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\begin{document}

\title{Hypocalcemia and Massive Pulmonary Embolism in SLE Patient with COVID-19
Infection, A Case Report}



\author[1]{Mohammed  Yousif Elnaeem Yousif }%
\author[2]{ Moh. Eljack}%
\author[3]{Mohammed   Alfatih}%
\author[3]{Mohammed   Abdulkarim }%
\author[4]{Abdirizak   Ibrahim mohamed}%
\author[5]{Khabab  Mohamed Ahmed}%
\author[5]{Mazin S. Hassan Haroun}%
\affil[1]{University of Gezira Faculty of Medicine}%
\affil[2]{Wad Medani center For heart disease and Surgery }%
\affil[3]{Alzaiem Alazhari University Faculty of Medicine}%
\affil[4]{University of Bakhtalruda Faculty of Medicine and Health Sciences}%
\affil[5]{University of Khartoum Faculty of Medicine}%


\vspace{-1em}



  
  \date{May 24, 2024}


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\begin{abstract}
A 16-year-old female presented to our ED with fever and coughing of
blood for 3 days. She is known to have SLE for 5 months and takes oral
prednisone. She was tested positive for COVID19. She developed
hypocalcemia with clinically-diagnosed massive pulmonary embolism. She
was treated with heparin and recovered.%
\end{abstract}%



\sloppy


Hypocalcemia and Massive Pulmonary Embolism in SLE Patient with COVID-19
Infection, A Case Report

Mohammed Yousif Elnaeem Yousif \textsuperscript{\textbf{1}} ,
Moh.Mah.Fadel Allah Eljack\textsuperscript{\textbf{2}} , Mohammed
Alfatih\textsuperscript{\textbf{3}} , Mohammed
Abdulkarim\textsuperscript{\textbf{4}} , Abdirizak Ibrahim
mohamed\textsuperscript{\textbf{5}} , Khabab Abbasher Hussien Mohamed
Ahmed\textsuperscript{\textbf{6*}} , Mazin S. Hassan
Haroun\textsuperscript{\textbf{7}}

\emph{Authors Affiliations:}

MD, Assistant Professor of Internal Medicine, University of Gezira,
Director of Wad Medani Isolation Centers, Khartoum, Sudan,

\emph{Mohammed\_elnaeem@yahoo.com}

MBBS, University of Bakht Alruda, Medani Heart Diseases and Surgery
Center, Khartoum, Sudan,

\emph{m.mahmmoud96@gmail.com}

MBBS, Alzaiem Alazhari University, Khartoum, Sudan,

\emph{mohammed.22.alfatih@gmail.com.}

MBBS, Alzaiem Alazhari University, Khartoum, Sudan,

\emph{mohd.karim0095@gmail.com}

\begin{enumerate}
\tightlist
\item
  MBBS, University of Bakht Alruda, Medical Doctor at Kiambu level 5
  hospital, Nairobi, Kenya, Dr.abdirizakmohamed2030@gmail.com
\item
  Medical student (MBBS student), University of Khartoum, Faculty of
  Medicine, Khartoum, Sudan, Khabab9722@gmail.com, ORCID ID:
  0000-0003-4608-5321, (Correspondence Author)
\item
  Medical student (MBBS student), University of Khartoum, Faculty of
  Medicine, Khartoum, Sudan,\emph{mazinsalaheldien@gmail.com}
\end{enumerate}

\textbf{*Correspondence Author :}

\textbf{Khabab Abbasher Hussien Mohamed Ahmed}

\textbf{Email:}\emph{Khabab9722@gmail.com}

\textbf{ORCID ID: 0000-0003-4608-5321}

\textbf{Khartoum State, Postal code:11111, Sudan, Mobile:00249907712134}

\textbf{Key Words :}

\textbf{Hypocalcemia, Pulmonary Embolism, SLE, COVID-19, Wad-madani}

\textbf{Abstract}

A 16-year-old female presented to our ED with fever and coughing of
blood for 3 days. She is known to have SLE for 5 months and takes oral
prednisone. She was tested positive for COVID19. She developed
hypocalcemia with clinically-diagnosed massive pulmonary embolism. She
was treated with heparin and recovered.

