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         <span class="citation_publisher">Hindawi Publishing Corporation</span>
         <h2 class="citation-title">Another Report of Acalculous Cholecystitis in a Greek Patient with Infectious Mononucleosis:
            A Matter of Luck or Genetic Predisposition?
         </h2>
         <span class="doi">10.1155/2016/6080832</span>
         <div class="contrib-group">contrib: 
            	  CONT
            	  
            <span class="citation_author">Theocharis Koufakis</span>
            <span class="citation_author_institution_ref">*</span>
            <span class="citation_author">Ioannis Gabranis</span>
            <span class="citation_author_institution_ref"></span>
         </div>
         <span class="email">[thkoyfak@hotmail.com]</span>
         <span class="conflict">[]</span>
         <span class="contribs">[]</span>
         <span class="citation_pubdate">[2016-1-14]</span>
         <span class="citation_copyright">[Copyright 2016: ]</span>
         <span class="citation_licence">[Licence This is an open access article distributed under the Creative Commons Attribution
            License, which permits unrestricted use, distribution, and reproduction in any medium,
            provided the original work is properly cited.]
         </span>
         <span class="citation_funding">[]</span>
         <span class="citation_pagecount">[]</span>
         <span class="citation_data">[]</span>
      </head>
      <div id="abstract" tag="abstract">
         <h2>Abstract</h2>
         <p>We here report a case of a young, male patient who presented with jaundice and was
            diagnosed with acalculous cholecystitis during the course of a primary Epstein-Barr
            Virus (EBV) infection. The coexistence of cholestatic hepatitis and acalculous cholecystitis
            in patients with infectious mononucleosis is extremely uncommon and only few cases
            can be found in the literature. Moreover, almost one-fourth of the total reports of
            this rare entity are coming from Greece. Whether this is a result of physicians' high
            index of suspicion due to previous reports or a consequence of genetic predisposition
            is an issue that deserves further investigation in the future. More studies are required
            in order to clarify the pathophysiological and genetic backgrounds that connect acalculous
            cholecystitis and EBV infection.
         </p>
      </div>
      <div tagxxx="sec">
         <title>1. Introduction</title>
         <p>Infectious mononucleosis (IM), first described by Sprunt and Evans in 1920, is a clinical
            entity caused by the Epstein-Barr Virus (EBV). EBV, also known as human herpesvirus
            4, is a member of the herpes virus family, composed of a double helix of DNA of approximately
            172,000 base pairs and containing about 85 genes [
            <span ref-type="bibr" rid="B1">
               <sup>
                  <a href="#B1">1</a>
               </sup>
            </span>]. Apart from IM, the virus has been associated with the pathogenesis of various diseases,
            including Burkitt's lymphoma, Hodgkin's lymphoma, gastric cancer, nasopharyngeal carcinoma,
            multiple sclerosis, and lymphomatoid granulomatosis [
            <span ref-type="bibr" rid="B2">
               <sup>
                  <a href="#B2">2</a>
               </sup>
            </span>].
         </p>
         <p>IM is characterized by global geographical distribution, being more frequent among
            children and young adults [
            <span ref-type="bibr" rid="B3">
               <sup>
                  <a href="#B3">3</a>
               </sup>
            </span>]. Still, it can be diagnosed in patients of any age, from neonates to the elderly.
            The virus is transmitted through direct contact with an infected individual. In many
            cases, the infected subjects remain asymptomatic. When present, the characteristic
            clinical features include fever, pharyngitis, and lymphadenopathy [
            <span ref-type="bibr" rid="B4">
               <sup>
                  <a href="#B4">4</a>
               </sup>
            </span>]. Other common manifestations of the disease are fatigue, anorexia, nausea, splenomegaly,
            arthralgias, and myalgias.
         </p>
         <p>Liver involvement is not unusual during the course of EBV infection, usually being
            mild and self-limited [
            <span ref-type="bibr" rid="B5">
               <sup>
                  <a href="#B5">5</a>
               </sup>
            </span>]. However, jaundice is an atypical presentation of the disease, observed only in
            5% of patients with IM [
            <span ref-type="bibr" rid="B6">
               <sup>
                  <a href="#B6">6</a>
               </sup>
            </span>]. The exact pathophysiological background of jaundice development in IM is still
            uncertain. Cholestasis and virus-induced hemolysis have been proposed as the most
            probable mechanisms [
            <span ref-type="bibr" rid="B5">
               <sup>
                  <a href="#B5">5</a>
               </sup>
            </span>, 
            <span ref-type="bibr" rid="B7">
               <sup>
                  <a href="#B7">7</a>
               </sup>
            </span>]. Moreover, the coexistence of cholestatic hepatitis and acalculous cholecystitis
            in patients with IM is extremely uncommon and only few reports can be found in the
            literature.
