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\begin{document}

\title{Acute arthritis revealing Hashimoto's Thyroiditis}



\author[1]{Maroua SLOUMA}%
\author[1]{Takwa Mehmli}%
\author[1]{Siwar Ben Dhia}%
\author[1]{Leila Metoui}%
\author[1]{Rim Dhahri}%
\author[1]{Imen Gharsallah}%
\author[1]{Bassem Louzir}%
\affil[1]{Military Hospital of Instruction of Tunis}%


\vspace{-1em}



  
  \date{May 26, 2024}


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\selectlanguage{english}
\begin{abstract}
Rheumatic manifestations can reveal hypothyroidism, such as arthritis
and non-specific musculoskeletal symptoms. We report herein the case of
an acute polyarthritis revealing Hashimoto's thyroiditis. Hormone
replacement therapy leads to the resolution of arthritis related to
Hashimoto's thyroiditis, suggesting the role of thyroid hormone in the
pathogenesis of arthritis.%
\end{abstract}%



\sloppy


\emph{Title:Acute} \textbf{arthritis revealing Hashimoto's Thyroiditis}

\emph{Authors:}

Maroua SLOUMA\textsuperscript{1,3}, MD, Takwa
MEHMLI\textsuperscript{1,3}, MD, Siwar BEN DHIA\textsuperscript{1,3},
MD, Leila METOUI\textsuperscript{1,3}, MD, Rim
DHAHRI\textsuperscript{1,3}, MD, Imen GHARSALLAH\textsuperscript{1,3},
MD, Bassem LOUZIR\textsuperscript{2,3}, MD.

\emph{Authors Affiliation:}

\begin{enumerate}
\tightlist
\item
  Department of Rheumatology, Military Hospital, Tunis, Tunisia,
\item
  Department of Internal Medicine, Military Hospital, Tunis, Tunisia,
\item
  Tunis El Manar University -- Tunisia
\end{enumerate}

\emph{Corresponding author} : Maroua SLOUMA

ORCID: 0000-0002-6889-9687

Address: Department of Rheumatology, Military Hospital, Tunis, Tunisia,
1007

Mail:\emph{maroua.slouma@gmail.com}

Tel: + 216 55~117~316



\textbf{Authors' contributions~}

- Dr. Takwa MEHMLI: Roles/Writing - original draft

- Dr. Maroua SLOUMA: Methodology and Writing - review \& editing

- Dr. Rim DHAHRI: data curation and formal analysis

- Dr. Siwar BEN DHIA: data curation

- Dr. Imen GHARSALLAH: visualization

- Dr. Leila METOUI: conceptualization

- Dr. Bassem LOUZIR: validation

\textbf{DECLARATION}

\textbf{Conflict of interest:} none

\textbf{Funding:} The authors declare that they have no funding for this
study

\emph{}

\emph{Abstract} \textbf{(50 words)\emph{:}}

Rheumatic manifestations can reveal hypothyroidism, such as arthritis
and non-specific musculoskeletal symptoms. We report herein the case of
an acute polyarthritis revealing Hashimoto's thyroiditis. Hormone
replacement therapy leads to the resolution of arthritis related to
Hashimoto's thyroiditis, suggesting the role of thyroid hormone in the
pathogenesis of arthritis.

\emph{}

\emph{Structured abstract:}

\emph{Introduction:}

Rheumatic manifestations such as arthritis and non-specific
musculoskeletal symptoms~can reveal hypothyroidism.

We report herein the case of an acute asymmetric polyarthritis revealing
Hashimoto's thyroiditis.

\emph{Case presentation:}

A 34-year-old woman presented to our department with acute seronegative
polyarthritis.

She had high thyroid-stimulating hormone levels, low thyroxine levels,
and positive thyroid peroxidase antibodies. Ultrasonography revealed a
thyroiditis aspect.

The diagnosis of Hashimoto's thyroiditis was made.

There were no clinical nor immunological features for the diagnosis of
Sj\selectlanguage{ngerman}ögren's syndrome, rheumatoid arthritis, systemic lupus erythematosus.

After three months of thyroid hormone replacement therapy, the
thyroid-stimulating hormone level had become within the normal range,
and polyarthritis had resolved.