\textbf{Key Clinical Message:}

In this study, we report a case of a 16-year-old female who is a known
case of systemic lupus erythematosus (SLE) for 5 months and is on
steroids presenting with hypocalcemia and massive pulmonary embolism
diagnosed clinically while she has COVID.

\textbf{Introduction}

Systemic lupus erythematosus (SLE) is an autoimmune disease that is
characterized with autoantibodies production with on and off clinical
course. It can affect any age or gender, but it has a particular
tendency to affect young females, with a female-to-male ratio of about
9:1 (1).

SLE can affect almost every organ system with a diverse scale of
manifestations. The disease severity can vary from a very mild illness
to a systemic life-threatening illness (2-4). Although manifestations
can affect almost every system in the body, cardiac and lung
manifestations have a significant impact on patients' everyday life and
outcome. Respiratory affection can affect the lung, pleura or lung
vasculature with various degrees of affection from an asymptomatic
illness to severe respiratory compromise.

\textbf{Case history / examination}

A 16-year-old female has presented to our accidents and emergency
department complaining of fever and coughing of blood for 3 days. Her
condition started three days prior to admission with a gradual-onset,
high-grade fever that was associated with rigors. She also had a
productive cough of red bloody sputum. There was no associated chest
pain, shortness of breath, syncopal attack nor lower limb edema.

On review of her systems including GI, GU and CNS, she reported burning
epigastric pain with no abdominal distension, nausea, vomiting, diarrhea
or constipation. There was no weight loss nor change in her appetite.

When it comes to her past medical history, she reported that she had
been diagnosed with systemic lupus erythematosus (SLE) 5 months ago when
she sought medical advice regarding recurrent facial rashes and small
joints pain. Her SLE has been immunologically confirmed using
anti-double stranded DNA antibodies (100 IU/mL) and ANA factor (400
IU/mL) for which she currently takes prednisone 5 mg once daily and
hydroxychloroquine tabs 200 mg tabs twice daily with good adherence to
treatment and regular follow-up since then. Apart from SLE, she reported
no DM, HTN or any other coagulation or autoimmune diseases and she has
never been hospitalized before. Her family history is unremarkable.

Her examination revealed a tachypneic drowsy patient with a Glasgow coma
scale (GCS) of 8. There was a photosensitive malar rash over her cheeks.
Cardiac examination was normal with no murmurs and her lung auscultation
revealed no abnormalities. Abdominal examination was normal and her
musculoskeletal system examination was completely normal with no joints
swellings or deformities. Her vitals at time of admission were as
follows: PR: 110 bpm, RR: 24, BP: 80/50 mmHg and SaO2 of 81\% on Room
Air.

\textbf{Differential diagnosis and investigations}

Up to this point, we have made a diagnosis of massive PE clinically on
the basis of her modified well's score of 5.5 (HR\textgreater{}100,
Hemoptysis as well as no alternative diagnoses more likely than PE) in
addition to the hemodynamic instability that our patient has suffered
from which cannot be explained by any cardiac condition (given her
normal cardiac exam and normal echocardiography excluding cardiac causes
of her hemodynamic instability). A very high level of d-dimer (10000)
has supported that diagnosis. Nevertheless, we were not able to do the
CT pulmonary angiography scan of the chest due to financial and logistic
causes as well as the patient's hemodynamic instability. A transthoracic
echography was normal ruling out cardiac causes of possible
presentation.

\textbf{Treatment, outcome and follow-up}

When it comes to the treatment provided to our patient, we divided it
into 2 phases. First, is the phase of stabilization in which the patient
was resuscitated using saline infusion that resulted in raising her BP
to 110/70 as well as an IV bolus of hydrocortisone 200 mg every 6 hours.
Second, is the maintenance phase in which the patient was commenced on
hydroxychloroquine, meropenem and pantoprazole. We also provided
adequate analgesia in addition to zinc and vitamin C supplements.

24 hours after admission, her fever improved, and the hemoptysis as well
as the epigastric pain subsided. Nonetheless, she was still drowsy with
a GCS of 11 and SaO2 of 90\% off oxygen. Her vitals were as follows: PR=
110, BP= 100/60, RR= 28. We continued the same management plan but
replacing hydrocortisone with methylprednisolone 500 mg, Clexane 6000 IU
S.C every 12 hours with quinine, doxycycline and also adding
N-acetylcysteine to the regimen. We also added vitamin D and Iron
tablets.

