D-Dimer as a prognostic marker of morbidity and mortality among HIV patients: a call for attention

2016 ◽  
Vol 48 (11-12) ◽  
pp. 860-861 ◽  
Author(s):  
Federico Aranda ◽  
Silvia Perés Wingeyer ◽  
Gabriela de Larrañaga
2019 ◽  
Vol 40 (1) ◽  
pp. 102-106 ◽  
Author(s):  
Yuki Yamada ◽  
Ryuji Kawaguchi ◽  
Kana Iwai ◽  
Emiko Niiro ◽  
Sachiko Morioka ◽  
...  

2021 ◽  
Author(s):  
Riju Maharjan ◽  
Anup Bastola ◽  
Nabaraj Adhikari ◽  
Komal Raj Rijal ◽  
Megha Raj Banjara ◽  
...  

Abstract Background Bacterial opportunistic infections are quite common in HIV patients. Besides HIV-TB coinfection, lower respiratory tract infections by multidrug-resistant bacteria cause significant morbidity and mortality among HIV patients. This study was done to evaluate the bacterial coinfection of LRT and detect plasmid-mediated blaTEM and blaCTX−M genes among Extended-Spectrum β-Lactamase (ESBL) producing isolates from sputum samples in HIV patients. Methods A total of 263 sputum samples from HIV-positive cases were processed with standard microbiological methods to isolate and identify the possible pathogens. The identified bacterial isolates were assessed for antibiotic susceptibility pattern by using modified Kirby Bauer disk diffusion method following Clinical Laboratory Standard Institute (CLSI) guidelines. Plasmid DNA was extracted from multidrug-resistant and ESBL producers for screening of ESBL genes; blaCTX−M and blaTEM by conventional PCR method using specific primers. Results Of 263 sputum samples, 67 (25.48%) were culture positive showing Klebsiella pneumoniae; 17(25.37%) as the most predominant one. A higher rate of infection (4/8, 50%) was observed among old-aged people of 61 -70 years, whereas no infection was observed below 20 years. About 30.0% (15/50) of smokers, 32.86% (23/70) cases with previous pulmonary tuberculosis and 52.38% (11/21) with CD4 count <200 cells/µl were found to be susceptible to LRTIs. Among 53 bacterial isolates, 52.83% (n=28) were multidrug-resistant and 43.4% (n=23) were ESBL producers. All ESBL producers were sensitive to Colistin and Polymyxin B. Of 23 ESBL producers, 47.83% (11/23) and 8.6% (2/23) possessed only blaCTX−M and blaTEM genes respectively and 43.48% (10/23) possessed both ESBL genes. Conclusion The increasing rate of MDR bacterial infections mainly ESBL producers of LRTIs causes difficulty in the management of diseases leading to high morbidity and mortality of HIV patients.


2019 ◽  
Vol 156 (6) ◽  
pp. S-1350-S-1351
Author(s):  
Tanabute Limprukkasem ◽  
Bubpha Pornthisarn ◽  
Ratha-Korn Vilaichone ◽  
Soonthorn Chonprasertsuk ◽  
Patommatat Bhanthumkomol ◽  
...  

2021 ◽  
Vol 41 (6) ◽  
pp. 327-335
Author(s):  
Tayfun Birtay ◽  
Suzan Bahadir ◽  
Ebru Kabacaoglu ◽  
Ozgur Yetiz ◽  
Mehmet Fatih Demirci ◽  
...  

BACKGROUND: SARS-CoV2/COVID-19 emerged in China and caused a global pandemic in 2020. The mortality rate has been reported to be between 0% and 14.6% in all patients. In this study, we determined the clinical and laboratory parameters of COVID-19 related morbidity and mortality in our hospital. OBJECTIVES: Investigate the relationship between demographic, clinical, and laboratory parameters on COVID-19-related morbidity and mortality. DESIGN: Retrospective observational study. SETTINGS: Tertiary care hospital. PATIENTS AND METHODS: Patients diagnosed with COVID-19 pneumonia from March until the end of December were included in the study. MAIN OUTCOME MEASURES: The relationship between demographic, clinical, and laboratory parameters and the morbidity and mortality rates of patients diagnosed with COVID-19. SAMPLE SIZE: 124 patients RESULTS: The mortality rate was 9.6% (12/124). Coronary artery disease ( P <.0001) diabetes mellitus ( P =.04) fever (>38.3°C) at presentation ( P =.04) hypertension ( P <.0001), and positive smoking history ( P <.0001) were significantly associated with mortality. Patients who died were older, had a higher comorbid disease index, pneumonia severity index, fasting blood glucose, baseline serum creatinine, D-dimer, and had lower baseline haemoglobin, SaO 2 , percentage of lymphocyte counts and diastolic blood pressure. Patients admitted to the ICU were older, had a higher comorbidity disease index, pneumonia severity index, C-reactive protein, WBC, D-dimer, creatinine, number of antibiotics used, longer O 2 support duration, lower hemoglobin, lymphocyte (%), and baseline SaO 2 (%). CONCLUSIONS: Our results were consistent with much of the reported data. We suggest that the frequency, dosage, and duration of steroid treatment should be limited. LIMITATIONS: Low patient number, uncertain reason of mortality, no standard treatment regimen, limited treatment options, like ECMO. CONFLICT OF INTEREST: None.


