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1.
Acta Medica Iranica ; 60(6):384-386, 2022.
Article in English | EMBASE | ID: covidwho-2033506

ABSTRACT

Safety monitoring of COVID-19 vaccination is paramount of importance. There are limited reports of Guillain-Barré syndrome (GBS) associated with the COVID-19 vaccination. The present study reported a case of GBS following the first dose of the Oxford-AstraZeneca SARS-CoV-2 vaccine. A 32-year-old man presented a history of progressive descending weakness and autonomic features within a month after receiving the Oxford-AstraZeneca SARS-CoV-2 vaccine. The neurological examination was consistent with acute polyneuropathy. The para-clinical investigations were in favor of acute demyelinating polyneuropathy. The patient was diagnosed with GBS, and IVIG was initiated as an acute treatment, which led to significant clinical recovery. We reported a case of GBS after receiving the Oxford-AstraZeneca vaccine. However, our findings dose not conclude a causal association between GBS and COVID-19 vaccination.

2.
Cells ; 11(16), 2022.
Article in English | EMBASE | ID: covidwho-2032864

ABSTRACT

Neurofilament light chain (NfL) is a specific biomarker of neuro-axonal damage. Matrix metalloproteinases (MMPs) are zinc-dependent enzymes involved in blood–brain barrier (BBB) integrity. We explored neuro-axonal damage, alteration of BBB integrity and SARS-CoV-2 RNA presence in COVID-19 patients with severe neurological symptoms (neuro-COVID) as well as neuro-axonal damage in COVID-19 patients without severe neurological symptoms according to disease severity and after recovery, comparing the obtained findings with healthy donors (HD). Overall, COVID-19 patients (n = 55) showed higher plasma NfL levels compared to HD (n = 31) (p < 0.0001), especially those who developed ARDS (n = 28) (p = 0.0005). After recovery, plasma NfL levels were still higher in ARDS patients compared to HD (p = 0.0037). In neuro-COVID patients (n = 12), higher CSF and plasma NfL, and CSF MMP-2 levels in ARDS than non-ARDS group were observed (p = 0.0357, p = 0.0346 and p = 0.0303, respectively). SARS-CoV-2 RNA was detected in four CSF and two plasma samples. SARS-CoV-2 RNA detection was not associated to increased CSF NfL and MMP levels. During COVID-19, ARDS could be associated to CNS damage and alteration of BBB integrity in the absence of SARS-CoV-2 RNA detection in CSF or blood. CNS damage was still detectable after discharge in blood of COVID-19 patients who developed ARDS during hospitalization.

3.
HemaSphere ; 6:1930-1931, 2022.
Article in English | EMBASE | ID: covidwho-2032125

ABSTRACT

Background: Bing-Neel syndrome (BNS) is a rare complication of lymphoplasmacytic lymphoma (LPL) comprising LPL infiltration in the central nervous system (CNS). Clinical and radiological features are diverse;the diagnosis is confirmed by cerebrospinal fluid (CSF) analysis using immunological and molecular techniques. Rarely, a tissue biopsy is required. The pattern of presentation including systemic involvement and CSF features inform treatment strategies, which include CNS-penetrating therapies. Aims: To evaluate the diagnostic characteristics of patients with BNS and their influence on therapy. Methods: Data from patients referred between 2011-2021 for management of BNS to our academic neurohaematology centre were retrospectively reviewed. Those with imaging features alone or where it was not possible to distinguish from high-grade transformation were excluded. Results: Thirty-five patients (22 male, 13 female) were identified. Median age at diagnosis of BNS was 65 years (range 48-85). All patients were symptomatic. In 12 patients (34%) BNS was the de novo presentation of the IgM-related disorder, of which 3 (25%) had no detectable bone marrow (BM) infiltration of LPL at diagnosis. Approximately half (17;49%) had previously received therapy for LPL;median time to BNS diagnosis in these was 49 months (range 3-125). At BNS diagnosis, BM involvement with LPL ranged from 0-95%. More than half (14/26;54%) had <10% infiltrate and almost a fifth (4/26) >60%. All patients had leptomeningeal involvement and 8 (23%) additionally had parenchymal CNS disease. The majority had kappa light-chain predominance: IgMκ (n=26), non-IgMκ (n=5), IgMλ (n=3), one unknown. The BNS diagnosis was made on CSF analysis (n=28;80%), leptomeningeal tissue biopsy (n=3;9%) where CSF was non-informative, or by expert opinion based on supportive clinical, radiological and non-definitive CSF features (n=4;11%). Of those with a diagnosis based on CSF studies, B-cell clonality was confirmed by flow cytometry (27/28;96%), MYD88L265P mutation (18/28;64%) and immunoglobulin gene rearrangement (12/28;43%). In 22 samples with a full dataset, median CSF white cell count was 25/ul (1-233), CSF protein 1.69g/l (0.35-6), CSF IgM 9.49mg/l (1.07-61.5). The majority were treated with intensive regimens (rituximab, methotrexate (MTX), cytarabine (ARA-C) + thiotepa/idarubicin;n=30) due to the presence of CNS disease bulk and clinical need, and less commonly ibrutinib (n=3), bendamustine-rituximab (BR, n=1);one patient had intrathecal therapy (MTX, ARA-C) at the height of the COVID pandemic. Of those who received 2 cycles of intensive chemotherapy, 3 had >4 cycles followed by BCNU/thiotepa autologous stem cell transplant;10 proceeded to 'consolidation' (indefinite) ibrutinib to limit intensive chemotherapy or tackle systemic disease. At a median follow up of 26 months (range 1-121), median survival was not reached;2-year overall survival was 91% (95% CI 74-97). Three patients died during treatment (1 invasive fungal infection post COVID-19 during ibrutinib consolidation post MTX/ARA-C based therapy) and 2 during MTX-ARA-C based therapy;7 patients relapsed or progressed and were treated with ibrutinib: 1 relapsed after ibrutinib use, 1 patient was intolerant of ibrutinib and switched to BR. Image: Summary/Conclusion: Our cohort confirms that BNS may present with leptomeningeal disease and/or parenchymal disease, de novo and without systemic disease. Overall outcomes are excellent with intensive regimens, consolidated with or followed by ibrutinib;however, there are treatment-related toxicities emphasising the need for a tailored approach.

