα αφέθηκε ελεύθερος με προφορική εντολή εισαγγελέα.
«Ο πελάτης μου είπε το αυτονόητο. Χωρίς να δημιουργήσει καμία ένταση με τη διευθύντρια του σχολείου, ζήτησε να του δώσει και εγγράφως την απόφασή της να αποχωρήσει ο πελάτης μου από το σχολείο, διότι δεν είναι δυνατό να εγκαταλείψει κάποιος την εργασία του σε μία δημόσια υπηρεσία μόνο με προφορική εντολή. Είναι απολύτως λογικό να θέλει να είναι καλυμμένος και έτσι δεν έφυγε από το σχολείο, από τη στιγμή που η διευθύντρια αρνήθηκε να του προσκομίσει και εγγράφως την απόφασή της», είπε στο ethnos.gr ο δικηγόρος του καθηγητή, Αποστόλης Τζαρός.
Όσο για το λόγο για τον οποίο ο καθηγητής δεν έκανε self test, ο κ. Τζαρός είπε: «Το έκανε ακολουθώντας τις οδηγίες χρήσης των τεστ. Η πρώτη κιόλας οδηγία χρήσης αναφέρει ξεκάθαρα ότι δεν πρέπει να κάνουν το τεστ, όσα άτομα δεν έχουν συμπτώματα. Επειδή ο πελάτης μου δεν είχε συμπτώματα και ακολουθώντας την οδηγία χρήσης, δεν έκανε το τεστ», λέει ο δικηγόρος του καθηγητή.
newsbreak.gr και https://www.triklopodia.gr/%cf%83%cf%85%ce%bd%ce%b5%ce%bb%ce%ae%cf%86%ce%b8%ce%b7-%ce%ba%ce%b1%ce%b8%ce%b7%ce%b3%ce%b7%cf%84%ce%ae%cf%82-%ce%b3%cf%85%ce%bc%ce%bd%ce%b1%cf%83%ce%af%ce%bf%cf%85-%ce%bc%ce%b5%cf%84%ce%ac-%ce%b1/
ΌΝΤΩΣ ,ΤΟΥΣ ΕΙΧΑΝ ΠΑΡΑΣΥΡΕΙ ΣΤΟ ΝΕΟ ΣΥΣΤΗΜΑ ,ΤΟΥ ΚΟΜΜΟΥΝΙΣΜΟΥ.
ΤΑΧΑ ΜΟΥ Ο ΕΡΓΆΤΗΣ ,ΤΑΧΑ ΜΟΥ Ο ΑΓΡΟΤΗΣ ΚΑΙ ΟΛΑ ΤΑ ΓΝΩΣΤΑ.
ΑΠΟ ΠΙΣΩ :Τ Α Ε Ρ Π Ε Τ Α.
ΠΙΣΩ ΑΠΟ ΤΗΝ ΚΟΥΡΤΙΝΑ ,Ο ΤΣΑΧΠΙΝΗΣ ΔΡΑΚΟΣ ΡΟΤΣΙΛΝΤ.
Ο Π.Ι.Ν.Δ.Α.Ρ.Ο.Σ
ΚΩΔΙΚΗ ΟΝΟΜΑΣΙΑ.
ΧΑΖΑΡΟΠΡΑΜΑ Ο ΧΙΤΛΕΡΑΚΟΣ.
ΒΟΥΝΤΟΥ ΜΕΣΑ ΣΤΑ ΔΑΣΗ ΟΙ ΝΑΖΙΣΤΕΣ.
ΣΕΛΗΝΗ ΚΑΙ ΤΑ ΣΥΝΑΦΗ.
ΣΕΞΟ ΤΕΤΟΙΑ ,ΞΕΒΡΑΚΩΜΑΤΑ , ΕΠΙΚΛΉΣΕΙΣ ΚΑΙ ΤΑ ΤΟΙΑΥΤΑ.
ΟΛΟΙ ΤΟΥΣ.
ΕΒΡΑΙΟΣ Ο ΧΙΤΛΕΡΑΚΟΣ ΚΑΙ ΑΠΟ ΔΥΟ ΓΟΝΕΙΣ.
ΣΙΓΑ !.
ΑΜΑ ΑΥΤΟΣ ΗΤΑΝ ΙΟΥΔΑΙΟΣ ,ΕΓΩ ΕΙΜΑΙ Ο ΦΟΥ ΜΑΝ ΤΣΟΥ.
