scholarly journals 293: HIGH-DOSE DEXAMETHASONE IN PATIENTS WITH SARS-COV-2 INFECTION REQUIRING OXYGEN IN MEDICAL ICU

2021 ◽  
Vol 50 (1) ◽  
pp. 132-132
Author(s):  
Muhammad Ahmad ◽  
Rajesh Kunadharaju ◽  
arjun Saradna ◽  
Sri Harika Meka ◽  
Gregory Fuhrer
2021 ◽  
Author(s):  
Archrob Khuhapinant ◽  
Tarinee Rungjirajittranon ◽  
Bundarika Suwanawiboon ◽  
Yingyong Chinthammitr ◽  
Theera Ruchutrakool

Abstract BackgroundVaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare but fatal complication of Coronavirus Disease 2019 vaccine. Many reports of VITT have mostly been in the Caucasian population. Here, we present first reported case from an oriental population.Case presentationA 26-year-old female who had severe headache and severe thrombocytopenia 8 days after administration of the ChAdOx1 nCoV-19 vaccine developed by AstraZeneca. Although no thrombosis was demonstrated by imaging studies, she had very highly elevated d-dimer level during hospitalization. Serology for antibody against platelet factor 4 was positive on several days with very high optical density readings. Furthermore, we found the antibody could induce spontaneous platelet aggregation without the presence of heparin. We decided to treat her with intravenous immunoglobulin, high-dose dexamethasone, and a prophylactic dose of apixaban. She improved rapidly and was discharged from the hospital 6 days after admission. Neither thrombocytopenia nor thrombosis was subsequently detected at three weeks follow-up.ConclusionsDespite lower rate of thrombosis, VITT can present in Asian population. Early detection and prompt treatment of VITT can improve patients’ clinical outcome. Thromboprophylaxis of non-heparin anticoagulants also results in prevention of clot formation.


2007 ◽  
Vol 293 (3) ◽  
pp. G552-G559 ◽  
Author(s):  
Lawrence A. Scheving ◽  
Renee Buchanan ◽  
Michael A. Krause ◽  
Xiuqi Zhang ◽  
Mary C. Stevenson ◽  
...  

Glucocorticoids paradoxically exert both stimulatory and inhibitory effects on the proliferation of cultured rat hepatocytes. We studied the effects of dexamethasone, a synthetic glucocorticoid, on the proliferation of cultured rat hepatocytes. The timing of growth factor addition modified the action of high-dose dexamethasone (10−6 M) on DNA synthesis. When we added transforming growth factor-α at the time of plating, 10−6 M dexamethasone weakly stimulated DNA synthesis by 26% relative to cells cultured in dexamethasone-free media. When we delayed growth factor addition until 24–48 h after plating, 10−6 M dexamethasone inhibited DNA synthesis by 50%. Using immunological methods, we analyzed the expression and signaling patterns of the ErbB kinases in dexamethasone-treated cells. High-dose dexamethasone stabilized the expression of epidermal growth factor receptor (EGFr) and ErbB3, and it suppressed the de novo expression of ErbB2 that occurs during the third and fourth day of culture in 10−8 M dexamethasone. High-dose dexamethasone by 72 h suppressed basal and EGF-associated phosphorylation of ERK and Akt. The reduction in ERK1/2 phosphorylation correlated with suppression of a culture-dependent increase in Son-of sevenless 1 (Sos1) and ERK1/2 expression. High-dose dexamethasone in hepatocytes stabilized or upregulated several inhibitory effectors of EGFr/ErbB2 and ERK, including receptor-associated late transducer (RALT) and MKP-1, respectively. Thus 10−6 M dexamethasone exerts a time-dependent and redundant inhibitory effect on EGFr-mediated proliferative signaling in hepatocytes, targeting not only the ErbB proteins but also their various positive and negative effectors.


Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 13-14
Author(s):  
Ramil Fatkhullin ◽  
Vasily Shuvaev