4.
Annals of Clinical Psychiatry ; 34(3):16-17, 2022.
Article in English | EMBASE | ID: covidwho-2030844

ABSTRACT

BACKGROUND: Catatonia is a psychomotor syndrome characterized by abnormal movements and decreased responsiveness. Diagnosis is made by observing or eliciting at least 3 of the following 12 criteria: stupor, catalepsy, waxy flexibility, mutism, negativism, posturing, mannerism, stereotypy, agitation, grimacing, echolalia, and echopraxia. It is commonly associated with psychiatric disorders but can also be secondary to a medical condition, more commonly neurologic or metabolic conditions. CASE DESCRIPTION: Patient was a 17-year-old female brought in by her guardian for evaluation at a psychiatric assessment center following a month of regressive behavior and concerns of possible hallucinations. While at the assessment center, the patient began hyperventilating and had 3 seizures. She was transferred to a nearby hospital and continued to seize, becoming hypoxic and requiring intubation. Computed tomography was unremarkable;urine drug testing was positive for THC and benzodiazepines. The patient was transferred to the intensive care unit of a children's hospital. She continued to have poverty of speech, decreased responsiveness, and disorganized behavior after extubation. Child psychiatric services was consulted for these concerns, and differential included psychotic disorder and catatonia, either secondary to psychiatric or medical cause. Patient underwent extensive medical evaluation, which was overall unremarkable, to rule out medical causes (including electroencephalography, cerebrospinal fluid studies, complete blood counts, C-reactive protein, and anti-NMDA antibodies). She did test positive for COVID, which resulted in delay of brain magnetic resonance imaging (MRI) being obtained. She had partial response to lorazepam challenge, and scheduled doses of lorazepam were started after. Bush Francis Catatonia Scale scores did lower partially with scheduled lorazepam, but full resolution of symptoms was not observed. MRI done on day 10 showed findings suspicious for superior sagittal thrombosis. Brain magnetic resonance venography showed superior sagittal and bilateral transverse venous thrombosis. The patient was started on anticoagulation therapy and discharged from hospital with the recommendation of psychiatry and neurology outpatient follow-up. She did not follow up with neurology but did have slow resolution of symptoms per outpatient psychiatry records. DISCUSSION: Catatonia typically results in resolution of symptoms with treatment of underlying cause along with benzodiazepines or electroconvulsive therapy. It is commonly associated with psychiatric disorders, but it is important to evaluate for medical causes as well, especially when there are concerning signs/symptoms. In this patient, there was only a partial response to benzodiazepines, but further improvement with anticoagulation therapy. This along with no previous psychiatric history supports an underlying medical cause. This patient had no history of health conditions associated with hyper-coagulopathies. However, COVID has been associated with risk for arterial and venous thromboembolic complications.

5.
Archives of Disease in Childhood ; 107(Suppl 2):A456-A457, 2022.
Article in English | ProQuest Central | ID: covidwho-2019929

ABSTRACT

AimsMain purpose of presenting this clinical case is that RSV BRONCHIOLITIS can present with lobar pneumonia,Fulminant viral septic shock with DIC,pulmonory haemorrhage and asystole. Viral VS Bacterial sepsis- clinically difficult to differentiate.Methods1 month old girl,unwell for 2 days with cough,decrease oral intake, seen by GP in the morning and diagnosed as BRONCHIOLITIS,same day evening presented to the hospital with apnoea in the car arrived at PAU within 3 mins of apnoea.O/E-no HR or breathing,bleeding from nose and mouth,pale looking,mottled, CRT 5 sec.CPR started and connected to monitor showed asystole.Immediate cardiac arrest call was activated.Intubated, cannula inserted, 2 doses of adrenaline given IV,Bolus of normal saline 10mls/kg thrice,partial septic screening done and covered with triple antibiotics amoxycillin,gentamycin and cefotaxime.After 10 mins of resuscitation baby responded. Given vitamin K and transfused with O negative blood and FFP.Blood gas showed mixed metabolic and respiratory acidosis and hence connected to ventilator started on morphine,maintenance fluids,ionotropes,morphine infusion and transferred to tertiary centre. In tertiary centre admitted for 11 days,extubated to CPAP on day 5, weaned to high flow on day 6, RA on day 9. Ionotropes for 1 day,acylovir, vitamin k for 9 and 6 days respectively.Neuroprotective measures followed.ResultsNPA for RSV positive, covid 19 PCR negative, blood c/s,CSF c/s and CSF PCR for bacteria and viruses negative, X ray chest consolidation upper lobes bilateral,CT Angiogram subsegmental consolidation and possible intraparenchymal haemorrhage. Initial Echo pulmonory hypertension and repeat Echo normal.MRI Brain -hypersensitivity in posterior putamina. Deranged coagulation profile.APTT more than 180, PT 16.2, INR 1.4ConclusionRSV positive bronchiolitis with all complications can mimic bacterial sepsis and its clinically difficult to differentiate between viral and bacterial septic shock.As this baby’s blood C/S was negative only positive thing was RSV in NPA, We have to consider this case as RSV BRONCHIOLITIS with fulminant septic shock with pneumonia, DIC, Pulmonory Haemorrhage leading to Asystole.Management of bacterial and viral Septic shock is pretty much the same except in certain cases we may have to use antivirals drugs when indicated.

6.
Journal of Basic and Clinical Pharmacy ; 11(3):2-2, 2020.
Article in English | CAB Abstracts | ID: covidwho-2012257

ABSTRACT

This editorial provides a brief information on how the coronavirus initially enters into the central nervous system (CNS) via the synaptic route followed by first capturing the Peripheral nerves, where trans-synaptic transfer in avian bronchitis and HEV67 virus. It has been observed in the study that SARS-CoV possess ananalogous potential with SARS-CoV-2, and both are highly similar. The mechanism about the entry of coronavirus into the nose, invade in CNS through olfactory bulb while nasal infection which leads to cause demyelination and inflammation, Further it reaches to the whole brain via Barrier of Blood-Brain and CSF via Blood-CSF barrier within 7 days which leads to respiratory disease due to the inability of air into the lungs as the defects in respiration controlled by the nervous systemand patients show symptoms like neurologic signs. According to theepidemiology study, the first symptom is dyspnoea which shows within 5 days, followed by admission in hospital at 7 days and intensive care at 8 days for SARS-CoV-2 and this latency period is sufficient for the virus to enter into CNS and destroy the medullary neurons which further causes respiratory problems.