On the third day of admission, calcium carbonate tabs 500 mg every 8
hours were also added to aid with managing her hypocalcemia (Serum Ca =
7.1 mg/dL, Procalcitonin = 1.5). She also received a packed red cell for
a few days during her admission resulting in her Hb level being raised
from 6.9 to 10.6 gm/dL. Over the next few days and by the
8\textsuperscript{th} day of admission, her fever subsided and she
gradually regained her normal mental status and level of consciousness.
Her vitals were also stabilized and they were as follows: PR= 75,
BP=120/70, RR=14 and SaO2 of 98\% off oxygen. Her nasal swab for COVID
came back negative and she was then discharged on oral cefditoren,
hydroxychloroquine, prednisone, iron tablets, omeprazole as well as
calcium carbonate. She has been followed up a month later without
complications.

\textbf{Discussion}

We report a case of a 16-year-old female with established systemic lupus
erythematosus (SLE) diagnosis for 5 months and is currently on steroids
presenting with hypocalcemia and pulmonary embolism diagnosed clinically
in the setting of COVID19 infection.

In terms of infections, SLE increases the risk of infections, both
common and opportunistic, with the lung being the most affected organ.
It does so through impairing both arms of the immune system, the
cellular and humoral immunity (5). COVID-19 is not an exception.
Coronavirus disease 2019 (COVID-19) is a respiratory tract infection
caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2),
a coronavirus that spreads mainly through respiratory droplets (6).
COVID19 infections, on the other hand, are also thought to increase the
risk of autoimmune diseases through the production of autoantibodies and
autoimmunity (7).

With regard to thrombotic phenomenon, both COVID19 infection and SLE
have been thought to cause such presentation. Complement activation in
COVID19 can cause thrombotic microangiopathy that can mediate organ
damage in severe cases, resembling a complement-mediated thrombotic
microangiopathy (8,9). Some factors that may be implicated in thrombosis
in SLE include immune response through the circulating complexes along
with auto-antibodies and the high state of inflammation that ensues
during the disease activity (10).

Hypocalcemia with COVID19 infection has been reported many times in the
literature along with low lymphocytes and elevated LDH, liver enzymes,
CK as well as CRP and is a frequent finding including a case of Italian
patient with acute severe hypocalcemia. Mechanisms for such finding
include a viral action requiring calcium for pathogenesis, malnutrition
as well as abundance of unsaturated fatty acids that present in high
levels during this viral infection, therefore, its severity can predict
the outcome for patients, hence proper evaluation and management should
be done (11).

\textbf{Conclusion:}

A combination of SLE with hypocalcemia and pulmonary embolism in the
setting of COVID19 infection, while expected, has not been reported in
the literature. This can be alarming since patients with SLE are already
immunosuppressed with high risk of thrombosis. Adding the risk of
thrombosis from COVID19, this can result in a massive pulmonary embolism
as in our reported patient. Hence, in such patients, hypocalcemia should
be thoroughly investigated, properly addressed and adequately managed.

\textbf{Abbreviations:}

SLE: Systemic lupus erythematosus.

ED: Emergency department.

HTN: Hypertension

DM: Diabetes Mellitus

\textbf{Ethical approval:}

Ethical approval was obtained from Gezira State Ministry of Health and a
written informed consent was taken from the patient.

\textbf{Conflict of interest}

Authors report no conflict of interest of any sort

\textbf{Authors contribution:}

MYE, MMF served as the first author and the second author, collected the
data, analyzed the results, and wrote the manuscript. MA and MA served
as the third and the fourth authors, wrote the manuscript, revised the
manuscript, and did editing. AI, KAH and MSH served as the fifth, the
sixth and the seventh authors, collected, analyzed the data, wrote and
revised the final draft. All authors read and approved the final
manuscript.

\par\null

\textbf{Funding:}

No funds.

\textbf{Acknowledgment:}

Not applicable.

\textbf{References}

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