Increased numbers of COVID-19 infection make the study of its systemic manifestations more and more important. Despite of SARS-Cov-2 main clinical respiratory syndrome other clinical infection signs as immune thrombocytopenia without respiratory failure were identified. We have seen case series of patients with thrombocytopenia and active COVID-19 infection during present epidemic outbreak. Patient 1, female, 31 years old was admitted at our hospital with ecchymoses, epistaxis, gingival hemorrhage and metrorrhagia. There were also signs of COVID-19 infection - fever up to 40oC, short of breathes with room air. The pulmonary infiltrates about to 25% were revealed by CT scan. The CBC parameters were as follows: WBC 8.9x109/l, Hb 11,2 g/dl, PLT 3 x109/l by microscopy. The patient was treated with high-dose dexamethasone 40 mg QD for 4 days. The treatment resulted to stable complete platelet response as 189x109/l in fourteen days after start of therapy. At that time, the cancer in situ of cervix uteri there was revealed by gynecologic examination, that was successfully local treated. Patient 2, female 30 years old presented epistaxis, metrorrhagia, cutaneous and gingival hemorrhagic syndrome as previous patient. There were WBC 6.4x109/l, Hb 12,6 g/dl, PLT 3x109/l by microscopy in CBC. She had no respiratory signs and abnormality in pulmonary CT. The COVID-19 infection was identified by PCR and antibody screening. The patient also received high-dose dexamethasone 40 mg QD for 4 days and yielded of platelet elevation to 25x109/l with no hemorrhagic syndrome in five days of treatment. Patient 3, female 68 years old with chronic course of immune thrombocytopenia and resistance to glucocorticoid, after splenectomy and presence of HBsAg. All relapses of thrombocytopenia in this patient were associated with virus infection. The first episode was in 2009, patient was treated with glucocorticoid with no effect. The complete platelet response was achieved after splenectomy. The relapse occurred in 2015 and was associated with acute respiratory distress syndrome (probably H7N9 flu). There treatment with prednisone 1 mg/day resulted to complete platelet response. At present time, the COVID-19 infection on this patient manifested with 75% of pulmonary volume lesions. At the recovery (25% of pulmonary infiltrates) the relapse of immune thrombocytopenia with cutaneous bleeding occurred. In CBC there were WBC 5.9x109/l, Hb 15,1 g/dl, PLT 5x109/l by microscopy. Given that history of therapy we treated this patient with high-dose dexamethasone 40 mg QD for 4 days and romiplostime 2 mqg/kg. The complete resolution of hemorrhagic signs and platelet response (65x109/l) was reached in seven days of treatment. Discussion. The virus-associated thrombocytopenia is usual in common practice. In recent COVID-19 infection outcome meta-analysis (G. Lippi et al. Clinica Chimica Acta 506 (2020) 145-148) the platelet count was significantly lower in severe course of disease. The presence of platelet below the lower limit was associated with fivefold of risk of severe COVID-19 and was a factor of mortality. The platelet decline could be as sign of disease worsening at one hand and have an own risk of mortality by bleeding at other hand. There is a need for guideline to thrombocytopenia management in COVID-19 patients. Now we are continuing to search and include the patients with COVID-19 infection and thrombocytopenia in our study. Disclosures Shuvaev: Novartis:Honoraria, Speakers Bureau;BMS:Honoraria, Speakers Bureau;Pfizer:Honoraria, Speakers Bureau.


2010 ◽  
Vol 28 (33) ◽  
pp. 4976-4984 ◽  
Author(s):  
Meletios A. Dimopoulos ◽  
Evangelos Terpos ◽  
Asher Chanan-Khan ◽  
Nelson Leung ◽  
Heinz Ludwig ◽  
...  

Renal impairment is a common complication of multiple myeloma (MM). The estimated glomerular filtration rate (eGFR) using the Modification of Diet in Renal Disease formula is the recommended method for the assessment of renal function in patients with MM with stabilized serum creatinine. In acute renal injury, the RIFLE (risk, injury, failure, loss and end-stage kidney disease) and Acute Renal Injury Network criteria seem to be appropriate to define the severity of renal impairment. Novel criteria based on eGFR measurements are recommended for the definition of the reversibility of renal impairment. Rapid intervention to reverse renal dysfunction is critical for the management of these patients, especially for those with light chain cast nephropathy. Bortezomib with high-dose dexamethasone is considered as the treatment of choice for such patients. There is limited experience with thalidomide in patients with myeloma with renal impairment. Thus, thalidomide can be carefully administered, mainly in the context of well-designed clinical trials, to evaluate if it can improve the rapidity and probability of response that is produced by the combination with bortezomib and high-dose dexamethasone. Lenalidomide is effective in this setting and can reverse renal insufficiency in a significant subset of patients, when it is given at reduced doses, according to renal function. The role of plasma exchange in patients with suspected light chain cast nephropathy and renal impairment is controversial. High-dose melphalan (140 mg/m2) and autologous stem-cell transplantation should be limited to younger patients with chemosensitive disease.


2003 ◽  
Vol 285 (2) ◽  
pp. L451-L455 ◽  
Author(s):  
Liliana Moreno ◽  
David B. Jacoby ◽  
Allison D. Fryer

In the lungs, neuronal M2 muscarinic receptors inhibit acetylcholine release from the parasympathetic nerves. Parainfluenza virus infection causes loss of M2 receptor function, which increases acetylcholine release and vagally mediated bronchoconstriction. Because glucocorticoids are known to inhibit airway hyperresponsiveness, we tested whether dexamethasone (6.5 or 65 μg/kg ip) prevents virus-induced hyperresponsiveness and M2 receptor dysfunction in guinea pigs. In controls, pilocarpine, a muscarinic agonist, inhibited vagally induced bronchoconstriction, demonstrating functional M2 receptors. However, in virus-infected animals, pilocarpine failed to inhibit vagally induced bronchoconstriction, demonstrating M2 receptor dysfunction. Frequency-dependent bronchoconstriction was greater in virus-infected animals than in controls, indicating airway hyperresponsiveness. Low-dose dexamethasone (6.5 μg/kg ip) treatment prevented virus-induced airway hyperresponsiveness, ameliorated M2 receptor dysfunction, and decreased viral content in the lungs without inhibiting virus induced inflammation. High-dose dexamethasone (65 μg/kg ip) prevented virus-induced hyperresponsiveness, completely reversed M2 receptor dysfunction, decreased viral titers, and decreased virus-induced inflammation. This high-dose dexamethasone also increased M2 receptor function in uninfected animals. In conclusion, dexamethasone prevented virus-induced hyperresponsiveness and M2 receptor dysfunction via multiple mechanisms.


Sign in / Sign up

Export Citation Format

Share Document