\emph{Conclusion:}

We highlight the link between thyroid disorders and rheumatic
manifestations. The diagnosis of hypothyroidism should be considered in
patients with rheumatic complaints. Hormone replacement therapy leads to
the resolution of arthritis related to Hashimoto's thyroiditis,
suggesting the role of thyroid hormone in the pathogenesis of arthritis.

\emph{Key clinical message:}

Hypothyroidism should be considered in polyarthritis patients.

Rheumatic manifestations can be due to thyroid dysfunction or
autoimmunity, or associated connective tissue diseases.

Thyroid hormone replacement therapy leads to arthritis resolution.

\textbf{Written informed consent} was obtained from the patient for
publication of the clinical information and any accompanying images.

\emph{}

\emph{Introduction:}

Hashimoto's thyroiditis (HT) is autoimmune thyroid disease and one of
the common causes of primary hypothyroidism {[}1{]}. It can be
responsible or associated with several rheumatic manifestations {[}2{]}.

Rheumatic manifestations, such as arthritis and non-specific
musculoskeletal symptoms, can reveal hypothyroidism. These
manifestations can be related to thyroid dysfunction, connective tissue
diseases associated with HT, or thyroid autoimmunity {[}3{]}.

We report the case of an acute polyarthritis revealing primary
hypothyroidism caused by Hashimoto's thyroiditis.

We emphasize clinical, biological, and management of this condition.

\emph{}

\emph{Case presentation:}

A 34-year-old woman with no medical history presented to our department
with a five-day history of arthritis affecting the small joints of the
left hand, wrist, right elbow, and ankle. She had myalgia without sicca
symptoms.

Physical examination showed a normal blood pressure of 110/60 mmHg,
synovitis of the left wrist and metacarpophalangeal joints, right elbow,
and ankle.

Laboratory findings revealed a high C-reactive protein level (28 mg/L,
Normal value (N) \textless{} 6), normocytic anemia (hemoglobin: 7.7
g/dL, N \selectlanguage{english}[?] 12 g/dL, mean corpuscular volume: 96.5 femtoliter, N: 80 --
100), high Lactate dehydrogenase (LDH) level (280 IU/L, N: 91 -- 260),
and high Creatine-phosphokinase (CPK) level (485 IU/L, N: 22 -- 269).
Liver and renal tests were within the normal range.

Anti-nuclear antibodies (ANA), anti-SSA, SSB, rheumatoid factor, and
anti-citrullinated protein antibodies (ACPA) were negative.

C3 and C4 complement levels were normal. Thyroxine (T4) level was low
(2.8 pmol/L, N: 7.9 -- 14.4), and thyroid-stimulating hormone (TSH)
level was high (39 \selectlanguage{greek}µ\selectlanguage{english}IU/L, N: 0.34 -- 5.6). The thyroid peroxidase
antibodies were positive (670 IU/mL, N: \textless{}35 IU/mL), whereas
anti-thyroglobulin antibodies were negative.

Radiographs of hands, feet, and pelvic were without abnormalities.
Musculoskeletal ultrasound showed synovial thickening of the left wrist
and the right elbow with hyperemia in power Doppler imaging. There was
also synovial thickening of the left metacarpophalangeal joints, right
ankle, and tenosynovitis of the~posterior tibial~ and fibular tendons.
The chest radiograph was normal. Thyroid ultrasound showed inhomogeneous
and hypoechogenic thyroid parenchyma. However, ultrasonography of the
salivary glands was without abnormalities.

The diagnosis of primary hypothyroidism related to Hashimoto thyroiditis
was made. There were not enough criteria to make the diagnosis of
Sjogren's syndrome.

A thyroid hormone replacement therapy was started at 25\selectlanguage{greek}µ\selectlanguage{english}g daily and
increased progressively to reach 150 \selectlanguage{greek}µ\selectlanguage{english}g daily.

After three months of treatment, the TSH level had become within the
normal range, and polyarthritis had disappeared. The TSH level remained
stable, and the patient didn't develop a recurrence of the polyarthritis
after 20 months of follow-up.

Consent from the patient for publication of this case study was
obtained.\emph{}

\emph{Discussion:}

We report a case of acute polyarthritis revealing Hashimoto's
thyroiditis. Hashimoto's thyroiditis is the most frequent auto-immune
endocrine disorder {[}4{]} and the most common etiology of
hypothyroidism {[}1{]}. It results from a diffuse lymphocytic
infiltration of the thyroid.