7.
Annals of the Rheumatic Diseases ; 81:1736, 2022.
Article in English | EMBASE | ID: covidwho-2009026

ABSTRACT

Background: Familial Hemophagocytic lymphohistiocytosis (fHLH) categorized as FHL2 (PRF1), FHL3 (UNC13D), FHL4 (STX11), and FHL5 (STXBP2) encoding for Perforin, Munc13-4, Syntaxin11, and Syntaxin binding protein 2, respectively. There is limited information available about the clinical and mutational spectrum of FHL patients in Indian population. Objectives: To delineate clinical and laboratory features of late onset familial Hemophagocytic Lymphohistiocytosis. Methods: A 12-years-old well nourished sick looking boy, born to a non-consanguineous parents with normal birth, development and immunization history with uneventful past presented to us with 6 days history of high fever, cough, breathing difficulty and severe headache. He had occasional vomiting, abdominal pain, polyarthragia & chest pain from last 10 days. Mother also had given history of throat pain, backache & some non-specifc papular rashes over face before the onset of fever. His vitals were normal. Examination revealed faint diffuse fxed erythematous rash all over the body, pallor, icterus and hepatos-plenomegaly. Musculoskeletal examination was unremarkable. Lab evaluation revealed HB 8.9gm%, TLC 4700/cumm with neutrophils 40% and lymphocytes 56% with 8-9% activated lympocytes. Further evaluation showed low ESR 6mm/hr, fbrinogen 97mg% and albumin 2.2 gm% with elevated CRP 40mg/L, ferritin 2000ng/ml, LDH 658IU/L, SGPT 110IU/L, SGOT 221 IU/L, total bilirubin 6mg%, D-dimer 4355 ng:EFU/ml and Triglycerides 441mg%. His blood, urine, CSF and bone marrow cultures were sterile for endemic bacterial and viral infections in our area. His EBV PCR, CoVID RT PCR and CoVID antibody (Total & IgG) test were negative. His immunoglobulin leves were normal. HRCT Chest showed bilateral mild-moderate plural effusions, mild interstitial thickening in both the lower lobes, few fbrotic opacities & old areas of consolidation bilaterally. 2D echo showed mild pericardial effusion. Bone marrow examination showed Hypercellular marrow with iron depletion and occasional hemophagocytosis with CD8 T lymphocytes proliferation (55.2%) and double positive CD4 & CD8 (1.2%). He was initially commenced on supportive therapy, oxygen & intravenous antibiotics. In view of most probable non-infectious, non-malignant hemophagocytic lymphohistiocytosis, he was fnally given intravenous immunoglobulin (2gm/kg) and intravenous pulse methylprednisolone (30mg/kg). He responded well to above regimen within 3 days. He was discharged with tapering steroids over few weeks. Clinical exome by NGS revealed Homozygous Mutation in STXBP2 gene Intron 14, c.1280-1G>C (3' Splice Site) His parents has been counselled for hematopoietic stem cell transplantation and their decision is still pending. Results: We compared our patietnt with a reference to the largest Indian series of pediatric HLH1. Conclusion: Primary HLH type 5 can present frst time during childhood and adolescence. Any child presenting with unexplained HLH features should undergo genetic analysis irrespective of person's past and family history.

8.
Annals of the Rheumatic Diseases ; 81:1669, 2022.
Article in English | EMBASE | ID: covidwho-2008861

ABSTRACT

Background: We present a case of a 36 year-old female who developed Acute Immune-mediated Demyelinating Polyneuropathy (AIDP) after receiving the second dose of Pfzer COVID-19 vaccine. Objectives: To report a rare auto-immune complication of COIVD-19 vaccination. To educate and inform physicians about the approach to diagnosing AIDP and narrowing down its etiology. Methods: Case report and literature review Results: A 36 year-old female with no signifcant past medical history presented to the hospital with progressive bilateral paresthesia. She started to experience numbness and tingling sensation in her extremities 1 week after receiving the second dose of Pfzer COVID-19 vaccine. Following 5 days of symptoms onset, she was no longer able to hold onto objects and experienced difficulty ambulating without assistance. Physical exam was notable for decreased distal sensation to touch and pain in all 4 limbs, otherwise, the rest of her neurological and musculoskeletal evaluation was normal. MRI-head showed small scattered foci of increased FLAIR signal in the white matter, suggesting an underlying infammatory process. Electromyography (EMG) was performed and showed evidence of acute diffuse sensorimotor neuropathy with mixed axonal and demyelinating features. These results along with the clinical features allowed us to diagnose our patient with Acute Immune-mediated Demyelinating Polyneuropathy (AIDP). Extensive autoimmune workup, including anti-GM1, GD1b, Gq1b, ANA, DS-DNA, RF, CCP, and C/P ANCA, were unremarkable. She had positive anti-Ro atb but did not have any clinical or physical features that would suggest Sjogren's Syndrome. Vitamin levels (B12, folate, thiamine) were found to be normal. Infectious workup of serum and CSF which included hepatitis serologies, Campylobacter jejuni serology, Lyme atb, CMV atb, EBV atb were all negative. The possible etiology of her disease was attributed to Pfzer COVID-19 vaccine given the temporal correlation. She was subsequently treated with 6 cycles of IVIG which resulted in moderate symptomatic improvement. Conclusion: AIDP is an autoimmune-guided infammatory neuropathy which result in axonal degeneration of myelinated nerves [1]. In some extremely rare cases, molecular mimicry following vaccination may lead to this disease [1]. There have been reports of AIDP linked to Johnson & Johnson and AstraZeneca COVID-19 vaccines [2]. Recently, a few cases have also been observed with Pfzer COVID-19 vaccine [2-3]. Interestingly, the majority of these cases occurred after the frst dose of the vaccine, making our case even more peculiar [2]. We report this case as physicians should be made aware that AIDP is a potential complication of COVID-19 vaccination. Given the extreme rarity of these cases, it is also important to note that more common infectious and autoimmune etiology of AIDP should be investigated before attributing any potential causal relationship to COVID-19 vaccines.

