\documentclass[10pt]{article}

\usepackage{fullpage}
\usepackage{setspace}
\usepackage{parskip}
\usepackage{titlesec}
\usepackage[section]{placeins}
\usepackage{xcolor}
\usepackage{breakcites}
\usepackage{lineno}
\usepackage{hyphenat}





\PassOptionsToPackage{hyphens}{url}
\usepackage[colorlinks = true,
            linkcolor = blue,
            urlcolor  = blue,
            citecolor = blue,
            anchorcolor = blue]{hyperref}
\usepackage{etoolbox}
\makeatletter
\patchcmd\@combinedblfloats{\box\@outputbox}{\unvbox\@outputbox}{}{%
  \errmessage{\noexpand\@combinedblfloats could not be patched}%
}%
\makeatother


\usepackage{natbib}




\renewenvironment{abstract}
  {{\bfseries\noindent{\abstractname}\par\nobreak}\footnotesize}
  {\bigskip}

\titlespacing{\section}{0pt}{*3}{*1}
\titlespacing{\subsection}{0pt}{*2}{*0.5}
\titlespacing{\subsubsection}{0pt}{*1.5}{0pt}


\usepackage{authblk}


\usepackage{graphicx}
\usepackage[space]{grffile}
\usepackage{latexsym}
\usepackage{textcomp}
\usepackage{longtable}
\usepackage{tabulary}
\usepackage{booktabs,array,multirow}
\usepackage{amsfonts,amsmath,amssymb}
\providecommand\citet{\cite}
\providecommand\citep{\cite}
\providecommand\citealt{\cite}
% You can conditionalize code for latexml or normal latex using this.
\newif\iflatexml\latexmlfalse
\providecommand{\tightlist}{\setlength{\itemsep}{0pt}\setlength{\parskip}{0pt}}%

\AtBeginDocument{\DeclareGraphicsExtensions{.pdf,.PDF,.eps,.EPS,.png,.PNG,.tif,.TIF,.jpg,.JPG,.jpeg,.JPEG}}

\usepackage[utf8]{inputenc}
\usepackage[english]{babel}



\usepackage{float}








\begin{document}

\title{Nasal Tip Necrosis as a Sign of Leprosy: Case Report}



\author[1]{Rana Alramyan}%
\author[2]{RAED ALMUTAIRI}%
\author[2]{Majed Althobaiti}%
\affil[1]{King Saud bin Abdulaziz University for Health Sciences College of Medicine}%
\affil[2]{Security Forces Hospital in Riyadh}%


\vspace{-1em}



  
  \date{June 07, 2024}


\begingroup
\let\center\flushleft
\let\endcenter\endflushleft
\maketitle
\endgroup





\selectlanguage{english}
\begin{abstract}
Leprosy is a chronic granulomatous disease caused by Mycobacterium
leprae. Leprosy occurrence in Saudi Arabia is rare, it was reported that
242 freshly diagnosed leprosy cases were in Saudi Arabia from 2003 to
2012. This report aims to provide awareness, avoid misdiagnosis, and to
introduce the manifestations of leprosy.%
\end{abstract}%



\sloppy


\textbf{Nasal Tip Necrosis a Sign of Leprosy: Case Report}

Rana Alramyan \textsuperscript{1}, Raed Almutairi \textsuperscript{2},
Majed Althubaiti \textsuperscript{2}

\textbf{Abstract}

Leprosy is a chronic granulomatous disease caused by Mycobacterium
leprae, which is an obligate intracellular pathogen. It is usually found
in tropical and developing countries. Leprosy occurrence in Saudi Arabia
is rare, it was reported that 242 freshly diagnosed leprosy cases were
in Saudi Arabia from 2003 to 2012. This report aims to provide
awareness, avoid misdiagnosis, and to introduce the manifestations of
leprosy, with the emphasis of nasal tip necrosis as it could be a
manifestation of leprosy.

\textbf{Ethical consideration}

A consent has been taken from the patient

\textbf{Introduction}

Mycobacterium leprae, an acid-fast, rod-shaped bacillus, obligate
intracellular pathogen causing leprosy, or Hansen disease. Leprosy is a
chronic slowly growing granulomatous disease involving the skin,
peripheral nerves, eyes, and mucosa of upper respiratory tract.
According to the Ridley and Jopling classification system, there are
five types of leprosy: lepromatous (LL), tuberculoid (TT), borderline
borderline (BB), borderline lepromatous (BL) and borderline tuberculoid
(BT). They have also used the term indeterminate leprosy (IL) when a
biopsy sample shows evidence of leprosy without a clear clinical
manifestation. (3) If left untreated, leprosy can cause progressive and
permanent damage to the skin, nerves, limbs, and eyes. Thus, rapid
recognition is crucial to avoid complications of leprosy.

