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\begin{document}

\title{Ulcerative colitis associated mononeuritis multiplex in 75-year-old
patient: rare case report}



\author[1]{omid pourbagherian}%
\author[1]{Mehdi Jafarpour}%
\author[1]{Sepideh  Tahsini}%
\author[2]{Amirtaher  Eftekharsadat}%
\author[1]{Maryam Javid}%
\affil[1]{Tabriz University of Medical Sciences}%
\affil[2]{Department of Pathology, Tabriz University of Medical Sciences, Tabriz, Iran}%


\vspace{-1em}



  
  \date{May 28, 2024}


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\textbf{Introduction}

Inflammatory bowel disease (IBD) refers to a collection of chronic,
idiopathic inflammatory/autoimmune disorders of the gastrointestinal
tract characterized by relapsing and remitting episodes(1). The two main
types of IBD are Crohn's disease and ulcerative colitis which lead to a
various type of debilitating symptoms such as abdominal pain, rectal
bleeding, weight loss, and diarrhea. The precise mechanisms underlying
IBD pathogenesis remain unclear but are thought to involve a
dysfunctional interplay between host genetics, the intestinal immune
system, and environmental factors(2). Current evidence suggests IBD
results from an aberrant immune response directed against commensal gut
bacteria in genetically susceptible individuals(3). Multiple genetic
loci have been implicated in IBD risk, including genes involved in
epithelial barrier function, microbial sensing, and immunoregulation.
However, genetics alone cannot explain IBD's rising incidence,
highlighting the likely contribution of environmental risk factors like
diet, smoking, medications, stress, and the microbiome. Ongoing research
aims to better delineate the complex immunopathogenesis of IBD in order
to identify improved diagnostic markers, prognostic indicators, and
therapeutic targets(4). Moreover, Individuals diagnosed with IBD
frequently encounter an array of difficulties that extend beyond the
gastrointestinal system. One such challenge is the emergence of
mononeuritis multiplex. This association between ulcerative colitis and
mononeuritis multiplex underscores the intricate and multifaceted nature
of these autoimmune disorders. The occurrence of symptoms of one
condition in individuals afflicted by the other warrants careful
examination by medical specialists. This necessitates a thorough
investigation into the underlying reasons and the implementation of
preventive measures. In this case report, we will report a patient who
has encountered ulcerative colitis related to mononeuritis multiplex.

\textbf{Case presentation}

A 75-year-old male patient, with a prior medical history including
long-standing hypertension, recurring episodes of peripheral joint
arthritis, leg skin lesions reminiscent of erythema nodosum, and
persistent chronic diarrhea over the past two years, was recently
hospitalized at the rheumatology department of Imam Reza Hospital in
Tabriz. His admission was prompted by a worsening of diarrhea and the
development of polyarthritis in the peripheral joints. Furthermore, he
exhibited distinctive palm skin lesions (as depicted in Figure 1), along
with sensations of tingling and paresthesia in his extremities and an
increase in blood creatinine levels. Throughout the patient's hospital
stay, a series of diagnostic assessments were conducted, encompassing
procedures such as colonoscopy (as shown in Figure 2), Electromyography
and nerve conduction studies (EMG-NCS), echocardiography, renal
ultrasonography, and standard hematological analyses (Table 1). Notably,
the colonoscopy result was: Multiple ulcers with congested
and~erythematous and friable mucosa, prompting a subsequent intestinal
biopsy that yielded findings consistent with a diagnosis of ulcerative
colitis (Figure 3) . The result of the EMG-NCS was reported as follows:
moderate axonal sensory motor~polyneuropathy with superimposed newly
onset left median and ulnar neuropathy compatible with mononeuritis
multiplex neuritis. In echocardiography EF (Ejection Fraction) 35-40\%
with normal LV (Left Ventricular Size) and RV (Right Ventricular) size
was reported. Ultrasound of kidney and urinary tract did not reveal any
abnormalities and shape, size, and echogenicity of the kidneys were
reported as normal.

Based on a comprehensive array of diagnostic findings, encompassing both
colon and skin and nerve biopsies, the patient's medical condition was
ascertained. The colon biopsy confirmed the presence of active
ulcerative colitis while excluding any associated vasculitis-related
indicators. Simultaneously, the skin and nerve biopsy yielded no
indications of vasculitis. Consequently, the patient received a formal
diagnosis of ulcerative colitis concomitant with mononeuritis
multiplex~and underwent the following therapeutic regimen.

The initial phase of treatment involved the administration of
corticosteroid pulse therapy at a dosage of 1 gram per day, administered
consecutively for three days. Additionally, the patient received a 750
mg ampoule of cyclophosphamide as part of the prescribed therapeutic
protocol.

