Covid 19 laboratory parameters - Abdulsalam Al-Ani

COVID-19COVID-19
Laboratory ParametersLaboratory Parameters
Dr. Abdulsalam Al-Ani
Consultant Hematologist

OBJECTIVES
• Coronavirus.
• Pathophysiology of Immune Response.
• Immune Response to SARS-CoV-2.
• Pathophysiology of COVID-19 Infection
• COVID-19-induced Coagulopathy
• Laboratory Parameters Changes.
DR. ABDULSLAM AL-ANI / CONSULTANT HEMATOLOGISTCOVID-19 LABORATORY PARAMETERS

CORONAVIRUS
• Family species of RNA viruses with 4 forms; alpha, beta, gamma, and delta ( α,
β, ɣ, and δ) infecting living mammals, both human and animals.
• The known six human coronaviruses (HCV), and the novel coronavirus are of 2
main genotypes; (3 of alpha; α and 4 beta; β).
• Novel Coronavirus (severe acute respiratory syndrome coronavirus 2 (SARS-
CoV-2) belongs to the β-coronavirus family, and is partially related with the
known SARS-CoV (~79% similarity) and MERS-CoV (~50% similarity) according
to genome sequencing.

Same as SARS-CoV,
SARS-CoV-2 uses for
angiotensin-converting
enzyme 2 (ACE2) as its
S-protein main receptor,
which is broadly
expressed in vascular
endothelium,
respiratory epithelium,
alveolar monocytes, and
macrophages.

✓ The main transmission route is through respiratory tract exposure
(direct or indirect).
✓ SARS-CoV-2 is capable of active replication in the upper respiratory
tissues, as viral subgenomic messenger RNA (sgRNA) detected in cells of
upper respiratory tract.
✓ Secondary viremia develops, followed by extensive attack against target
organs that express ACE2, such as heart, kidney, gastrointestinal tract
and vast distal vasculature.

✓Infection with HCVs causing variable degree of illness from simple common
cold to acute respiratory distress syndrome (ARDS).
✓According to the World Health Organization (WHO), most people who
contract COVID-19 only experience mild flu-like symptoms. Occasionally, the
infection can cascade into a severe case of pneumonia that can be lethal,
especially for older people and those with underlying medical conditions.
✓Of note, two distinctive features have been noticed in severe and critical
patients with COVID-19, progressive increase of inflammation and an
unusual trend of hypercoagulation

Pathophysiology
Of
Immune Response

IMMUNE SYSTEM
Composed of 2 main components;
1- Innate Immune Response; performed by myeloid cell lineage origin cells
(granulocytes, monocytes and macrophages) and lymphoid cells (Natural
Killer and cytotoxic T cells).
2- Adaptive Immune Response; performed by the lymphoid cells, through
specific interaction of both T- and B- cells.

Hematopoietic
Stem Cells
Produce Cells in
Blood
and
Lymph
The Biology Project,
The University of Arizona

Neutrophil

❖ Innate Immune Response
✓ The body’s general reaction to any virus or attacking organism it does not recognize.
✓ Mainly performed by NK cells and T lymphocytes with the release of INFs.
✓ Natural killer (NK) cells kill virally infected cells via degranulation, receptor
mediated apoptosis, and antibody-dependent cell-mediated cytotoxicity.
✓ Innate immune cells secrete proinflammatory cytokines that inhibit viral replication,
stimulate the adaptive immune response, and recruit other immune cells to the site
of infection.
✓ The innate immune response prevents infections or reduces the severity of a
disease and its strength is influenced by many factors including health and age.
✓ Many people have a strong and healthy immune response to the new coronavirus
which may also give them protection against future infections

✓ Granulocytes degranulate in response to extracellular pathogens, releasing
enzymes and toxic proteins.
✓ Monocytes traffic to tissues and differentiate into monocyte-derived
macrophages and dendritic cells (mDCs).
✓ Macrophages and neutrophils phagocytose and destroy pathogens as well as
infected cells
✓ Activated DCs present pathogen-derived antigens to naive helper T cells to
initiate the adaptive immune response.
✓ Finally, the complement system plays a role in immune cell recruitment,
activation, and destruction of pathogens.

