<?xml version="1.0" encoding="UTF-8"?><!DOCTYPE article  PUBLIC "-//NLM//DTD Journal Publishing DTD v3.0 20080202//EN" "http://dtd.nlm.nih.gov/publishing/3.0/journalpublishing3.dtd"><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" dtd-version="3.0" xml:lang="en" article-type="research article"><front><journal-meta><journal-id journal-id-type="publisher-id">OJPed</journal-id><journal-title-group><journal-title>Open Journal of Pediatrics</journal-title></journal-title-group><issn pub-type="epub">2160-8741</issn><publisher><publisher-name>Scientific Research Publishing</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.4236/ojped.2020.104077</article-id><article-id pub-id-type="publisher-id">OJPed-106291</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group><subj-group subj-group-type="Discipline-v2"><subject>Medicine&amp;Healthcare</subject></subj-group></article-categories><title-group><article-title>
 
 
  Etiology of Pediatric Jaundice: Observation in the Pediatric Ward of the Gabriel Toure University Hospital
 
</article-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>K.</surname><given-names>Sacko</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>A.</surname><given-names>A. Diakité</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>F.</surname><given-names>Traoré</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>B.</surname><given-names>Maiga</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>P.</surname><given-names>Togo</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>O.</surname><given-names>Coulibaly</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>G.</surname><given-names>Guindo</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>D.</surname><given-names>Konaté</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>A.</surname><given-names>K. Doumbia</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>H.</surname><given-names>Konaré</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>S.</surname><given-names>Sagara</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>A.</surname><given-names>Dembélé</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>A.</surname><given-names>Touré</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>F.</surname><given-names>L. Diakité</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>L.</surname><given-names>N. Sidibé</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>H.</surname><given-names>Diall</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>M.</surname><given-names>Traoré</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Y.</surname><given-names>A. Coulibaly</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>M.</surname><given-names>E. Cissé</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>A.</surname><given-names>Sangaré</given-names></name><xref ref-type="aff" rid="aff3"><sup>3</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>A.</surname><given-names>Ibrahim</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>F.</surname><given-names>T. Dicko</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>M.</surname><given-names>Sylla</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>B.</surname><given-names>Togo</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib></contrib-group><aff id="aff3"><addr-line>Pediatric Service of the Mali Hospital, Bamako, Mali</addr-line></aff><aff id="aff2"><addr-line>Pediatric Service of the Reference Health Center of Municipality 5, Bamako, Mali</addr-line></aff><aff id="aff1"><addr-line>Pediatric Department of Gabriel Toure University Hospital, Bamako, Mali</addr-line></aff><pub-date pub-type="epub"><day>04</day><month>11</month><year>2020</year></pub-date><volume>10</volume><issue>04</issue><fpage>759</fpage><lpage>768</lpage><history><date date-type="received"><day>3,</day>	<month>November</month>	<year>2020</year></date><date date-type="rev-recd"><day>28,</day>	<month>December</month>	<year>2020</year>	</date><date date-type="accepted"><day>31,</day>	<month>December</month>	<year>2020</year></date></history><permissions><copyright-statement>&#169; Copyright  2014 by authors and Scientific Research Publishing Inc. </copyright-statement><copyright-year>2014</copyright-year><license><license-p>This work is licensed under the Creative Commons Attribution International License (CC BY). http://creativecommons.org/licenses/by/4.0/</license-p></license></permissions><abstract><p>
 
 
  Objective: Pediatric jaundice is caused by various conditions. Although some data is available on this issue, data from Mali is insufficient. The present retrospective observational study was an attempt to determine the etiology of pediatric jaundice in the pediatric department of Gabriel Tour&#233; teaching hospital in Bamako, Mali. Methods: We reviewed all pediatric patients with jaundice who were hospitalized and treated in this department 
  during
   January 1 to December 31, 2016 (n = 168). Result: Pediatric jaundice patients accounted for 1.88% of the hospitalized patients, with 
  median
   age of 6 years and 
  male
  /female ratio being 1.6. Infectious, cholestatic, and hemolytic jaundice accounted for 75%, 11% 
  and
   10%, respectively. Malaria and sickle cell disease accounted for 67% and 9%, respectively. Hepatomegaly and splenomegaly were observed in 49 (29%) and 23 (13.7%) patients, respectively. Of 168, 9 patients died. Conclusion: Infectious jaundice, especially jaundice due to malaria, was the most frequent. However, 
  variety
   of etiologies was observed, 
  of
   which the practitioners should be 
  aware
  . The observation presented here may become fundamental data in health-policy making in this area.