\textbf{Pulse Corticosteroid} : The treatment began with a high dose of
corticosteroids \textbackslash{} administered intravenously at 1 gram
per day for three consecutive days. This approach is aimed at rapidly
reducing inflammation.

\textbf{Cyclophosphamide} : On the same day, the patient received an
injection of cyclophosphamide at a dose of 750 mg. Cyclophosphamide is
an immunosuppressive medication often used to treat vasculitis by
suppressing the overactive immune response.

\textbf{Mesalamine:} Based on a consultation with a gastrointestinal
specialist, the patient was prescribed mesalamine

During the hospitalization, the patient's diarrhea ceased, and their
hydration improved. Additionally, their creatinine levels
decreased(creatinine =1.1), indicating a positive response to treatment.
As a result, the patient was discharged from the hospital with the
following medications:

\textbf{Prednisolone} : The patient was prescribed prednisolone at a
dose of 20 mg three times a day (TDS).

\textbf{Mesalasine} : Mesalasine is another medication commonly used in
the treatment of IBD.

\textbf{Cotrimoxazole and Monthly Cyclophosphamide Injection} : The
patient received cyclophosphamide injections on a monthly basis.

In accordance with the patient's recent follow-up conducted over the
past 20 days, it is notable that recurrent episodes of diarrhea have not
been reported. Additionally, the patient has shown substantial
amelioration in parathesis and tingling symptoms, and notably, the
previously evident arthritis has demonstrated complete resolution. These
observed clinical improvements signify a promising response to the
treatment and suggest a positive trajectory in the management of the
patient's condition.

\textbf{Discussion}

In this case report, we highlight and present a unique and uncommon
clinical scenario involving 75-year-old patient with a history of
ulcerative colitis. To the best of our knowledge this is the first case
of ulcerative colitis associated mononeuritis multiplex. The exact
etiology and cause of ulcerative colitis remain incompletely understood,
and it is believed to be a complex interplay of genetic, environmental,
immunological, and microbial factors(5). Mononeuritis multiplex is a
rare neurological disorder characterized by multifocal nerve damage(6).
These two distinct diseases may have some connections in the context of
extraintestinal manifestations of UC and autoimmune processes.
Ulcerative colitis (UC) and mononeuritis multiplex appear to stem from
similar underlying processes - an aberrant immune reaction. The
inflammatory bowel disease known as UC arises when the immune system
overreacts within the gastrointestinal tract, provoking inflammation and
sores in the colon. Mononeuritis multiplex occurs due to the immune
system assaulting peripheral nerves, impairing neurological function.
Although UC centers around the digestive system while mononeuritis
multiplex involves nerve damage, the common autoimmune component points
to a plausible association between these two conditions. Uncovering the
precise immune pathways responsible could clarify how an overactive
immune system in UC may occasionally give rise to nerve inflammation and
injury remotely, manifesting as mononeuritis multiplex. Elucidating the
mechanisms linking intestinal autoimmunity with neuronal autoimmunity
will enable better understanding of the scope of extraintestinal
manifestations in inflammatory bowel disease.

The precise etiology and pathophysiology underlying both ulcerative
colitis (UC) and mononeuritis multiplex remain incompletely elucidated,
likely involving a constellation of factors(7). Given the intricate
nature of autoimmune diseases and their potential for systemic effects,
overlapping mechanisms could potentially contribute to the pathogenesis
of both conditions. However, direct causal links between UC and
mononeuritis multiplex are yet to be established, and they constitute
distinct clinical entities. Nevertheless, indirect associations such as
autoimmune processes and shared immune system involvement imply that
individuals with UC may be at heightened risk for developing other
autoimmune diseases, including mononeuritis multiplex. Therefore, UC
patients presenting with unexplained neurological signs and symptoms
warrant comprehensive diagnostic workup to exclude neurological
complications like mononeuritis multiplex, followed by prompt initiation
of appropriate therapy. Further research into the complex immunological
interactions in UC and the mechanisms underlying secondary systemic
manifestations like mononeuritis multiplex will provide greater insight
into the spectrum of extraintestinal disease in patients with
inflammatory bowel disease.

R. Okiyama et.al presented a case of a 40-year-old woman experienced
rectal bleeding, diarrhea, weight loss, and tenesmus, leading to a
diagnosis of ulcerative colitis affecting the ascending colon to the
rectum. Initial treatment with oral salazosulfapyridine (SASP) was
effective, resulting in a remission lasting 7 years. UC exacerbation
occurred, prompting treatment with higher SASP and prednisolone. SASP
was stopped due to suspected side effects, after which the patient
experienced a severe UC relapse, accompanied by paresthesia and weakness
in the lower extremities and right hand. This patient presented with
acute mononeuritis multiplex characterized by distinct right-sided
predominance. Nerve conduction studies and biopsy supported axonal
degeneration as the primary neuropathological process. Notably, the
neuropathy's development and course closely paralleled UC activity,
suggesting a strong correlation. This case represents a unique
manifestation of neuropathy associated with UC(8).