9.
Journal of Neuroimaging ; 32(4):767-768, 2022.
Article in English | EMBASE | ID: covidwho-2008752

ABSTRACT

Background and Purpose: Balo's concentric sclerosis (BCS) is a rare inflammatory demyelinating disorder of the central nervous system (CNS) characterized pathologically and radiologically by concentric lamella of alternating demyelinated and partially myelin-preserved white matter. Whether BCS is a variant of multiple sclerosis (MS) or a distinct entity remains debatable. Here, we report an unusual case of MS complicated by Balo's lesions, post-Coronavirus disease 2019 (COVID-19), focusing on the evolution ofMRI findings. Methods: Single-case study. Results: The patient is a 42-year-old woman with relapsing-remitting MS diagnosed at age of 19 who was treated with teriflunomide for the past 5 years. She developed a febrile illness and arthralgia for a week;however, COVID-19 testing was deferred. Two weeks later, she presented with vertigo followed by profound right-hemiparesis, gait impairment, and encephalopathy. Cerebrospinal fluid analysis revealed a protein of 56 mg/dl, increased immunoglobulinG(IgG) index, and>l10 unique oligoclonal bands. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) IgG was detected in serum, but viral ribonucleic acid was absent in the CSF. BrainMRI demonstrated, for the first time, several Balo-like and tumefactive lesions, with contrast enhancement and restricted diffusion. She received plasma exchange alternating with pulse steroids, yet was left with ataxic hemiparetic gait. She was later switched to an anti-CD20 monoclonal antibody therapy. Followup brain MRIs showed continuous regression of the tumefactive and Balo-like lesions. Conclusion: This case adds to the emerging spectrum of COVID-19- associated radiological findings regarding inflammatory demyelination in the CNS. It remains unknown whether potential neurotropism of SARS-CoV-2 or parainfectious mechanisms might have contributed to the fulminant disease in our patient.

10.
Journal of Neuroimaging ; 32(4):770-771, 2022.
Article in English | EMBASE | ID: covidwho-2008751

ABSTRACT

Background and Purpose: Since the implementation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination, we see continued hesitancy across the world regarding the potential emergence of immune and thromboembolic complications with these injections. This has included temporary pauses over concerns for thromboembolic events and cardiac inflammation.We provide discussion of a 57-year-old patient who suffered multiple ischemic strokes, with no prior history of vascular events after receiving her SARSCoV- 2 (messenger ribonucleic acid [mRNA]) vaccination with workup suggesting CNS vasculitis in the setting of multiple positive immune markers and propose the need for further investigation in this area. Methods:Review of case presentation, testing, imaging, and laboratory studies. Results: CT angiography was performed but could not identify any vascular pathology in the large vasculature. Brain MRI/MR angiography demonstrated strokes in multiple vascular territories (similar findings on first and second admission). Conventional angiogram was completed, which also did not demonstrate large vessel abnormalities. Telemetry was unremarkable. Echocardiogram (transthoracic and transesophageal) was performed without cardioembolic source identified. Serum and CSF laboratory studies were completed and suggestive of a CNS immune process and given the overall clinical picture were most consistent with probable small vessel CNS vasculitis. Conclusion: In presenting this patient's background and medical history, which includes autoimmune hepatitis, we propose there may be a subpopulation who could be at higher risk of immune reactions in the setting of these vaccinations and that while generally still safe for the overall population, in these particular subpopulations increased caution may be warranted pending further investigation, particularly if considering the newermRNA vaccinations.

11.
Indian Journal of Critical Care Medicine ; 26:S73-S74, 2022.
Article in English | EMBASE | ID: covidwho-2006362

ABSTRACT

Aim and objective: During the recent COVID-19 pandemic various vaccines have been developed and approved for emergency use, including adenovirus vector-based ChAdOx1 nCov-19. There are few reports of serious adverse events following immunization (AEFI). Materials and methods: Here, we report two cases of serious AEFI who required ICU admission. Results: Case 1: A 55-y-m hospitalized with complaints of giddiness for 4 days and onset of weakness of all four limbs with altered sensorium for 1 day. He had no history of any comorbidity, non-smoker and non-alcoholic, and no previous episodes of transient ischemic attacks. He was vaccinated with a second dose of adenoviral vector-based ChAdOx1 nCov-19 vaccine (8 days before the onset of first symptoms). After hospitalization, immediate intubation was done for airway protection. His neurological examination revealed blinking of eyes spontaneously, motor power of 0/5 in all four limbs, deep tendon reflex of +2, and mute plantar. MRI Brain was done on the next day (day of illness, DOI-4), which revealed acute infarct in the pons and bilateral cerebellar hemisphere. He was referred to our ICU on DOI-12. Repeat MRI Brain on DOI-16 showed subacute infarcts in the pons, bilateral middle cerebellar peduncles, and left cerebral hemisphere with thrombosed basilar artery. Lipid profile, homocysteine levels, auto-immune work-up were normal. Echocardiography showed normal LV function with no evidence of LA clot. Carotid Doppler showed normal carotid vessels. In view of ischemic stroke and basilar artery thrombosis anti-platelet agent and therapeutic anticoagulation continued. Over the next 3 weeks, he showed gradual improvement in motor power (3/5 in upper limbs and 2/5 in lower limbs) and weaned off from mechanical ventilation. Case 2: A 19-y-m hospitalized with complaints of acute onset paraesthesia and progressive weakness in both lower limbs for 4 days and difficulty in speech and swallowing for 1 day. He had no history of any comorbidity, and no history of preceding viral/bacterial infection except that he had received the first dose of the adenoviral vector-based ChAdOx1 nCov-19 vaccine (16 days before the onset of first symptoms). After hospitalization, he required intubation in view of pooling of oral secretions and respiratory distress. Clinical examination revealed bifacial weakness, severe neck muscle weakness, and flaccid areflexic quadriparesis with prominent proximal upper and lower limb weakness. Pin-prick sensation was distally reduced in both lower limbs with associated autonomic instability in the form of tachycardia and hypertension. MRI Brain was normal in the study. In further work, Guillain-Barré syndrome (GBS) was diagnosed. CSF showed albumin-cytologic dissociation (protein 1.14 g/L and nil cell), and bilateral motor nerve axonal neuropathy on nerve conduction study. Immunoglobulin (IVIG) therapy was started on DOI-6. He did not show significant improvement and was referred to our ICU for further management. During the 5th week of illness, the IVIG dose was repeated without any improvement and continuing requirement of mechanical ventilation. Conclusion: Though vaccination is one of the important public health interventions implemented to tackle the COVID-19 pandemic, there are known and unknown serious AEFI being reported. Both cases presented quadriparesis with different diagnoses, who received vaccination for COVID-19.