         </p>
      </div>
      <div tagxxx="sec">
         <title>2. Case Presentation</title>
         <p>A 21-year-old male patient presented to the emergency department complaining about
            icteric skin 24 hours earlier. His past medical history was unremarkable and he was
            not on any medication. He denied any history of smoking or alcohol intake and there
            was no significant family history. Patient's physical examination revealed icteric
            skin and sclera. He did not mention unprovoked abdominal pain. Tenderness of upper
            right quadrant was noticed only during abdomen palpation (positive Murphy sign). Interestingly,
            no peripheral lymphadenopathy or exudative pharyngitis was observed. Low-grade fever
            was noticed during the time of hospitalization.
         </p>
         <p>Laboratory tests on admission were as follows: aspartate aminotransferase 172 IU/L
            (normal &lt; 40 IU/L), alanine aminotransferase 232 IU/L (normal &lt; 40 IU/L), total bilirubin
            6.31 mg/dL (normal &lt; 1 mg/dL), direct bilirubin 4.96 mg/dL (normal &lt; 0.3 mg/dL), alkaline
            phosphatase 179 IU/L (normal &lt; 140 IU/L), gamma-glutamyl transferase 350 IU/L (normal
            &lt; 30 IU/L), lactate dehydrogenase 1141 IU/L (normal &lt; 350 IU/L), prothrombin time
            14.2 s (normal 11–14 s), international normalized ratio (INR) 1.07, C-Reactive Protein
            3.3 mg/dL (negative &lt; 0.5 mg/dL), and white cell count 11 × 10
            <sup>3</sup> with 57% lymphocytes. Abdominal ultrasound revealed mild splenomegaly, thickening
            of the gallbladder wall (4.5 mm) (
            <span ref-type="fig" rid="fig1">Figure 1</span>), and positive sonographic Murphy sign. No stones, dilatation of the biliary tract,
            gallbladder swelling, or debris was detected.
         </p>
         <p>The diagnosis of IM was established by high levels of IgM antibodies against EBV viral
            capsid antigen (&gt;320 U/mL, normal &lt; 20 U/mL). Viral hepatitis markers as well as antibodies
            for other hepatotropic viruses, human immunodeficiency virus (HIV) test, and blood
            and urine cultures proved to be negative.
         </p>
         <p>No special treatment was administered apart from intravenous fluids. Our patient had
            an uneventful recovery and was discharged 10 days after admission, presenting significant
            improvement of his laboratory tests. Surgical intervention was thought to be unnecessary.
            In his follow-up visits, he remained in good physical condition and his liver tests
            gradually normalized within the next 2 months. Abdominal ultrasound repeated 30 days
            after admission demonstrated normal findings.
         </p>
      </div>
      <div tagxxx="sec">
         <title>3. Discussion</title>
         <p>Acute acalculous cholecystitis (AAC) is identified as the cause of about 5 to 10%
            of all cases of acute cholecystitis [
            <span ref-type="bibr" rid="B8">
               <sup>
                  <a href="#B8">12</a>
               </sup>
            </span>]. Being more frequent among patients with severe underlying conditions such as trauma
            and sepsis, it has been linked with higher percentages of mortality and complications
            when compared to the calculous type of the disease [
            <span ref-type="bibr" rid="B9">
               <sup>
                  <a href="#B9">13</a>
               </sup>
            </span>]. Though viral AAC is generally uncommon, several case reports of hepatitis A virus-induced
            AAC have been published in the literature [
            <span ref-type="bibr" rid="B10">
               <sup>
                  <a href="#B10">14</a>
               </sup>
            </span>, 
            <span ref-type="bibr" rid="B11">
               <sup>
                  <a href="#B11">15</a>
               </sup>
            </span>]. Direct invasion of the gallbladder wall by the EBV could be a possible explanation
            of the development of AAC during the course of IM [
            <span ref-type="bibr" rid="B12">
               <sup>
                  <a href="#B12">16</a>
               </sup>
            </span>]; still other mechanisms might be also involved. Attilakos et al. [
            <span ref-type="bibr" rid="B13">
               <sup>
                  <a href="#B13">9</a>
               </sup>
            </span>] discuss a potential contributing role of Gilbert's syndrome to the development of
            AAC in children with acute EBV infection. Fretzayas et al. [
            <span ref-type="bibr" rid="B14">
               <sup>
                  <a href="#B14">11</a>
               </sup>
            </span>] consider that biliary dyskinesia could be an alternative explanation of impaired
            gallbladder contractility in EBV infection.