Peripheral Innate Immune Response:
-Some peripheral CD14+ monocytes have an
inflammatory phenotype and secrete T cell-
activating cytokines, whereas others have
decreased HLA class II expression, which
could result in decreased antigen presentation
to naive T cells.
Monocytes and activated granulocytes, such
as neutrophils, might phagocytose or
degranulate in response to opsonized infected
cells.
Prior to exhaustion, NK cells might kill
infected cells via direct killing or ADCC.
Although a decrease in the abundance of DCs
is reported, the behavior of DCs is currently
unknown.
DC, dendritic cell; NK cell, natural killer cell; ADCC,
antibody-dependent cellular cytotoxicity.

Innate Immune Reaction in the Lung:
There are increased levels of both
inflammatory macrophages and activated
neutrophils in the lung.
Inflammatory macrophages secrete IL-1β,
activating T cells.
Activated DCs are also present and likely take
up viral antigens to present to naive T cells.
NK cells, inflammatory macrophages, and
activated neutrophils could kill infected type II
alveolar epithelial cells by a variety of
mechanisms. Additionally, formation of the
MAC might also result in lysis of infected cells.
Complement proteins and chemokines
produced by lung epithelial cells and other
cell types at the site of infection recruit
additional immune cells.
DC, dendritic cell; NK cell, natural killer cell;
MAC, complement membrane attack complex.

The innate immune response and
adaptive immune responses of
Coronaviruses (CoV) infection during an
infection. CoV infects macrophages, and
then macrophages present CoV antigens
to T cells. This process leads to T cell
activation and differentiation, including
the production of cytokines associated
with the different T cell subsets (ie, Th17),
followed by a massive release of cytokines
for immune response amplification. The
continued production of these mediators
due to viral persistence has a negative
effect on NK, and CD8 T cell activation.
However, CD8 T cells produce very
effective mediators to clear CoV.
Inhibitory effects
Activating effects
Li, Geng, et al. Coronavirus infections and immune responses. Journal of medical virology 92.4 (2020):
424-432.

Attachment of CoV to DPP4R, also known as adenosine deaminase
complexing protein 2 or CD26 - cluster of differentiation 26) on the
host cell through S (Spike) protein leads to the appearance of
genomic RNA in the cytoplasm. An immune response to dsRNA can
be partially generated during CoV replication. TLR‐3 sensitized by
dsRNA and cascades of signaling pathways IRFs; are activated to
produce IFNs and proinflammatory cytokines. The production of
IFNs is important to enhance the release of antiviral proteins for the
protection of uninfected cells. Sometimes, accessory proteins of CoV
can interfere with TLR‐3 signaling and bind the dsRNA of CoV
during replication to prevent TLR‐3 activation and evade the immune
response. TLR‐4 might recognize S protein and lead to the activation
of proinflammatory cytokines through the MyD88‐dependent
signaling pathway. Virus‐cell interactions lead to the strong
production of immune mediators. The secretion of large quantities of
chemokines and cytokines (IL‐1, IL‐6, IL‐8, IL‐21, TNF‐β, and
MCP‐1) is promoted in infected cells in response to CoV infection.
These chemokines and cytokines, in turn, recruit lymphocytes and
leukocytes to the site of infection.
Li, Geng, et al. Coronavirus infections and immune responses. Journal of medical
virology 92.4 (2020): 424-432.
DPP4R; Dipeptidyl Peptidase-4 Receptor, S (Spike), TLR; Toll-like receptor, IRFs;
interferon regulatory factors B cells, TIRAP, TRAM; adapter molecules associated with
toll-like receptors, MyD88; Myeloid differentiation factor 88, TIR; Toll/IL-1 receptor,
TRIF: TIR-domain-containing adaptor-inducing IFN-b

❖ Mechanism of lymphocyte deficiency in COVID-19:
Multiple mechanisms mentioned might work together to cause
lymphopenia, and further researches are needed.
1. Lymphocytes and macrophages express the coronavirus receptor ACE2
and may be a direct target of viruses resulting redistribution of the circulating
lymphocytes or death by apoptosis or pyroptosis.
2. The virus might directly destroy lymphatic organs (thymus and spleen ).
3. Inflammatory cytokines (IL-6 and tumour necrosis factor; TNFα)
disordered, perhaps leading to lymphocyte apoptosis.
4. Elevated blood levels of metabolic molecules (lactic acid, hyperlactic
acidemia) inhibit lymphocytes proliferation and function.