 
</p></abstract><kwd-group><kwd>Jaundice</kwd><kwd> Etiology</kwd><kwd> Paediatrics</kwd><kwd> Mali</kwd></kwd-group></article-meta></front><body><sec id="s1"><title>1. Introduction</title><p>Jaundice is one of the reasons for frequent consultation in pediatrics. It is often reported by parents. At times, it is observed by the pediatrician due to the existence of another clinical symptom evoking a liver disease or hemolytic [<xref ref-type="bibr" rid="scirp.106291-ref1">1</xref>]. In practice, the pediatrician often comes across one of these following four situations: jaundice and stool discoloration, jaundice, haemolysis and isolated jaundice [<xref ref-type="bibr" rid="scirp.106291-ref2">2</xref>] [<xref ref-type="bibr" rid="scirp.106291-ref3">3</xref>]. Jaundices etiologies are many; we can divide them into two big categories according to the increase of serum bilirubin which can be non-conjugated bilirubin or conjugated bilirubin and of mixed cause as well [<xref ref-type="bibr" rid="scirp.106291-ref1">1</xref>].</p><p>In Mali, we don’t have statistics related to child and infant’s jaundice, which is the reason why we conducted this study of the infant and child’s jaundices etiologies in the paediatric ward at Gabriel Toure university hospital centre.</p></sec><sec id="s2"><title>2. Methods and Patients</title><p>It was a prospective study led from 1<sup>st</sup> January to 31<sup>st</sup> December 2016 (12 months) in the paediatric ward of the university hospital centre of Gabriel Toure. The university hospital center of Gabriel Toure is a third reference hospital in the Bamako city, Mali’s capital, sahelo-saharan country. All infants and hospitalized children in the ward with icterus were included at the entry examination witin the study. The parameters studied within the searching were: anamnestic, clinical, paraclinical, treatment and scalable. The data were collected on a survey sheet, entered by Word and Excel software and then analyzed by SPSS version 20 software.</p></sec><sec id="s3"><title>3. Results</title><p>During the study we collected 168 files of infants and children with jaundice out of 8924 hospitalization or a frequency of 1.8%.</p><sec id="s3_1"><title>3.1. Soci-Demographic Data</title><p>The average age was 6 years and 3 months with a standard deviation of 4 years and the median age was 6 years. The most represented age group was from 1 to 5 years old with 39.5% (66 patients). The male sex predominated with 62.5%, the sex ratio was 1.66%. Patients from outside Bamako accounted for 42.9%.</p></sec><sec id="s3_2"><title>3.2. Clinical Data</title><p>The vaccination according to Mali’s Expanded Program on Immunization (EPI) was up to date in 65% of patients and 15.5% had been hospitalized for at least one year. We found 1<sup>st</sup> degree consanguinity in 126 patients (75%), the notion of jaundice was found in 20 (11.9%) and 7 (4.1%) were known to have sickle cell disease.</p><p>Anemia and fever were the most common reasons for consultation with 26.7% and 23.8% respectively. Icterus was the reason for consultation in 13% of patients. At the entrance clinical examination, 81% of patients presented with fever, 42.8% with digestive disorders and 20.82% with abdominal pain. Feces were discolored in 5.35% of patients and urine was dark in 6.5%. Jaundice was generalized in 112 patients (66.6%), limited to the conjunctiva in 40 (23.8%) and a subicterus in 18 (10.7%). The general condition was poor in 79 patients (47%), pallor was found in 140 (83.3%), hepatomegaly in 49 (29%) and splenomegaly in 23 (13.6%. Infectious jaundice class predominated with 75% followed by cholestatic jaundice (11%) and constitutional hemolytic jaundice (10%) (<xref ref-type="table" rid="table1">Table 1</xref>).