         </p>
         <p>Interestingly, the vast majority of patients previously reported with coexistence
            of AAC and EBV infection were females [
            <span ref-type="bibr" rid="B12">
               <sup>
                  <a href="#B12">16</a>
               </sup>
            </span>], suggesting a probable relationship between estrogens and the development of the
            disease [
            <span ref-type="bibr" rid="B15">
               <sup>
                  <a href="#B15">17</a>
               </sup>
            </span>]. Additionally, abdominal pain was prominent in most of the cases and it was the
            main reason that urged patients to seek medical advice. Differently, peripheral lymphadenopathy
            was generally absent, in contrast with the typical pattern of IM.
         </p>
         <p>Most cases come from Europe and it is worth pointing out that 6 of them have been
            already reported from Greece [
            <span ref-type="bibr" rid="B7">
               <sup>
                  <a href="#B7">7</a>
               </sup>
            </span>–
            <span ref-type="bibr" rid="B14">
               <sup>
                  <a href="#B14">11</a>
               </sup>
            </span>] (
            <span ref-type="table" rid="tab1">
               <a href="#tab1">Table 1</a>
            </span>). Whether this is a result of physicians' high index of suspicion due to previous
            reports or a consequence of genetic predisposition is an issue that deserves further
            investigation in the future.
         </p>
         <p>It is worth mentioning that most of formerly described cases received antibiotics,
            while only one was subjected to cholecystectomy, because of severe clinical condition
            [
            <span ref-type="bibr" rid="B18">
               <sup>
                  <a href="#B18">18</a>
               </sup>
            </span>]. However, existing evidence suggests that supportive care and close monitoring of
            liver function tests are usually adequate management strategies for patients with
            EBV-induced AAC. The possibility of rash development associated with antibiotic treatment
            in subjects with IM [
            <span ref-type="bibr" rid="B19">
               <sup>
                  <a href="#B19">19</a>
               </sup>
            </span>] should also be considered.
         </p>
         <p>Gallbladder wall thickening has been also reported in patients with acute hepatitis
            [
            <span ref-type="bibr" rid="B20">
               <sup>
                  <a href="#B20">20</a>
               </sup>
            </span>]. However, we consider that the wall thickening of patient's gallbladder in the reported
            case was a consequence of the developed AAC. Currently, there are no universally accepted
            criteria for the diagnosis of AAC. Gallbladder wall thickening of over 3 mm, distention
            of the gallbladder, localized tenderness, and pericholecystic fluid and sludge have
            been proposed as suitable ones [
            <span ref-type="bibr" rid="B21">
               <sup>
                  <a href="#B21">21</a>
               </sup>
            </span>, 
            <span ref-type="bibr" rid="B22">
               <sup>
                  <a href="#B22">22</a>
               </sup>
            </span>]. The combination of two or more of the above criteria, in a compatible clinical
            setting, is considered to be diagnostic [
            <span ref-type="bibr" rid="B21">
               <sup>
                  <a href="#B21">21</a>
               </sup>
            </span>]. Our patient met two of the reported criteria, that is, wall thickening (4.5 mm)
            and localized tenderness. Generally, a gallbladder wall thickness of at least 3.5 mm
            is accepted to be diagnostic of AAC [
            <span ref-type="bibr" rid="B8">
               <sup>
                  <a href="#B8">12</a>
               </sup>
            </span>].
         </p>
         <p>In contrast with previous reports, our patient was a male and older than the majority
            of other cases. Moreover, he did not present with abdominal pain, but his main clinical
            manifestation was jaundice. Consistent with other cases, he did not develop pharyngitis
            and lymphadenopathy.