12.
Indian Journal of Critical Care Medicine ; 26:S70-S71, 2022.
Article in English | EMBASE | ID: covidwho-2006360

ABSTRACT

Aim and background: Cases of thrombotic thrombocytopenia induced by coronavirus disease 2019 (COVID-19) vaccines have been reported recently. Herein, we describe hemophagocytic lymphohistiocytosis (HLH) following COVID-19 vaccination. Case report: A 35-year-old male, chronic alcoholic, 3 years into abstinence received first dose Covishield vaccine. He started developing a fever, testicular pain, diminished sensorium requiring invasive ventilation, and decreased urine output 4 days after getting vaccinated. Initial workup for NCCT brain and HRCT chest was normal, tropical fever panel was negative, cultures for blood and endotracheal aspirate were sterile, liver and renal functions showed mild derangement, CSF study was normal. Ultrasound examination of the abdomen revealed mild hepatosplenomegaly, mild testicular swelling, and suprainguinal lymphadenopathy, with no focus of infection. Subsequently, he developed bicytopenia with haemoglobin 9.0 g/dL and platelet counts 50 × 109/L, ferritin 2130 μg/L, triglyceride 353 mg/dL, and decreased fibrinogen 1.41 g/L. Bone marrow as well as lymph node biopsy showed haemophagocytosis with engulfment of neutrophils, lymphocytes, and normoblasts making HLH a likely diagnosis. Soluble CD25 and NK cell function could not be performed. Extensive evaluation was done to look into the etiology of HLH. SARS-CoV-2 reverse transcriptase-polymerase chain reaction (RT-PCR) test was negative. RT-PCR test for Epstein-Barr virus (EBV), influenza A (H1N1, H3N2), influenza B, cytomegalovirus (CMV) performed from endotracheal aspirate (ETA) was negative. Similarly, the RT-PCR test from serum samples for EBV, Parvo B-19, CMV, and from CSF sample for EBV, Parvo B-19, CMV, and HSV-1 was negative. Hepatitis B, C, and HIV serologies were negative. Culture and sensitivity repeated from blood, ETA and urine was sterile. Autoimmune panel including complements levels were negative. Peripheral smear, bone marrow, and lymph node biopsy were normal and did not reveal abnormal or malignant cells. He had persistent fevers to 38.6°C during the first 6 days of his admission, with a rise in his ferritin to 1950 μg/L. The patient received steroids but not etoposide. By the 8th day, his fevers resolved, with improvement in his lethargy and malaise. Two weeks later, his ferritin had reduced to 510 μg/L, platelet count rose to 180 × 109/L, and repeat ultrasound abdomen demonstrated resolution of his splenomegaly. In our patient, there was no clear precipitant of HLH other than the Covishield vaccine. There was no evidence of an infection or malignancy. Due to our patient's clinical stability, resolution of symptoms, and improvement of HLH parameters he did not require HLH specific therapy. It is unclear if he had a pre-existing genetic predisposition to HLH as genetic testing is pending, however, it is unlikely as he has reached the age of 35 and suffered from previous viral infections without developing HLH.

13.
Frontiers in Cellular and Infection Microbiology ; 12, 2022.
Article in English | EMBASE | ID: covidwho-2005850

ABSTRACT

Purpose: The Corona Virus Disease 2019 (COVID-19) pandemic has become a challenge of world. The latest research has proved that Xuanfei Baidu granule (XFBD) significantly improved patient’s clinical symptoms, the compound drug improves immunity by increasing the number of white blood cells and lymphocytes, and exerts anti-inflammatory effects. However, the analysis of the effective monomer components of XFBD and its mechanism of action in the treatment of COVID-19 is currently lacking. Therefore, this study used computer simulation to study the effective monomer components of XFBD and its therapeutic mechanism. Methods: We screened out the key active ingredients in XFBD through TCMSP database. Besides GeneCards database was used to search disease gene targets and screen intersection gene targets. The intersection gene targets were analyzed by GO and KEGG. The disease-core gene target-drug network was analyzed and molecular docking was used for verification. Molecular dynamics simulation verification was carried out to combine the active ingredient and the target with a stable combination. The supercomputer platform was used to measure and analyze the number of hydrogen bonds, the binding free energy, the stability of protein target at the residue level, the solvent accessible surface area, and the radius of gyration. Results: XFBD had 1308 gene targets, COVID-19 had 4600 gene targets, the intersection gene targets were 548. GO and KEGG analysis showed that XFBD played a vital role by the signaling pathways of immune response and inflammation. Molecular docking showed that I-SPD, Pachypodol and Vestitol in XFBD played a role in treating COVID-19 by acting on NLRP3, CSF2, and relieve the clinical symptoms of SARS-CoV-2 infection. Molecular dynamics was used to prove the binding stability of active ingredients and protein targets, CSF2/I-SPD combination has the strongest binding energy. Conclusion: For the first time, it was found that the important active chemical components in XFBD, such as I-SPD, Pachypodol and Vestitol, reduce inflammatory response and apoptosis by inhibiting the activation of NLRP3, and reduce the production of inflammatory factors and chemotaxis of inflammatory cells by inhibiting the activation of CSF2. Therefore, XFBD can effectively alleviate the clinical symptoms of COVID-19 through NLRP3 and CSF2.