“ΝΑΖΙΣΜΟΣ ,ΜΥΣΤΙΚΗ ΕΤΑΙΡΕΙΑ ”
ΒΡΕΙΤΕ ΤΟ ΒΙΒΛΙΟ.
ΠΑΠΑΡΑΣ ΗΤΑΝ .ΕΝΑΣ ΠΑΠΑΡΑΣ ΚΑΙ ΜΙΣΟΣ.
ΑΥΤΟΣ ΟΜΩΣ ΤΟΥΣ ΕΚΑΝΕ ,ΑΥΤΟΝ ΒΑΛΑΝΕ.
ΑΛΛΟΙ ΚΟΥΛΑΝΤΡΙΖΑΝ ΑΠΟ ΠΙΣΩ.
ΤΟ ΧΡΗΜΑ ΔΕΝ ΤΟ ΕΙΧΑΝ ΟΙ ΦΤΩΧΟΜΠΙΝΕΔΕΣ ΙΟΥΔΑΙΟΙ.
ΤΟ ΕΙΧΑΝ ΟΙ ΧΑΖΑΡΟ ΑΙΜΑΤΟΙ.
ΙΟΥΔΑΙΟΙ ΠΛΕΟΝ ΣΤΟ ΘΡΗΣΚΕΥΜΑ.
ΣΑΝ ΤΟΥΣ ΧΑΜΑΙΛΕΟΝΤΕΣ ,ΟΠΟΥ ΕΜΕΝΑΝ ,ΑΥΤΗΣ ΤΗΣ ΠΕΡΙΟΧΗΣ ΘΡΗΣΚΕΥΜΑ ΑΚΟΛΟΥΘΟΥΣΑΝ.
ΑΥΤΟ ΤΟΥΣ ΕΝΔΙΕΦΕΡΕ ;ΤΟ ΘΡΗΣΚΕΥΜΑ ;
ΚΑΘΟΛΟΥ.
ΕΙΝΑΙ ΧΡΙΣΤΙΑΝΟΣ Ο ΜΠΙ ΣΚΑΤΑ ΚΙΣ ;
ΕΙΝΑΙ ΧΡΙΣΤΙΑΝΟΣ Ο ΑΛ 6;
Ο ΣΗΜΙΤΗΣ ;
Ο ΜΠΕΝΑΚ ;
Ο ΤΖΕΦΡΥ ;
ΠΟΣΟΙ ΚΑΙ ΠΟΣΟΙ ΑΛΛΟΙ.
ΑΝΤΕ ,ΒΑΖΑΝΕ ΚΑΙ ΚΑΝΑ ΟΡΙΤΖΙΝΑΛ ΟΒΡΙΟ -ΙΟΥΔΑΙΟ ΣΤΑ ΔΙΚΑ ΤΟΥΣ ,ΤΟΝ ΤΑΙΖΑΝΕ ΚΑΛΑ ,ΒΛΕΠΕ ΡΟΚΦΕΛΕΡ ΚΑΙ ΤΟΝ ΕΙΧΑΝ ΠΙΑ ΣΤΟ ΧΕΡΙ.
Ο ΓΕΡΜΑΝΙΚΟΣ ΣΤΡΆΤΟΣ ,ΕΙΧΕ ΜΈΣΑ ΠΟΛΛΟΥΣ ΕΒΡΑΙΟΥΣ.
ΣΤΡΑΤΙΩΤΕΣ ,ΑΞΙΩΜΑΤΙΚΟΥΣ.
Ο ΟΔΗΓΟΣ ΤΟΥ ΧΙΤΛΕΡ ΗΤΑΝ ΕΒΡΑΙΟΣ.
ΠΡΟΣΠΑΘΗΣΕ ΝΑ ΤΟΥΣ ΠΕΤΑΞΗ ΕΞΩ ΑΠΟ ΤΙΣ ΤΡΑΠΕΖΕΣ ΚΑΙ ΠΟΛΥΕΘΝΙΚΕΣ.
ΕΙΝΑΙ ΑΛΗΘΕΙΑ ΟΜΩΣ ΑΥΤΟ ;
Ή ΚΑΠΟΙΑ ΕΓΙΝΑΝ ΓΙΑ ΤΑ ΜΑΤΙΑ ΤΟΥ ΚΟΣΜΟΥ.
ΞΕΡΟΥΜΕ ,ΟΤ ΠΙΣΩ ΚΑΙ ΑΠΟ ΤΟΥΣ ΔΥΟ ΠΑΓΚΟΣΜΙΟΥΣ ,ΗΤΑΝ ΤΑ ΕΡΠΕΤΑ.