         </p>
         <p>In conclusion, the coexistence of cholestatic hepatitis and acalculous cholecystitis
            represents a rare and atypical presentation of infectious mononucleosis. Physicians
            should be aware of this uncommon combination and suspect in time a possible EBV infection,
            in order to avoid unnecessary use of antibiotics or surgical procedures. Further studies
            are required in order to clarify the pathophysiological and genetic backgrounds that
            connect acalculous cholecystitis and EBV infection.
         </p>
      </div>
      <back>
         <div tagxxx="sec">
            <title>Conflict of Interests</title>
            <p>The authors declare that there is no conflict of interests regarding the publication
               of this paper.
            </p>
         </div>
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      </back>
      <div tagxxx="floats-group">
         <fig>
            <label>Figure 1</label>
            <caption>
               <p>Abdominal ultrasound revealing thickening of the gallbladder wall and absence of stones
                  or dilatation of the biliary tract.
               </p>
            </caption>
            <graphic></graphic>
         </fig>
         <div id="tab1">
            <label>Table 1</label>
            <caption>
               <p>Main characteristics of cases with EBV-induced acute acalculous cholecystitis (AAC),
                  reported from Greece.
               </p>
            </caption>
            <table>
               <thead>
                  <tr>
                     <th>1st author, year (ref.)</th>
                     <th>Age, sex</th>
                     <th>ALT (IU/L)</th>
                     <th>Total bilirubin</th>
                     <th>ALP (IU/L)</th>
                     <th>Surgical intervention</th>
                  </tr>
               </thead>
               <tbody>
                  <tr>
                     <td>Prassouli, 2007 [
                        <span ref-type="bibr" rid="B7">
                           <sup>
                              <a href="#B7">7</a>
                           </sup>
                        </span>]
                     </td>
                     <td>13, female</td>
                     <td>674 (5–45)</td>
                     <td>4 mg/dL</td>
                     <td>721 (&lt;248)</td>
                     <td>No</td>
                  </tr>
                  <tr>
                     <td>Lagona, 2007 [
                        <span ref-type="bibr" rid="B16">
                           <sup>
                              <a href="#B16">8</a>
                           </sup>
                        </span>]
                     </td>
                     <td>4, female</td>
                     <td>304 (5–45)</td>
                     <td>4.6 mg/dL</td>
                     <td>236 (38–148)</td>
                     <td>No</td>
                  </tr>
                  <tr>
                     <td>Attilakos, 2009 [
                        <span ref-type="bibr" rid="B13">
                           <sup>
                              <a href="#B13">9</a>
                           </sup>
                        </span>]
                     </td>
                     <td>5, male</td>
                     <td>257 (5–45)</td>
                     <td>1.8 mg/dL</td>
                     <td>919 (38–148)</td>
                     <td>No</td>
                  </tr>
                  <tr>
                     <td>Cholongitas, 2009 [
                        <span ref-type="bibr" rid="B17">
                           <sup>
                              <a href="#B17">10</a>
                           </sup>
                        </span>]
                     </td>
                     <td>19, female</td>
                     <td>584</td>
                     <td>6.5 mg/dL</td>
                     <td>710</td>
                     <td>No</td>
                  </tr>
                  <tr>
                     <td>Fretzayas, 2014 [
                        <span ref-type="bibr" rid="B14">
                           <sup>
                              <a href="#B14">11</a>
                           </sup>
                        </span>]
                     </td>
                     <td>11, female</td>
                     <td>198</td>
                     <td>31 
                        <i>μ</i>mol/L
                     </td>
                     <td>536</td>
                     <td>No</td>
                  </tr>
                  <tr>
                     <td>Fretzayas, 2014 [
                        <span ref-type="bibr" rid="B14">
                           <sup>
                              <a href="#B14">11</a>
                           </sup>
                        </span>]
                     </td>
                     <td>12, female</td>
                     <td>195</td>
                     <td>Not provided</td>
                     <td>Not provided</td>
                     <td>No</td>
                  </tr>
                  <tr>
                     <td>Present case</td>
                     <td>21, male</td>
                     <td>232 (&lt;40)</td>
                     <td>6.31 mg/dL</td>
                     <td>179 (&lt;140)</td>
                     <td>No</td>
                  </tr>
               </tbody>
            </table>
         </div>
      </div>
   </article>
</html>