\textbf{Case report}

A 56-year-old lady, known to have diabetic mellitus, hypertension,
dyslipidemia, hypothyroidism, and sinusitis. She presented to the
outpatient department of ear nose and throat (ENT) six months prior to
admission complaining of bilateral nasal obstruction on and off for five
months associated with nasal discharge, facial rash, and erythema around
nasal bridge started four months ago. She had no post-nasal drip, no
change of smell, no facial pain, no ear symptoms, no throat symptoms, no
hair loss nor photosensitivity. She had a history of on and off joint
pain. Her social history is remarkable as she was born in Al-Khurma and
lived there for fifteen years. Family history remarkable for rheumatoid
arthritis in both her brother and son. On examination, she was vitally
stable, afebrile. Nasal examination showed deviated nasal septum with
thick nasal discharge, hypertrophied inferior turbinate, the middle
meatus and nasopharynx were clear, no septal perforation. Ear exam:
bilateral intact tympanic membrane. Throat exam: grade I tonsil
bilaterally. Neck examination: no neck masses. Facial rash, nasal and
perinasal swelling and tenderness with palpation were noted. Lower limb:
no deformity, no scar, no swelling. The plan in the clinic was to give
nasal spray, order sinuses computed tomography (CT), follow CT result,
and to refer to rheumatology and dermatology.

Two months later, the patient was seen in dermatology clinic and was
treated conservatively with local creams as acne vulgaris. At that time,
she was also seen by rheumatology. Laboratory workup was done. Table1
shows the results of the laboratory workup. CT sinuses reported small
poorly delineated non-enhancing soft tissue swelling seen at
anterosuperior aspect of nasal cavities, associated with invovment of
subcutenious fat and thicking of skin at the inferior aspect of nasal
bone. Nasal bone and nasal septum appeared intact.

Two days prior to ER presentation the patient came to the outpatient ENT
clinic complaining of skin edema, nasal tip necrosis associated with
needle prick sensation, and on/off nasal obstruction. She had no nasal
discharge, no paroxysmal nocturnal dyspnea, no smell loss, nor cough. On
examination, there was midfacial necrotizing lesion localized to dorsum
of the nose with exposed cartilage, with surrounding erythema and
inflammation. The lesion started as pustule with pus and underlying
facial erythema localized to central face. No joint pain no rash, no
hematuria, hemoptysis

Then the patient presented to emergency department (ER) with the same
complaint. The ENT team were contacted. Then, she was admitted for
further investigation. In ER, three biopsies were taken, mid nasal
dorsum, left and right nasal dorsum. All showed acute inflammatory cells
with no malignant cells. Also, culture was taken in ER and showed normal
skin flora moderate growth. Blood culture was negative. Hepatitis A, B,
and C negative. The patient was started on empirical antibiotic,
tazocin. At that time, our differential was either midline NK T cell
lymphoma, Wegner granulomatosis, leprosy, or vasculitis.

During her stay, Infectious diseases (ID) team were consulted, their
recommendation was to discontinue tazocin and start ceftriaxone 500mg OD
and metronidazole q8hrs, amphotericin B 300mg IV. They also requested
for acid fast bacilli, and culture. All came with negative results.
Rheumatology team were also consulted, they requested for C-ANCA,
P-ANCA, ANA, SSA, and SSB. All were negative except for ANA it came with
positive result. Also, a chest x-ray was ordered and showed no cavities.

Next day the patient was taken to operating room (OR). Endoscopic
examination was normal, and no abnormality was seen except the nasal
tip. Twelve biopsies were taken under general anesthesia. From right and
left middle nasal turbinate, nasal septum. The result of the biopsies
showed granulation tissue formation with dense acute inflammatory cells
and no malignancy. Biopsies from the skin of right nasal nostril, skin
of left nasal nostril were also taken, it showed chronic inflammation,
no histopathological evidence of vasculitis, and no malignancy. Culture
from wound and tissue came with a negative result, no organisms were
seen.

Dermatology team were contacted, they took two punch biopsies from
healthy tissues (cheeks) and sent for H\&E. Fungal, bacterial,
mycobacterial swabs were also sent. Fungal culture and acid-fast bacilli
were both negative. LDH normal 136. The biopsy was reported as a
granuloma in deep dermis mainly around peripheral nerve. Fite's acid
fast stain (FITE) reveals scanty acid-fast bacilli-like organisms around
the nerve suggestive of leprosy. GMS and PAS stains were negative.