The diagnosis of Hashimoto's thyroiditis relies on clinical features
which vary from subclinical hypothyroidism to typical myxedema,
positivity of serum thyroid antibodies (mainly thyroperoxidase (90\%)
and thyroglobulin), and reduced echogenicity on thyroid ultrasonography
{[}5{]}.

Hashimoto's thyroiditis can be responsible for various rhematic
manifestations due to thyroid dysfunction. These manifestations often
reveal this disease.

It is also closely associated with several autoimmune diseases, which
can be themselves responsible for articular and muscular manifestations,
such as Sj\selectlanguage{ngerman}ögren's syndrome, rheumatoid arthritis, systemic lupus
erythematosus, or scleroderma {[}6{]}{[}7{]}{[}8{]}{[}9{]}. Therefore,
it is necessary to rule out these diagnoses before attributing articular
manifestations to Hashimoto's thyroiditis.

In our case, apart from arthritis, there were no clinical nor
immunological features for the diagnosis of systemic lupus
erythematosus, Sjögren's syndrome, or rheumatoid arthritis. Moreover,
thyroid hormone replacement therapy led to a complete resolution of
polyarthritis.

Musculoskeletal symptoms related to hypothyroidism {[}10{]} occur in 25
to 79\% of cases. Muscular signs may include pain, cramps, and
weakness.The muscle enzyme levels (CK, myoglobin, and lactate
dehydrogenase) {[}10{]} can be increased. The CK levels correlated with
TSH levels {[}11{]}{[}12{]}, and hypothyroid myopathy symptoms usually
resolve after thyroxin supplementation {[}11{]}{[}13{]}.

Polyarthralgia is the most frequent rheumatic symptom occurring during
hypothyroidism {[}3{]}. The classic clinical presentation of hypothyroid
arthropathy is less frequent, it is characterized by synovial thickening
and joint effusions typically affecting the knees, metacarpophalangeal,
proximal interphalangeal, and metatarsophalangeal joints. Synovial fluid
can be non-inflammatory with highly increased viscosity
{[}14{]}{[}15{]}{[}16{]}{[}17{]}.

Other rheumatic manifestations were also reported in patients with
hypothyroidism, such as frozen shoulder {[}18{]}, chondrocalcinosis
{[}19{]}, and carpal tunnel syndrome {[}20{]}. The incidence of
osteoarthritis seemed to be increased in patients with hypothyroidism
{[}21{]}.

Rheumatological manifestations in patients with hypothyroidism result
from hormonal dysfunction {[}17{]} and deposition of
mucopolysaccharides, notably hyaluronic acid in articular and
peri-articular structures {[}22{]}. Indeed, the excess of hyaluronic
acid in patients with primary hypothyroidism is due to the stimulation
of hyaluronic acid synthesis by the increased TSH levels and the
inhibition of hyaluronic acid degradation caused by thyroxine deficiency
{[}23{]}{[}24{]}{[}25{]}{[}26{]}{[}17{]}.

The role of TSH in the pathogenesis of arthropathy was also highlighted
because normalization of TSH levels under thyroid hormone substitution
therapy leads to improvement and complete resolution of articular
symptoms {[}27{]}{[}14{]}{[}28{]}{[}15{]}{[}17{]}{[}29{]}.

However, other studies showed that rheumatic manifestations may occur in
patients with chronic lymphocytic thyroiditis, even in those with TSH
levels within normal ranges {[}3{]}{[}30{]}{[}31{]}{[}25{[}{[}28{]}.
Besides, LeRiche et al. {[}32{]} reported cases of inflammatory
polyarthritis (joint stiffness, tenderness, and effusion) in patients
with HT with no improvement of arthritis under thyroid replacement.
These findings suggest that rheumatological manifestations can be
related to either inflammatory or serological features of Hashimoto's
thyroiditis {[}32{]}.

\emph{}

\emph{Conclusion:}

The diagnosis of hypothyroidism should be considered in patients with
articular impairment, even without classic signs of hypothyroidism.

Thyroid replacement can lead to alleviation or complete resolution of
hypothyroid arthropathy.

\emph{References :}

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