❖ Adaptive Immune System
✓ Most viral infections are controlled by the innate immune system. However,
if viral replication outpaces innate defenses, the adaptive response must be
mobilized.
✓ The cells of the adaptive immune system are B- and T-lymphocytes.
✓ B-cells derived from the bone marrow, become the cells that produce
antibodies, while T cells mature in the thymus and differentiate into cells
that either participate in lymphocyte maturation, or kill virus-infected cells.
✓ The interaction between the innate and adaptive systems is so crucial that
the adaptive response cannot occur without an innate immune system.
✓ The adaptive defense consists of antibodies and lymphocytes, often called
the humoral response and the cell mediated response respectively.

✓ Antibodies generally bind to virus, thereby blocking the spread of infection. In
contrast, T cells recognize and kill infected cells.
✓ A key feature of the adaptive immune system is memory. Repeat infections by
the same virus are met immediately with a strong and specific response that
usually effectively stops the infection with less reliance on the innate system.
✓ The first adaptive response against a virus - called the primary response -
often takes days to mature.
✓ Memory response develops within hours of infection. This maintained by a
subset of B and T lymphocytes called memory cells which survive for years in
the body.
✓ Memory cells remain ready to respond rapidly and efficiently to a subsequent
encounter with a pathogen.
✓ This so-called secondary response is often stronger than the primary response
to infection.
✓ Uncontrolled or inappropriate adaptive response can also be damaging.

After binding an
antigen to the B cell
receptor (BCR), a B
cell internalizes the
antigen and presents
it on MHC II.
Helper T recognizes
the MHC II–antigen
complex and activates
the B cell.
As a result, memory
B cells and plasma
cells are made.

Virus-specific IgM and IgG are
detectable in serum between
7 and 14 days after the onset
of symptoms.
Viral RNA is inversely
correlated with neutralizing
antibody titers. Higher titers
have been observed in
critically ill patients, but it is
unknown whether antibody
responses somehow
contribute to pulmonary
pathology. The SARS-CoV-1
humoral response is relatively
short lived, and memory B
cells may disappear altogether,
suggesting that immunity with
SARS-CoV-2 may wane 1–2
years after primary infection.

Pathogenesis
Of COVID-19

❖INFECTION
✓The virus, SARS-CoV-2, enters the body - generally through the mouth or nose.
From there, the virus makes its way down into the lung alveoli
✓In the alveoli, the virus uses its distinctive spike (S) proteins to “hijack” cells
(primarily type II alveolar cells).
✓The primary genetic programming of any virus is to make copies of itself, and
COVID-19 is no exception. Once the virus’ RNA has entered a cell, new copies
are made and the cell is killed in the process, releasing new viruses to infect
neighboring cells in the alveolus.
✓This process can occur initially without a person being aware of the infection,
which is one of the reasons COVID-19 has been able to spread so effectively.

Nick Routley. Visualizing what COVID-19 does to your body, Healthcare

(S protein)
Nick Routley. Visualizing what COVID-19 does to your body, Healthcare

❖IMMUNE RESPONSE
✓The process of “hijacking” cells to reproduce causes inflammation in the
lungs, which triggers an immune response.
✓As this process continues, fluid begins to accumulate in the alveoli, causing
a dry cough and making breathing difficult.
✓For 80-85% of people infected by COVID-19, these symptoms will run their
course much as they would with a case of the flu.
✓Progression of the inflammatory process with increased effect of its signals
and cytokines, more fluid accumulate within the alveolar spaces with
subsequent impairment of gas exchange leading to hypoxia and SOB in the
form of moderate degree of illness.

✓The immune system’s response can cause what’s known as a ‘Cytokine Storm’ this
response can cause more damage to the body’s own cells than to the virus it’s trying
to defeat, and is thought to be the main reason for why the conditions of young,
otherwise healthy individuals can rapidly deteriorate.
✓At this stage, the surfactant that helps keep alveoli from collapsing has been diluted,
and fluid containing cellular debris is impairing the gas exchange.
✓In the most severe cases, systemic inflammatory response syndrome (SIRS) occurs
as the protein-rich fluid from the lungs enters the bloodstream, resulting in septic
shock and multi-organ failure. This is often the cause of death for people who have
succumbed to a COVID-19 infection.
✓A part from the inflammatory reaction alveolar walls may develop fibrosis, which
can be of permanent changes.