After the biopsy result, ID were contacted, and they advised to start
the patient on a triple antibiotic regimen which is dapsone 100mg orally
once daily, rifampicin 600mg orally once monthly, clofazimine 50mg
orally once daily, and follow up in their clinic.

\textbf{Discussion}

Since the first meeting of the World Health Organization's Leprosy
Expert Committee in 1956, the prevalence of leprosy has decreased
worldwide. However, there are still endemic leprosy areas, such as India
and Indonesia. Regarding the epidemiology of leprosy in Saudi Arabia,
Asiri et al. reported the occurrence of 242 new leprosy cases over a
10-year period spanning 2003-2012. Leprosy is known to exist in Saudi
Arabia, with a geographical distribution showing clustering of cases in
the South-Western and Eastern regions of the country. Unlike our case,
as she presented in Riyadh, at the central region of the country.
However, she was born and lived fifteen years of her life in Al-Khurma,
which is a city in the western region of the country. Emphasizing the
importance of taking a thorough past medical and social history.

Of diagnosed leprosy patients in Saudi Arabia, 57\% are immigrants, and
leprosy is more common in males than females at a ratio of 3:1. Our
patient is of a Saudi nationality, with no direct physical contact with
immigrants nor recent contact with patients known to have leprosy. She
had no history of travelling abroad.

Dermatological lesions and peripheral neuropathy are the cardinal
clinical features of leprosy. Unlike our case, Swain SK. and his
colleagues report that the clinical presentation in their case was
chronic unilateral nasal obstruction and unilateral/ same side
intermittent epistaxis. Other case presented with chronic nasal
congestion, rhinorrhea, intermittent epistaxis, and headache. Our
patient was complaining of on/off bilateral nasal obstruction for five
months associated with nasal discharge, facial rash, and erythema around
nasal bridge started four months prior to her first presentation. No
epistaxis.

Upon physical examination, the case report done by Swain SK presented
with a small reddish mass in the anterior part of nasal cavity. Al-Aboud
et al. reported a case with asymptomatic reddish plaque over the nose
extending to malar area measuring 12 cm in diameter for six months.
Nasal tip drop, or saddle nose, has been reported in the literature due
to cartilaginous destruction with no nasal tip necrosis. Our patient,
however, presented with midfacial edema with no septal perforation. Then
nasal tip necrosis in a later presentation. This unusual presentation
led to a delay in the final diagnosis which was based on
histopathological examination.

\textbf{Conclusion}

Because of the decrease of reported cases over the past several years,
leprosy is not considered as a major public health problem in Saudi
Arabia. Nevertheless, it has not been eradicated yet. Up to our
knowledge, no similar case was reported regarding nasal tip necrosis.
Leprosy could be one of the differential diagnoses of nasal tip
necrosis, which has not been reported before. This case shows the
importance of maintaining a high suspicion index for leprosy even in
non-endemic areas.

\textbf{Figures}\selectlanguage{english}
\begin{longtable}[]{@{}l@{}}
\toprule
\textbf{WBC}: 11.4\tabularnewline
\midrule
\endhead
\textbf{Hgb}: 161 g/l\tabularnewline
\textbf{Electrolytes}: normal\tabularnewline
\textbf{Liver function test:} normal\tabularnewline
\textbf{Bone profile:} normal\tabularnewline
\textbf{ESR:} 42 (high)\tabularnewline
\textbf{CRP:} 9 (high)\tabularnewline
\textbf{Antinuclear antibody:} positive\tabularnewline
\textbf{Rheumatoid factor:} negative\tabularnewline
\textbf{C3 and C4:} within normal range\tabularnewline
\textbf{DAT:} weak positive\tabularnewline
\textbf{Anti IgG:} weak positive\tabularnewline
\textbf{Anti C3d:} negative\tabularnewline
\textbf{Urine analysis:} unremarkable\tabularnewline
\textbf{Anti-DNA:} negative\tabularnewline
\textbf{ELISA IgG and IgM:} negative\tabularnewline
\textbf{Anti gly IgG and IgM:} negative\tabularnewline
\textbf{SS-A and SS-B:} negative\tabularnewline
\textbf{SM, RNP, JO-1 and SCL-70:} negative\tabularnewline
\textbf{Hepatitis A, B and C:} negative\tabularnewline
\bottomrule
\end{longtable}

\textbf{Table 1:} Laboratory results.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

\textbf{Figure 1:} Clinical presentation showing nasal tip necrosis\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

\textbf{Figure 2:} CT sinuses.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

\textbf{Figure 4:} Six months of starting the treatment.

\textbf{Reference:}

\selectlanguage{english}
\FloatBarrier
\end{document}