2021 ◽  
Vol 72 (3) ◽  
pp. 70-77
Author(s):  
Predrag Miljić

Coagulopathy in COVID-19 represents a thrombo-inflammatory condition, and it is one of the most important causes of morbidity and mortality in this disease. The occurrence of coagulopathy correlates with the intensity of the inflammatory response to SARS-Cov-2 virus infection, and its presence is characterized by laboratory markers of blood hypercoagulability and clinically pronounced prothrombotic condition. Although the mechanism of coagulopathy is not fully elucidated, dysregulated and overemphasized immune responses mediated by inflammatory cytokines, complement activation, leukocyte activation with release of free nucleic acids and histones into the circulation, hypoxia and endothelial damage play a very important role in its development. Thrombosis can occur in all parts of the circulatory system and is most often localized in the microcirculation and venous part of the vasculature. A number of studies have shown that the presence of thrombotic pulmonary embolism can be demonstrated by objective methods in approximately 15% of COVID-19 patients treated in intensive care units, while the incidence of total venous thromboembolism in this group of patients is over 20% despite antithrombotic prophylaxis. Although much less common than venous thrombosis, arterial thrombosis may also occur in COVID-19 patients, most often in the form of myocardial infarction, ischemic stroke and peripheral artery occlusion. Damage to the endothelium under the influence of virus or inflammatory response, activation of platelets and coagulation system with fibrin deposition leads to extensive thrombosis in the microcirculation of lungs and other tissues and directly contributes to respiratory failure, ARDS or multiorgan failure. Therefore, coagulopathy in COVID-19 is an integral part of the pathophysiological mechanism of the disease and contributes to its clinical manifestation and progression. Main laboratory characteristics of COVID-19 coagulopathy are elevated values of D-dimer in the blood, which occurs in the process of decomposition of precipitated fibrin under the action of fibrinolytic enzymes in the microcirculation of the lungs and other organs. Therefore, D-dimer values reflect the intensity of the inflammation in the lungs and have prognostic significance in recognizing patients at risk of serious complications and unfavorable course of the disease. In contrast to disseminated intravascular coagulation in sepsis, severe thrombocytopenia and hypofibrinogenemia as well as bleeding tendencies are rare in COVID-19 coagulopathy. Due to the high frequency and important role of coagulopathy in morbidity and mortality, the use of anticoagulant therapy is recommended in all hospitalized patients. However, the optimal way of treating coagulopathy and the intensity of antithrombotic prophylaxis are not known, and represent the subject of intensive research.


2020 ◽  
Vol 9 (5) ◽  
pp. 2431
Author(s):  
Izna ◽  
Puneeta Vohra ◽  
Sharayu Nimonkar ◽  
Vikram Belkhode ◽  
Suraj Potdar ◽  
...  

2013 ◽  
Vol 19 (5) ◽  
pp. 1-12
Author(s):  
Khaled Abd El-Twab ◽  
Hala Foaud ◽  
John youssef ◽  
Hala Metwally

2020 ◽  
Vol 11 ◽  
Author(s):  
Giris Jacob ◽  
Anat Aharon ◽  
Benjamin Brenner

The emerging novel coronavirus disease (COVID-19), which is caused by the SARS-CoV-2 presents with high infectivity, morbidity and mortality. It presenting a need for immediate understanding of its pathogenicity. Inflammation and coagulation systems are over-activated in COVID-19. SARS-CoV-2 damages endothelial cell and pneumocyte, resulting in hemostatic disorder and ARDS. An influential biomarkers of poor outcome in COVID-19 are high circulating cytokines and D-dimer level. This latter is due to hyper-fibrinolysis and hyper-coagulation. Plasmin is a key player in fibrinolysis and is involved in the cleavage of many viruses envelop proteins, including SARS-CoV. This function is similar to that of TMPRSS2, which underpins the entry of viruses into the host cell. In addition, plasmin is involved in the pathophysiology of ARDS in SARS and promotes secretion of cytokine, such as IL-6 and TNF, from activated macrophages. Here, we suggest an out-of-the-box treatment for alleviating fibrinolysis and the ARDS of COVID-19 patients. This proposed treatment is concomitant administration of an anti-fibrinolytic drug and the anticoagulant.


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