✓When SARS-CoV-2 infects cells expressing the surface receptors angiotensin-
converting enzyme 2 (ACE2) and Transmembrane Serine Protease 2
(TMPRSS2), the active replication and release of the virus cause the host cell
to undergo pyroptosis and release damage-associated molecular patterns,
including ATP, nucleic acids and apoptosis-associated speck-like protein (ASC)
oligomers.
✓These are recognized by neighboring epithelial cells, endothelial cells and
alveolar macrophages, triggering the generation of pro-inflammatory
cytokines and chemokines (including IL-6, IP-10, macrophage inflammatory
protein 1α (MIP1α), MIP1β and MCP1).
✓These proteins attract monocytes, macrophages and T cells to the site of
infection, promoting further inflammation (with the addition of IFNγ produced
by T cells) and establishing a pro-inflammatory feedback loop.

✓In a defective immune response, this may lead to further accumulation of immune
cells in the lungs, causing overproduction of pro-inflammatory cytokines, which
eventually damages the lung infrastructure. The resulting cytokine storm circulates to
other organs, leading to multi-organ damage. In addition, non-neutralizing antibodies
produced by B cells may enhance SARS-CoV-2 infection through antibody-dependent
enhancement (ADE), further exacerbating organ damage.
✓Alternatively, in a healthy immune response (right side), the initial inflammation
attracts virus-specific T cells to the site of infection, where they can eliminate the
infected cells before the virus spreads. Neutralizing antibodies in these individuals
can block viral infection, and alveolar macrophages recognize neutralized viruses and
apoptotic cells and clear them by phagocytosis. Altogether, these processes lead to
clearance of the virus and minimal lung damage, resulting in recovery.
G-CSF, granulocyte colony-stimulating factor; TNF, tumour necrosis factor.

MCP; Monocyte chemoattractant protein MIP ; Macrophage inflammatory protein
TMPRSS2;
Transmembrane
Serine Protease

COVID-19
Induced
Coagulopathy

HEMOSTASIS
Process of
response to
vascular damage,
performed by
interaction of;
Blood vessel wall
, Platelets and
Coagulation
factors

Coagulation Cascade
Through
Coagulation factors

❖Mechanism of Coagulopathy;
✓The novel coronavirus, SARS-CoV-2, activates the thrombotic
process in addition to the inflammatory reaction.
✓The disease it causes is associated with hypoxia, an increase in
inflammatory cytokines (cytokine storm) and coagulation
disorders, with predisposition to thrombus formation.
3 main mechanisms play as procoagulants predisposing for the
coagulopathy;
1. Severe and prolonged hypoxemia.
2. High incidence of cytokine storms.
3. Local pulmonary endothelial injury.

1. Hypoxia;
Hypoxia-inducible Factor (HIF) activation is the main resultant changes by COVID-
19 induced hypoxia, which enhance coagulopathy.
2
1
4
3

2. Inflammatory Effect;
✓Inflammation is the triggering factor for thrombogenesis.
✓Cytokines and chemokines have been associated with an important role in
immunity and immunopathology during viral infections.
✓The immune response to acute SARS-CoV-2 infection and the accompanying
surge of cytokines and inflammatory mediators (interleukin (ILs and chemokines)
can lead to activating pro-coagulant pathways.
✓On other hand, cytokines impaired the natural coagulation pathways and shut
down of fibrinolysis

✓ Mononuclear cells interact with activated platelets and the coagulation
cascade, which activate inflammatory cells by binding thrombin and tissue
factor with specific protease activated receptors and by binding fibrin to Toll-
like receptor 4.
✓ DIC develops as an advanced complication of sever infection and sepsis, with
causative factor of high mortality rate.

PARs; Protease-activated receptors
TLR4: Toll-like receptor 4

3. Endothelial Injury;
✓Inflammatory cytokines, together with endothelial injury, can up-regulate
tissue factor expression and further drive a pro-thrombotic state
✓Endothelial cell activation/damage due to the virus binding to the ACE2
receptor promoting acute inflammation and hypercoagulation may be of
paramount importance to explain the high thrombotic burden observed.

Difference of COVID-19 Coagulopathy from DIC
Disseminated Intravascular Coagulation is a generalized consumptive process
with microangiopathic hemolytic process, while COVID-19 is a localized pocess
mostly to the lung alveoli.
1. Mild thrombocytopenia.
2. Prothrombin time (PT) not always elevated.
3. Normal activated partial thromboplastin time (aPTT).
4. Elevations in fibrinogen and D-dimer levels.
5. No microangiopathic hemolytic process.