14.
Multiple Sclerosis and Related Disorders ; 59, 2022.
Article in English | EMBASE | ID: covidwho-2004361

ABSTRACT

Introduction: Since the declaration of COVID-19 pandemic, several cases of demyelination of both peripheral and central nervous systems have been reported. The association of viral infection and the development of CNS demyelination has long been studied, and this link has recently been reported following SARS-CoV-2 infection as well. Material(s) and Method(s): We report a case of a 36-year-old male who developed CNS demyelinating disease, that fulfilled the diagnostic criteria of multiple sclerosis (MS), 2 months after laboratory-confirmed infection with SARS-CoV-2. Result(s): A 36-year-old male developed CNS demyelination, 2-months following a laboratory-confirmed SARS-CoV-2 infection, that fulfilled the revised 2017 McDonald diagnostic criteria for MS. He presented with ataxia, and MRI showed multiple demyelinating lesions in the brain, and positive oligoclonal bands in CSF. Conclusion(s): To our knowledge, this is the second case report of MS in association with COVID-19 infection, and the first case from Middle East and North Africa (MENA) region. This case report adds to the growing body of evidence of a probable causal relationship between SARS‐CoV‐2 infection and the development of MS. SARS-CoV-2 could potentially trigger a demyelinating process, through an acute or delayed immune-mediated CNS inflammatory response.

15.
Multiple Sclerosis and Related Disorders ; 59, 2022.
Article in English | EMBASE | ID: covidwho-2004360

ABSTRACT

Background: CNS involvement in CLL is rare and it usually occurs in late-stage CLL disease. There is usual delay in the diagnosis due to its variable manifestations, challenging diagnosis process and possible misdiagnosis with a mimicker condition. I am sharing our relative successful experience with this challenging case that had satisfied outcome after going through comprehensive investigations and treatment journey treating his symptoms until arriving the final diagnosis and getting the best treatment option. Material(s) and Method(s): A 42 years old male, with recent COVID-19 infection, presented with multiple progressive neurologic symptoms over one month;started as numbness around the mouth, reduced facial sensation and a feeling of band like sensation below the costal margins. On exam, he had left abduction restriction, diplopia on left gaze and upbeat nystagmus, reduced facial sensation and hyperesthesia. The reflexes were 1+ in the upper limbs, 3+ in the lower limbs, up going planters, tingling from the feet up to T6 level and postural tremor bilaterally. His CSF showed high protein level. MRI brain/ spine revealed left frontal juxtacortical white matter and bilateral middle cerebral peduncles lesions with post-contrast enhancement and long segment spinal cord demyelinating plaques. He was initially treated as a case of Acute disseminated encephalomyelitis (ADEM) post viral infection in a background of CLL. The delayed diagnosis was due to temporal relation of neurological manifestation to viral infection, similar MRI lesions to ADEM and multiple negative CSF results of cytology and flow cytometry. He had persistent disabling symptoms and enhancing lesions in MRI despite being treated with IVMP, IVIG and PLEX. He was managed for ADEM based on responsiveness to the recommended therapy step by step. Firstly, he received a high-dose corticosteroids, secondly IV immunoglobulin but he was still progressing and considered as steroid-unresponsive ADEM. lastly, plasma exchange was done when he exhibited progressive symptoms with fair improvement. Interestingly, the patient showed significant improvement in the clinical and radiological parameters after starting him with a new anti-leukemia medication (Acalabrutinib) for his concurrent active condition. He run out of his medication for around 1 week and he experienced recurrent of the neurological manifestation and the previous lesions in the images. A repeated flow cytometry for the third time came positive for CLL cells and the final diagnosis of CNS involvement by CLL was established. The diagnosis was made after the exclusion of other etiologies. Result(s): The patient received Ibrutinib at a standard dose and as a monotherapy. It is an efficient chemotherapy that crosses the blood brain barrier and has showed a favorable clinical, biological and radiological outcome. The patient is back to his work and his daily activities have improved. Conclusion(s): In case of inconclusive work up, CSF analysis should be repeated testing for cytology and flow cytometry\immunophenotypes as the false negative results are common. Our patient had an active CLL proved in his investigations, and the fact that the patient responded very well to the new chemotherapy should alert the diagnosis of CNS involvement by CLL and directs towards repeating investigations and introducing aggressive treatment strategy to target both hematological and neurological complications of the condition.