F. Tripodi Cutr\selectlanguage{ngerman}ì et.al reported ulcerative colitis associated with
leukocytoclastic vasculitis of the skin. Ulcerative colitis may be
associated with a number of skin lesions such as erythema nodosum and
pyoderma gangrenosum. They describe an unusual case of a
33-year-old-caucasian male with ulcerative colitis and skin lesions
diagnosed as leukocytoclastic vasculitis. An initial treatment with oral
deflazacort led to little benefit, while treatment with oral Mesalasine
caused remission of the skin and intestinal manifestations in 2
weeks(9).

Scott R Levin et.al presented a prime example of the diverse
extraintestinal manifestations that can accompany inflammatory bowel
disease. As illustrated by the 58-year-old female described, ulcerative
colitis may present atypically with a constellation of cutaneous,
ocular, arthritic and hematologic abnormalities prior to the onset of
gastrointestinal symptoms. The tender skin lesions with characteristic
palmoplantar distribution, biopsy findings showing neutrophilic
infiltration, and resolution with ulcerative colitis treatment
collectively confirm the diagnosis of neutrophilic dermatosis(10). This
rare dermatosis highlights the neutrophil-mediated inflammation that
likely underpins many extra-intestinal manifestations of IBD. The
episodic course and response to systemic steroids aligns with previous
reports of neutrophilic dermatoses in IBD.

\textbf{Conclusion}

In conclusion, our case presented a A 75-year-old male patient which
developed Ulcerative colitis associated mononeuritis multiplex as a rare
case

\textbf{Acknowledgments}

The authors express their gratitude for the valuable contribution made
by the patient in providing biopsy and blood donation.

The authors appreciate support provided by Imam Reza Hospital, Tabriz,
Iran.

\textbf{Author contributions}

All authors approved the final manuscript.

\textbf{Availability of data and material}

Considering that this study is about a rare disease availability to
patients and data may hard to some extent.

\textbf{Funding}

Not applicable

\textbf{Competing interests}

The authors declare that they have no competing interests

\textbf{Ethical approval}

This study has been performed according to the Declaration of Helsinki.

\textbf{Consent}

Written informed consent was obtained from the patient to publish this
report in accordance with the journal's patient consent policy.

\textbf{Corresponding author e-mail address~}

jafarpourmehdi1360@gmail.com

\textbf{Tables}

\textbf{Table 1.} Laboratory parameters of the patient\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
\begin{minipage}[b]{0.22\columnwidth}\raggedright\strut
Test\strut
\end{minipage} & \begin{minipage}[b]{0.22\columnwidth}\raggedright\strut
Result\strut
\end{minipage} & \begin{minipage}[b]{0.22\columnwidth}\raggedright\strut
Normal range\strut
\end{minipage} & \begin{minipage}[b]{0.22\columnwidth}\raggedright\strut
Unit\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
HBS Ag*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Qualitative\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
HCV Ab*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Qualitative\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
HIV Ab*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Qualitative\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Serum protein *electrophoresis\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Normal\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
IU/Ml\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
ESR*\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
110\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
For males: 0-15 mm/hr (millimeters per hour) For females: 0-20
mm/hr\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
mm/hr\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
CRP*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
300\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Less than 10 mg/L\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
mg/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
F ANA*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Qualitative\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
C ANCA*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Qualitative\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
P ANCA*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Qualitative\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
S/C*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Qualitative\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Anti SSA\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Qualitative\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Anti SSB\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Qualitative\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Anti dsDNA*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Qualitative\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
S/E*\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
WBC: Moderate RBC: Moderate\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Qualitative\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Na*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
140\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
135 to 145\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\selectlanguage{greek}µ\selectlanguage{english}q/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
K*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
4.1\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
3.5 to 5.0\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\selectlanguage{greek}µ\selectlanguage{english}q/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
C3*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
102(90-180)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
90 - 180\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
mg/dL\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
C4*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
15 (10-40)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
10 - 40\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
mg/dL\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
Urine analysis*\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
RBC: 4-5 Protein: Trace\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
-\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Urea*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
138\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.7 to 1.3\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
mg/dL\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Creatinine*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
4.5\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
~0.6 to 1.1\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
mg/dL\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
AST*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
35\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
10-40\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
U/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
ALT*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
24\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
7-56\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
U/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
ALKP*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
571\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
44-147\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
U/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
TSH*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
2.8 (Normal)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.4 - 4.0\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
mIU/L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
WBC*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
18200\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
4,500 to 11,000\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
cells/\selectlanguage{greek}μ\selectlanguage{english}L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
MCV*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
91\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
80--100\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
fl\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
HB*\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
9.8 g/dl\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
males: 13.8 to 17.2 g/dL females: 12.1 to 15.1 g/dL\strut
\end{minipage} & \begin{minipage}[t]{0.24\columnwidth}\raggedright\strut
g/dL\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
RF*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
-\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
PLT*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
214000\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
150,000 to 450,000\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
platelets/\selectlanguage{greek}μ\selectlanguage{english}L\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Anti-CCP*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Negative\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
-\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
-\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Fe\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
26\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
70 to 175 mcg/dL\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
mcg/dL\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Ferritin\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Normal\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
TIBC\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Normal\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