ΜΕΧΡΙ ΤΟ 2016 ,ΕΙΧΕ ΝΙΚΕΣ Η ΓΕΡΜΑΝΊΑ.
ΜΕΤΑ ,ΛΕΝΕ ,ΟΙ ΕΒΡΑΙΟΙ ΚΑΤΕΔΩΣΑΝ ΜΥΣΤΙΚΑ ΣΤΟΥΣ ΑΛΛΟΥΣ ΧΑΖΑΡΟ ΕΒΡΑΙΟΥΣ ,ΤΗΣ ΑΓΓΛΙΑΣ.
ΜΑΛΙΣΤΑ.
Ο ΧΙΤΛΕΡ ,ΕΙΧΕ ΠΕΙ ΟΤΙ ΑΥΤΗ ΗΤΑΝ Η ΑΙΤΙΑ ΠΟΥ ΈΧΑΣΑΝ ΣΤΟΝ ΠΡΩΤΟ.
ΠΡΟΦΑΝΩΣ ,ΟΤΑΝ ΤΟΝ ΧΩΣΑΝ ΣΤΗΝ ΜΥΗΣΗ …ΠΗΡΕ ΤΑ ΕΠΑΝΩ ΤΟΥ ΤΟ ΧΑΖΑΡΙΚΟ ΑΙΜΑ.
ΕΤΣΙ ,ΠΗΡΕ Η ΜΠΑΛΑ ΠΟΛΛΟΥΣ.
ΝΑ ΑΦΗΣΗ ΤΑ ΠΟΥΣΤΙΚΑ Ο ΧΙΤΛΕΡΑΚΟΣ ,ΓΙΑΤΙ ΑΝΤΕΣΤΡΕΨΕ ΟΛΑ ΤΑ ΕΛΛΗΝΙΚΑ ΣΎΜΒΟΛΑ ΚΑΙ ΤΑ ΜΑΥΡΙΣΕ ΚΙΟΛΑΣ.
ΠΟΙΟΣ ΤΟΥ ΤΟ ΕΙΠΕ ΑΥΤΟ ,ΤΟΥ ΑΓΡΑΜΜΑΤΟΥ ΔΕΚΑΝΕΑ ;
ΕΓΩ ;
ΚΑΙ ΓΙΑ ΝΑ ΞΕΡΟΥΜΕ ΑΛΛΟ ΕΝΑ :
Ο ΧΙΤΛΕΡ ,ΔΕΝ ΗΘΕΛΕ ΤΟΝ ΠΟΛΕΜΟ.
ΚΑΤΙ Ή ΚΑΠΟΙΟΙ ΟΜΩΣ ,ΤΟΝ ΕΣΠΡΩΧΝΑΝ ΠΡΟΣ ΤΑ ΕΚΕΙ.
ΕΙΠΑΜΕ :ΗΤΑΝ ΟΡΤΙΝΑΝΤΖΑ.
Ο ΕΥΦΥΕΣΤΑΤΟΣ ΛΕΝΙΝ…ΧΑΖΑΡΟ ΠΑΝΟΥΡΓΟΣ.
ΛΕΦΤΑ ΑΠΟ ΤΙΣ ΧΑΖΑΡΙΚΕΣ ΤΡΑΠΕΖΕΣ.
ΣΤΗΝ ΚΑΘΟΜΙΛΟΥΜΕΝΗ ,ΕΒΡΑΙΟΙ.
ΤΗΝ ΤΡΩΓΑΝ ΣΤΟΝ Κ@ΛΟ ΟΙ ΙΟΥΔΑΙΟΙ ΚΑΙ ΟΙ ΧΑΖΑΡΟΙ ,ΣΤΗΝ ΑΠΟΞΩ.
ΓΙΑ ΘΥΜΗΘΕΙΤΕ ΣΤΗΝ ΟΥ ΧΑΝ .
ΞΕΡΕΤΕ ΠΟΙΟΙ ΣΤΗΣΑΝ ΤΟ ΣΚΗΝΙΚΟ ;
ΑΠΟ ΜΕΣΑ ΑΠΟ ΤΟ ΚΟΜΜΟΥΝΙΣΤΙΚΟ ΚΟΜΜΑ.
ΔΗΛΑΔΗ ;
ΤΑ ΕΡΠΕΤΑ ,ΑΠΟ ΠΙΣΩ .ΔΡΑΚΟΙ.
ΤΟΥΣ ΕΝΟΙΑΞΕ ΕΑΝ ΓΚΡΕΜΙΣΑΝ ΚΑΤΑΓΗΣ ΧΙΛΙΑΔΕΣ ΚΙΝΕΖΟΥΣ ;
ΟΧΙ.