16.
EJVES Vascular Forum ; 54:e49-e50, 2022.
Article in English | EMBASE | ID: covidwho-2004043

ABSTRACT

Introduction: Aortic aneurysmal disease is an evolving pathology: when treating an aortic aneurysm, we must consider the possibility of a thoraco-abdominal evolution aneurysm, which might lead to further treatments. In case of challenging anatomies (narrow aortic lumen at the level of visceral arteries, aortic wall thrombus, true lumen in an aortic dissected aneurysm, and focal aortic narrow diameter), unfavourable both for fenestrated endovascular aneurysm repair (FEVAR) and branched endovascular aneurysm repair (BEVAR), an inner branched custom made device could represent a potential feasible solution. Inner branched endografts have a typical configuration that combines the advantageous characteristics of both fenestrated and side branched endografts, thus showing advantages over other custom made grafts. Our study aimed to investigate the potential role of this technique in a broad variety of aortic anatomies unfavourable for FEVAR and BEVAR, in patients who received different previous aortic treatments. Methods: In our institution, between July 2018 and July 2020, 20 consecutive patients underwent a FEVAR/BEVAR procedure to treat complex abdominal aortic aneurysm or thoracic aortic aneurysm. Nine patients who were deemed untreatable with a fenestrated/branched graft due to aortic anatomy and/or previous treatments were treated with a custom made, four inner branch E-xtra design endograft (I BEVAR). All patients were treated for a complex aortic abdominal and thoraco-abdominal aneurysm: two patients were previously treated with frozen elephant trunk and TEVAR;three patients were previously treated with TEVAR;and one with TEVAR + abdominal aortic surgical treatment. Two patients received abdominal aortic surgical treatment only. The last patient was previously treated with EVAR, which was then complicated with a type 1A endoleak (EL). Five of six TEVARs were placed before BEVAR as staged procedures, to decrease spinal cord ischaemia risk. All patients had a lumbar cerebrospinal fluid drainage during the BEVAR procedure. In total, the bridging stents placed included 43 balloon expandable and four self-expandable stents. Results: In our experience, all cases were treated with a four inner branch endograft with a total revascularisation of 36 target vessels. Technical success was achieved in all nine cases (100%), with precise deployment of the inner branched endograft and effective engagement and bridging of all branches. Major clinical complications occurred in three (33%) patients: one case of continuous veno-venous haemofiltration treatment for a transient acute renal failure in a chronic renal disease;one case of hepatic decompensation in patient with a chronic cirrhosis, which led to liver failure (Child Pugh C10, MELD 19, still under medical treatment);and one patient with a pulmonary infection disease (COVID-19 related), which then resolved. No patient suffered spinal cord ischaemia. The mean follow up was 12.8 months ± 6.79 months, with an estimated one year survival rate of 89%. One patient with a thrombophilic disorder died on postoperative day 48 as a result of multiple organ failure after acute four inner branches simultaneous occlusion. During follow up, the target vessel primary patency rate was 89%, associated with four (11%) bridging stent ELs. At 30 days, computed tomography angiography detected five BS ELs in four patients: one type III BS EL (2.7%), and four type I BS ELs (11%). Re-intervention was needed in one patient (11%) with a type III and I BS EL associated with an aneurysm sac enlargement treated with bridging stent relining in the left renal artery and superior mesenteric artery. Conclusion: Our experience shows the feasibility of treating complex aortic anatomies with an inner branched graft in patients which were anatomically unfit for FEVAR/BEVAR treatment, allowing complex visceral vessels recanalisation and an adequate sealing. When a re-intervention is needed, we have to consider that previous surgical and endovascular treatments modify the aortic anatomy, and the graft deploy ent may be tougher, with a higher risk of malrotation. Inner branched endograft could be a valid option in case of complex anatomies, but long term follow up is needed.

17.
Pediatrics ; 149, 2022.
Article in English | EMBASE | ID: covidwho-2003505

ABSTRACT

Introduction: Acute necrotizing encephalopathy (ANE) is a rare condition often triggered by infection and characterized by febrile prodromal illness, seizures, altered mental status and bilateral brain lesions. While many cases are isolated, a recurrent familial pattern has been linked to missense mutation of the gene encoding RAN binding protein 2 (RANBP2). Early administration of high dose steroids has been associated with improved outcomes, while IVIG and tocilizumab have also shown benefit. Case Description: A two-year-old male presented with vomiting, somnolence and seizure-like activity. Evaluation revealed positive SARS-CoV2, adenovirus and rhinovirus/enterovirus PCR by nasopharyngeal swab, and Mycoplasma pneumoniae IgM. MRI showed numerous foci of restricted diffusion and microhemorrhage as well as necrotic change in the internal capsules. He was diagnosed with ANE. He recovered to neurologic baseline following treatment with IVIG and corticosteroids. After six months, the patient presented with similar symptoms. SARS-CoV2 IgG was positive, but no new infectious pathogens were identified. Cerebrospinal fluid (CSF) analysis showed elevated IL-6 and IL-8 levels, suggestive of inflammatory breakdown of the blood-brain barrier. Brain MRI demonstrated worsened bilateral T2/fluid attenuated inversion reduction signal abnormalities and necrosis within the midbrain and pons bilaterally, concerning for recurrent ANE. Following multidisciplinary consultation, the patient was treated with corticosteroids and IVIG. Tocilizumab was later added due to elevated CSF IL-6. Worsening MRI findings (Figure 1) coupled with decrease in strength and spontaneous movement prompted plasma exchange (PLEX) therapy. While his exam improved after PLEX, treatment was discontinued due to development of a pericardial effusion. The patient steadily improved neurologically and was transitioned to inpatient rehabilitation with an ongoing steroid taper, monthly IVIG, and tocilizumab therapy. Given recurrence of ANE, an epilepsy genetic sequencing panel was ordered and revealed heterozygous mutation in RANBP2 (c.1966A>G p.Ile656Val). Discussion: During the patient's initial presentation, it was reasonable to conclude an infectious trigger for ANE given the presence of several potential inciting pathogens. Upon recurrence, investigation of underlying genetic predisposition was warranted. This patient exhibited the classic clinical and radiographic findings of recurrent ANE and was found to have RANBP2 mutation. Available literature suggests pathogenicity of the same mutation identified in this case due to its location in a highly conserved genetic region and its presence in affected members of a family with ANE. To our knowledge, this is the second report of this specific RANBP2 mutation in association with ANE. Conclusion: While ANE may present as a singular event following infection, recurrence is rare and should prompt evaluation of underlying genetic predisposition. Consideration of familial ANE with testing for RANBP2 mutation may lead to early genetic counseling. Our case also provides additional support for the pathogenicity of the RANBP2 (p.Ile656Val) mutation. (Figure Presented).