+HBS Ag: Hepatitis B Surface Antigen, HCV Ab: Hepatitis C Virus
Antibodies, HIV Ab: Human, ESR: Erythrocyte Sedimentation Rate, CRP:
C-Reactive Protein, F ANA: Fluorescent Antinuclear Antibody, C ANCA:
Cytoplasmic Antineutrophil Cytoplasmic Antibody, P ANCA: Perinuclear
Antineutrophil Cytoplasmic Antibody, Anti-smith ab, Anti SSA:
Anti-Sj\selectlanguage{ngerman}ögren's Syndrome A Antibodies, Anti SSB: Anti-Sjögren's Syndrome
B Antibodies, Anti dsDNA: Anti-Double-Stranded DNA Antibodies,C3:
Complement Component 3, C4: Complement Component 4, AST: Aspartate
Aminotransferase, ALT: Alanine Aminotransferase, ALKP: Alkaline
Phosphatase, LDH: Lactate Dehydrogenase: White Blood Cell Count, HB:
Hemoglobin, MCV: Mean Corpuscular Volume, PLT: Platelet Count

\textbf{Figures}

Fig1: Distinctive palm skin lesions\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

Fig2: Colposcopy of Patient\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

Fig3: Intestinal biopsy from patient, microscopic view (histologic) of a
biopsy of the intestine (A\&B) (H\&E, \selectlanguage{ngerman}×50)\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

\textbf{References}

1. Saez A, Herrero-Fernandez B, Gomez-Bris R, S\selectlanguage{ngerman}ánchez-Martinez H,
Gonzalez-Granado JM. Pathophysiology of inflammatory bowel disease:
innate immune system. International Journal of Molecular Sciences.
2023;24(2):1526.

2. Ramos GP, Papadakis KA, editors. Mechanisms of disease: inflammatory
bowel diseases. Mayo Clinic Proceedings; 2019: Elsevier.

3. Schirmer M, Garner A, Vlamakis H, Xavier RJ. Microbial genes and
pathways in inflammatory bowel disease. Nature Reviews Microbiology.
2019;17(8):497-511.

4. Wijnands AM, de Jong ME, Lutgens MW, Hoentjen F, Elias SG, Oldenburg
B, et al. Prognostic factors for advanced colorectal neoplasia in
inflammatory bowel disease: systematic review and meta-analysis.
Gastroenterology. 2021;160(5):1584-98.

5. Esiyok A, Yavasoglu I, Sargin G, Coskun A, Kadikoylu G, Meteoglu I,
Bolaman Z. A rare etiology of fever of unknown origin: ulcerative
colitis. European Geriatric Medicine. 2013;4(6):414-5.

6. Hellmann DB, Laing TJ, Petri M, Whiting-O'keefe Q, Parry GJ.
Mononeuritis multiplex: the yield of evaluations for occult rheumatic
diseases. Medicine. 1988;67(3):145-53.

7. Kaur A, Goggolidou P. Ulcerative colitis: understanding its cellular
pathology could provide insights into novel therapies. Journal of
inflammation. 2020;17:1-8.

8. Okiyama R, Yamada M, Tamaki M, Orimo S, Arai M. Mononeuropathy
multiplex with ulcerative colitis. Internal medicine. 1993;32 8:651-4.

9. Cutrì FT, Salerno R, Schiavo AL, Gravina AG, Romano M, Ruocco E.
Ulcerative colitis associated with leukocytoclastic vasculitis of the
skin. Digestive and liver disease : official journal of the Italian
Society of Gastroenterology and the Italian Association for the Study of
the Liver. 2009;41 7:e42-4.

10. Fine S. Extraintestinal Manifestations of Inflammatory Bowel
Disease. Rhode Island medical journal. 2022;105 9:13-9.

\textbf{Hosted file}

\verb`figure.docx`  available at \url{https://authorea.com/users/617984/articles/683695-ulcerative-colitis-associated-mononeuritis-multiplex-in-75-year-old-patient-rare-case-report}

\textbf{Hosted file}

\verb`table.docx`  available at \url{https://authorea.com/users/617984/articles/683695-ulcerative-colitis-associated-mononeuritis-multiplex-in-75-year-old-patient-rare-case-report}

\selectlanguage{english}
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\end{document}