Laboratory
Parameters
Changes

• Lymphopenia; Direct infection of macrophages and lymphocytes by SARS-CoV
and redistribution of the circulating lymphocytes or depletion of lymphocytes
through apoptosis or pyroptosis.
• Lymphopenia is an important feature of SARS patients, and decline of both
CD4+ and CD8+ T lymphocytes often preceded the radiographic changes.
•

Haematological and Risk Factors in COVID-19.
1- Haematological and coagulation parameters;
white blood cell count, neutrophil count, lymphocyte count, neutrophil to
lymphocyte ratio (NLR), prothrombin time, D-dimer, fibrin degradation products.
Platelets were significantly lower in patients with critical disease
C-reactive protein, and lactate dehydrogenase, IL-10
serum ferritin.

❖HAEMATOLOGICAL CHANGES
• Leukocytes (WBCs);
The WBC changes mainly of leukopenia, which is can be as reflection of the
decreased lymphocyte count
Lymphopenia is an important feature of SARS patients, and decline of both
CD4+ and CD8+ T lymphocytes often preceded the radiographic changes.

1- Hematological;
✓Complete blood count (CBC).
✓Coagulation; D-Dimer and APTT.
✓Blood film
✓Leukocytes Scattergram (New reports)
✓G6PD
2- Inflammatory markers (acute phase reactant);
✓CRP, Ferritin and Procalcitonin (PCT) and IL-6
3- Biochemical test;
✓LDH, CK (Creatine Kinase), AST / GOT (aspartate aminotransferase)
and ALT / GPT (alanine aminotransferase)
4- Cardiac biomarker; Troponin I.
5- Other screening tests for organ function;Bd Urea, S. Creatinine, S.
Bilirubin,S. Albumin

1- Hematological;
✓Complete blood count (CBC);
Most important; low Lymphocyte count (% or absolute), Lymphopenia is an
important feature of SARS patients, and decline of both CD4+ and CD8+ T
lymphocytes often preceded the radiographic changes.
✓Increased Neutrophils (neutrophilia)
✓Increased NLR (neutrophil lymphocytes ratio).
✓Platelets count (mild reduction)
✓Coagulation parameters; increased D-Dimer and prolonged APTT.
✓Blood film; presence of atypical lymphocytes
✓Leukocyte Scattergram (New data report)

L. Tan et al, Lymphopenia predicts disease severity of COVID-19: a descriptive and
predictive study, Target. Ther., vol. 5, no. 1, pp. 16–18, 2020

V. C. L. Chong, et al., Reactive lymphocytes in patients with COVID-19, Br. J. Haematol., 189.5;844, 2020

M. Gupta et al, Useful information provided by graphic displays of automated cell counter in hematological malignancies

2- Inflammatory markers;
✓ Most important; CRP, Ferritin and Procalcitonin (PCT)
✓ Triponin I.
3- Biochemical test;
✓ Most important is LDH
✓ Others; CK (Creatine Kinase), AST / GOT (aspartate aminotransferase),
ALT / GPT (alanine aminotransferase)

HORIBA; Infectious Screening Guidance

Cytokines StormCytokines Storm
Siddiqi HK, Mehra MR. COVID-19 illness in native and immunosuppressed states: a clinical therapeutic
staging proposal. J Heart Lung Transplant. 2020

Laboratory findings All Sever Non-Sever
WBC <4,000 per mm3 5.07 (4.90-5.24) 6.06 (5.67, 6.46) 5.39 (5.22, 5.55)
Lymphocytes <1,500 per mm3
83.2%
1.15 (1.08-1.22)
96.1%
0.80 (0.75-0.84)
80.4%
0.98 (0.92-1.04)
Platelets <150,000 per mm3
201.44
(175.75, 227.12)
212.58
(154.63, 270.53)
184.19
(178.04, 190.33)
C-reactive protein ≥10 mg/L
36.99
(33.31, 40.67)
60.91
(49.24, 72.5)
19.83
(16.67, 23.0)
Lactate dehydrogenase ≥250 U/L
271.82
(254.13, 289.52)
344.48
(307.08, 381.88)
224.20
(205.33, 243.07)
AST >40 U/L 30.66 (29.19, 32.13) 36.78 (33.69, 39.87) 26.24 (25.29, 28.18)
D-dimer ≥0.5 mg/L 0.61 (0.54, 0.67) 1.29 (1.03, 1.54) 0.47 (0.40, 0.53)
Disease Laboratory Tests at Diagnosis

Biochemical and hematological biomarkers of COVID-19 progression and severity. Citation: Clinical Chemistry and Laboratory Medicine (CCLM) 58, 7