18.
Pediatrics ; 149, 2022.
Article in English | EMBASE | ID: covidwho-2003484

ABSTRACT

Introduction: The COVID-19 pandemic has been widely described, however, there is limited data regarding neonatal infection. We present an extremely premature neonate with suspected COVID-19 pneumonia treated with Remdesivir. Case Description: Our patient is an infant born via emergency cesarean section for chorioamnionitis at 24 weeks gestational age with extremely low birth weight (ELBW). Mother is a 23-yearold primigravid female whose pregnancy was complicated by asymptomatic COVID-19 infection diagnosed by nasopharyngeal PCR ten days prior to delivery. Antenatal steroids were given for imminent premature delivery. Infant was intubated during initial resuscitation then extubated to non-invasive positive pressure ventilation (NIPPV) on day three of life. On day seven of life, she developed increasing apneic spells and feeding intolerance. Empiric antibiotics were initiated while awaiting blood and cerebrospinal fluid cultures. Blood culture grew Serratia marcescens and antibiotic coverage was tailored to cefepime monotherapy. Our patient remained stable on non-invasive respiratory support seven days into her sepsis event. Around this time, histopathological analysis of the placenta revealed acute villitis and intervillositis highly suggestive of COVID-19 placentitis. A positive nasopharyngeal COVID-19 PCR was noted on day ten of life. Our patient remained stable on non-invasive respiratory support until day fourteen of life, when she suddenly developed refractory hypoxemia requiring intubation. This coincided with acute changes in her chest x-ray (Fig 1). The negative bacterial respiratory culture, timing of clinical deterioration, and placental findings increased our suspicion for symptomatic co-infection with COVID-19. Patient continued to have refractory hypoxia and poor ventilation despite maximum settings and inhaled nitric oxide. After an extensive multidisciplinary discussion, patient received Remdesivir as a compassionate measure. Neonatal dosage was well tolerated with no adverse effects at 5 mg/kg loading dose followed by four days of maintenance dosing at 2.5 mg/kg. Significant clinical improvement was noted after the second day by decreasing FiO2 requirements. COVID-19 PCR remained positive ten days after Remdesivir treatment was completed. Patient was extubated to NIPPV on day thirty-six of life and is currently requiring no respiratory support at 37 weeks corrected age. Discussion: We present an ELBW neonate with placental findings typical of COVID-19 infection and refractory hypoxemia likely due to COVID-19 pneumonia. To date, the mechanism for this infant's infection is unclear. Based on the Acharya et al. Classification for Maternal-Fetal-Neonatal SARS-CoV-2 infection, our patient fits into probable neonatal infection acquired post-partum category. We have strong evidence of infection but lack of absolute proof to confirm congenital disease as no testing was done at birth. We acknowledge that part of the clinical course was complicated by sepsis, however, the peak of illness correlates with the typical clinical course for COVID-19 infection. Conclusion: To our knowledge, this may be the youngest patient documented to have COVID-19 pneumonia and received Remdesivir treatment.

19.
Biomedica ; 42:1-46, 2022.
Article in English | Web of Science | ID: covidwho-2003382

ABSTRACT

Neuroimmunology is a discipline that increasingly broadens its horizons in the understanding of neurological diseases. At the same time and in front of the pathophysiological links of neurological diseases and immunology, specific diagnostic and therapeutic approaches have been proposed. Despite the important advances in this discipline, there are multiple dilemmas that concern and filter into clinical practice. This article presents 15 controversies and a discussion about them, which are built with the most up-to-date evidence available. The topics included in this review are: steroid decline in relapses of multiple sclerosis (MS), therapeutic recommendations in MS in light of the SARS-CoV2 pandemic, evidence of vaccination in MS and other demyelinating diseases, overview current situation of isolated clinical and radiological syndrome, therapeutic failure in MS as well as criteria for suspension of disease-modifying therapies, evidence of the management of mild relapses in MS, recommendations for prophylaxis against strongyloides stercolaris, usefulness of a second course of immunoglobulin in the syndrome Guillain-Barre (GBS), criteria to differentiate an acute-onset inflammatory demyelinating chronic polyneuropathy versus GBS and the utility of angiotensin-converting enzyme in neurosarcoidosis. In each of the controversies, the general problem is presented and specific recommendations are offered that can be adopted in daily clinical practice.

20.
Pediatrics ; 149, 2022.
Article in English | EMBASE | ID: covidwho-2003274

ABSTRACT

Background: Pre-COVID literature suggests that viral infections account for about 90% of cases of fever in infants ≤56 days of age. Given the reduction in non-SARS-CoV-2 viral infections observed during the COVID-19 pandemic, we sought to determine if SBI accounted for a higher than usual proportion of fever cases in this age group during this period. Methods: We performed a multi-center, retrospective chart review of infants age ≤56 days presenting with fever to emergency departments (EDs) of six community hospitals affiliated with the same academic children's hospital. We compared the incidence of SBIs, viral meningitis, and viral bronchiolitis during March 2020 - February 2021 (pandemic year) with the same calendar months in the two preceding years (pre-pandemic years). Results: From March 2018 to February 2021, 543 febrile infants presented to the EDs, 95 during the pandemic year (Mar 2020-Feb 2021) compared to 231 and 217 in the pre-pandemic years (Mar 2018- Feb 2019 and Mar 2019-Feb 2020, respectively). The incidence of SBI was 28.4% (27/95) during the pandemic year compared to 11.6% (27/231) and 6.9% (15/217) in the pre-pandemic years (p<0.001);bacteremia 13.7% (13/95) during the pandemic year compared to 2.2% (5/231) and 1.4% (3/217) in the pre-pandemic years;and UTI 19% (18/95) during the pandemic compared to 11.3% (26/231) and 6.5% (14/217) in the pre-pandemic years (TABLE 1). Five patients were diagnosed with bacterial meningitis over the three-year period, four of them during the pandemic year, a rate of 4.2% (4/95). Rate of positivity for viral CSF PCR during the pandemic year was 6.4% (3/47) compared to 20.8% (25/120) and 20.4% (23/113) in the pre-pandemic years (Mar 2018-Feb 2019 and Mar 2019-Feb 2020 respectively;p=0.070). 2.1% (2/95) febrile young infants were admitted with a co-morbid diagnosis of bronchiolitis during the pandemic year compared to 4.3% (10/231) and 6.0% (13/217) in the pre-pandemic years (Mar 2018-Feb 2019 and Mar 2019-Feb 2020 respectively;p=0.310). The risk ratio for SBI (FIGURE 1) for pre-pandemic year 1 (referent;Mar 2018-Feb 2019) compared to the pandemic year (Mar 2020-Feb 2021) was 2.43 (95% CI 1.51-3.92;Bonferroni adjusted p=0.001);and the risk ratio for pre-pandemic year 2 (referent;Mar 2019-Feb 2020) compared to the pandemic year was 4.11 (95%CI 2.29-7.37;Bonferroni adjusted p<0.001). Conclusion: The COVID-19 pandemic led to an increase in the proportion of SBIs among febrile infants ≤56 days of age. This is likely a result of reduction in non-SARS-CoV-2 viral infections. Greater vigilance is thus warranted in the evaluation of febrile infants during the COVID-19 pandemic. (Table Presented).

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