ΕΙΝΑΙ ΟΛΟΙ ΓΙΑ ΜΑΣΑΜΠΟΥΚΑ.
ΞΕΡΩ ΕΒΡΑΙΟΥΣ ,ΠΟΥ ΔΕΝ ΗΤΑΝ ΠΛΟΥΣΙΟΙ.
ΕΒΡΑΙΟΙ…ΟΤΙ ΕΙΝΑΙ.ΙΟΥΔΑΙΟΙ.
ΠΩΣ ΓΙΝΕΤΑΙ ΑΥΤΟΙ ΝΑ ΜΗΝ ΕΙΝΑΙ ΣΤΗΝ ΠΟΛΙΤΙΚΗ ΚΑΙ ΣΤΗΝ ΜΑΣΑΜΠΟΥΚΑ ,ΣΤΙΣ ΤΡΑΠΕΖΕΣ ;
ΑΡΑ ,ΚΑΤΙ ΤΡΕΧΕΙ.
ΕΙΝΑΙ ΕΒΡΑΙΟΣ Ο ΜΠΙ ΣΚΑΤΑ ΚΙΣ ;
ΟΧΙ.
ΧΑΖΑΡΟΣ.
ΔΙΑΒΑΣΤΕ ΚΑΙ ΓΙΑ ΧΑΖΑΡΟΥΣ ,ΚΙΜΜΕΡΙΟΥΣ -ΣΙΚΑΜΒΡΟΥΣ.
ΔΙΑΒΑΣΤΕ ΚΙΜΜΕΡΙΟΙ ΣΥΚΑΜΒΡΟΙ.
ΠΑΝΑΓΙΩΤΗΣ ΛΕΝΤΖΟΣ Ο ΣΥΓΓΡΑΦΈΑΣ.ΔΙΚΗΓΟΡΟΣ.
ΦΙΔΟ ΑΙΜΑΤΑ.
ΑΝΑΚΑΤΩΣΟΥΡΕΣ ,ΔΟΛΟΠΛΟΚΟΙ ,ΜΗΧΑΝΟΡΡΑΦΟΙ ΚΟΠΤΟΓΑΖΩΤΡΙΕΣ !.
ΣΕ ΤΡΩΝΕ ΛΆΧΑΝΟ ΚΑΙ ΜΠΑΜΠΕΣΙΚΑ ΑΒΛΕΠΕΙ.
ΦΟΥΛ ΘΗΡΙΩΔΙΑ.
ΟΜΟΙΩΣ ,ΟΙ ΜΟΓΓΟΛΟΙ.
ΜΗΝ ΤΟ ΨΑΧΝΕΤΕ.ΤΩΡΑ ΕΙΝΑΙ ΔΙΑΣΠΑΡΤΟΙ ΠΑΝΤΟΥ.
ΤΙΓΚΑ ΣΤΟ ΕΡΠΕΤΙΚΟ ΑΙΜΑ Ο ΠΛΑΝΗΤΗΣ.
Ο ΚΥΡΙΟΣ ΣΤΑΛΙΝΑΚΟΣ ;
ΜΟΛΙΣ ΜΠΟΥΚΑΡΑΝ ΤΑ ΓΕΡΜΑΝΙΚΑ ΣΤΡΑΤΕΥΑΜΑΤΑ ΚΑΙ ΠΡΟΗΛΑΥΝΑΝ ,
ΕΧΩ ΔΙΑΒΑΣΕΙ ΣΤΡΑΤΙΩΤΙΚΗ ΙΣΤΟΡΙΑ.
ΜΟΥ ΑΡΕΣΕΙ ΠΟΛΥ.
ΤΟΥΣ ΚΑΘΑΡΙΖΕ ΤΟΥΣ ΑΞΙΟΥΣ ΣΤΡΑΤΙΩΤΙΚΟΥΣ ,ΣΑΝ ΣΤΡΑΓΑΛΙΑ.
Ο ΤΥΠΑΚΟΣ ,ΠΟΥ ΚΑΤΙ ΗΛΙΘΙΟΙ ΕΔΩ ,ΤΟΝ ΕΧΟΥΝ ΚΑΝΕΙ ΘΕΟ.
ΤΟΝ ΑΧΥΡΑΝΘΡΩΠΟ ΤΟΥ ΡΟΤΣΙΛΝΤ.
ΑΡΙΣΤΟΜΑΧΟΣ.