❖‫ه‬‫إضافات‬ ‫المريض‬ ‫لتجنيب‬ ‫المناسبة‬ ‫التحاليل‬ ‫اختيار‬ ‫اعاة‬‫ر‬‫م‬ ‫يمكن‬ ‫ل‬‫تبعات‬
‫معنوية؟‬ ‫و‬ ‫مادية‬
‫نعم‬....‫نعرف‬‫جيدا‬‫الحمل‬‫المادي‬‫من‬‫الناحية‬‫المادية‬‫بصرف‬‫مبالغ‬‫إضاف‬‫ية‬‫و‬
‫يض‬‫ر‬‫تع‬‫يض‬‫ر‬‫الم‬‫و‬‫العائلة‬‫لالختالط‬...‫و‬‫األهم‬‫من‬‫ذلك‬‫يض‬‫ر‬‫تع‬‫اد‬‫و‬‫الك‬‫ر‬
‫الصحية‬‫و‬‫يادة‬‫ز‬‫انتشار‬‫المرض‬
❖‫ان‬ ‫تقليل‬ ‫في‬ ‫الوسائل‬ ‫احد‬ ‫المختبرية‬ ‫اءات‬‫ر‬‫اإلج‬ ‫ن‬‫تكو‬ ‫ان‬ ‫باإلمكان‬ ‫هل‬‫تشار‬
‫المجتمع؟‬ ‫في‬ ‫المرض‬
‫نعم‬‫و‬‫هنا‬‫يكمن‬‫الفائدة‬‫من‬‫خالل‬‫اب‬‫و‬‫الج‬‫في‬‫ال‬‫ؤ‬‫الس‬‫خامسا‬

‫بشأنها‬ ‫التثقيف‬ ‫و‬ ‫لها‬ ‫ننتبه‬ ‫ان‬ ‫تحتاج‬ ‫الصورة‬ ‫في‬ ‫أخطاء‬...‫هي؟‬ ‫ما‬

References;
• W. Cao and T. Li, COVID-19: towards understanding of pathogenesis, Cell Research; 30, 367-369, 2020.
• Luca Antonioli et al. NKG2A and COVID-19: another brick in the wall, Cellular and Mol Imm; 17, 672–
674, 2020.
• Nick Routley. Visualizing what COVID-19 does to your body, Healthcare.
• The Biology Project, The University of Arizona.
• Li, Geng, et al. Coronavirus infections and immune responses. Journal of medical virology, 92.4, 424-
432, 2020.
• J. L. McKechnie and C. A. Blish, The Innate Immune System: Fighting on the Front Lines of Fanning the
Flames of COVID-19, Cell Host & Microbe; pp. 863-869, 2020.
• N. Vabre et al, Immunology of COVID-19: Current State of the Science. Immunity, 52, 2020
• J. Chen et al, Cellular Immune Responses to Severe Acute Respiratory Syndrome Coronavirus (SARS-
CoV) Infection in Senescent BALB/c Mice: CD4+ T Cells Are Important in Control of SARS-CoV Infection.
J. Of Virology, 1289–1301

• U. K. Kar & L. A. B. Joosten. Training the trainable cells of the immune system and beyond.
Nature Immunology, 115–119
• M. Z. Tay. The trinity of COVID-19: immunity, inflammation and intervention. Nature Imm.,
v20, 363-374,2020
• D. McGonagle et al. Immune mechanisms of pulmonary intravascular coagulopathy in
COVID-19 pneumonia. Lancet Rheumatol 2020; 2; 437–45
• B. Marchandot et al. COVID-19 Related Coagulopathy: A Distinct Entity?. J. Clin. Med. 2020,
9, 1651: 1-17
• C. S. Lim et al. Hypoxia-inducible factor pathway and diseases of the vascular wall. J. OF V.
Surgery, 58, 1; 219-230, 2013
• L. Tan et al, Lymphopenia predicts disease severity of COVID-19: a descriptive and predictive
study, Target. Ther., vol. 5, no. 1, pp. 16–18, 2020

Covid 19 laboratory parameters - Abdulsalam Al-Ani

Covid 19 laboratory parameters - Abdulsalam Al-Ani

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Covid 19 laboratory parameters - Abdulsalam Al-Ani

Similar to Covid 19 laboratory parameters - Abdulsalam Al-Ani (20)

Recently uploaded

Recently uploaded (20)

Covid 19 laboratory parameters - Abdulsalam Al-Ani