</p><p>The hemogram was performed at 97/168. The majority of patients (95%) had an anemia (Hemoglobin ≤ 11 g/dl) that was microcytic (average globular volume &lt; 70 fintolitre) in 62%. Hyperleukocytosis (WBC &gt; 10,000/mm&#179;) was found in 41% of patients and leukopenia in 4%. Increased in 56/72 patients and conjugated bilirubin (VN ≤ 5 &#181;mol/L) was elevated in 21/72 patients. Transaminases were achieved in 33/168 patients with elevated AST in 27/33 and increased ALT in 24/33. GGTs were increased in 14/18 patients and alkaline phosphatases were</p><table-wrap id="table1" ><label><xref ref-type="table" rid="table1">Table 1</xref></label><caption><title> Clinical characteristics</title></caption><table><tbody><thead><tr><th align="center" valign="middle" >Clinicla characteristics</th><th align="center" valign="middle" >Number</th><th align="center" valign="middle" >Percentage</th></tr></thead><tr><td align="center" valign="middle"  colspan="3"  >Age group</td></tr><tr><td align="center" valign="middle" >&lt;1 year</td><td align="center" valign="middle" >16</td><td align="center" valign="middle" >9.6</td></tr><tr><td align="center" valign="middle" >1 to 5 ans</td><td align="center" valign="middle" >66</td><td align="center" valign="middle" >39.5</td></tr><tr><td align="center" valign="middle" >5 to 10 years</td><td align="center" valign="middle" >52</td><td align="center" valign="middle" >31.1</td></tr><tr><td align="center" valign="middle" >&gt;10 years</td><td align="center" valign="middle" >33</td><td align="center" valign="middle" >19.8</td></tr><tr><td align="center" valign="middle"  colspan="3"  >Sex</td></tr><tr><td align="center" valign="middle" >Male</td><td align="center" valign="middle" >105</td><td align="center" valign="middle" >62.5</td></tr><tr><td align="center" valign="middle" >Female</td><td align="center" valign="middle" >63</td><td align="center" valign="middle" >37.5</td></tr><tr><td align="center" valign="middle"  colspan="3"  >Anamnestic signs</td></tr><tr><td align="center" valign="middle" >Dark urine</td><td align="center" valign="middle" >11</td><td align="center" valign="middle" >6.54</td></tr><tr><td align="center" valign="middle" >Discolored stools</td><td align="center" valign="middle" >9</td><td align="center" valign="middle" >5.35</td></tr><tr><td align="center" valign="middle" >Fever</td><td align="center" valign="middle" >136</td><td align="center" valign="middle" >81</td></tr><tr><td align="center" valign="middle" >Digestive disorders</td><td align="center" valign="middle" >72</td><td align="center" valign="middle" >42.85</td></tr><tr><td align="center" valign="middle" >Abdominal pain</td><td align="center" valign="middle" >35</td><td align="center" valign="middle" >20.83</td></tr><tr><td align="center" valign="middle" >pruritus</td><td align="center" valign="middle" >2</td><td align="center" valign="middle" >1.19</td></tr><tr><td align="center" valign="middle"  colspan="3"  >Physical signs</td></tr><tr><td align="center" valign="middle" >Poor general condition</td><td align="center" valign="middle" >79</td><td align="center" valign="middle" >47</td></tr><tr><td align="center" valign="middle" >Skin rashes</td><td align="center" valign="middle" >4</td><td align="center" valign="middle" >2.38</td></tr><tr><td align="center" valign="middle" >Pallor</td><td align="center" valign="middle" >140</td><td align="center" valign="middle" >83.33</td></tr><tr><td align="center" valign="middle" >jaundice</td><td align="center" valign="middle" >168</td><td align="center" valign="middle" >100</td></tr><tr><td align="center" valign="middle" >Hepatomegaly</td><td align="center" valign="middle" >49</td><td align="center" valign="middle" >29.16</td></tr><tr><td align="center" valign="middle" >Splenomegaly</td><td align="center" valign="middle" >23</td><td align="center" valign="middle" >13.69</td></tr><tr><td align="center" valign="middle" >Abdominal mass</td><td align="center" valign="middle" >4</td><td align="center" valign="middle" >2.38</td></tr><tr><td align="center" valign="middle" >Ascites</td><td align="center" valign="middle" >3</td><td align="center" valign="middle" >1.78</td></tr><tr><td align="center" valign="middle" >CVC</td><td align="center" valign="middle" >2</td><td align="center" valign="middle" >1.19</td></tr></tbody></table></table-wrap><p>elevated in 10/15 patients. Thick Drop was the most requested diagnostic adjunct test and was positive in 67% of patients. Hepatitis A serology was positive in 7% of patients and Hbs Ag was positive in 4%. Abdominal ultrasonography was performed in 45/168 patients and showed hepatomegaly in 15, splenomegaly in 6 and others (<xref ref-type="table" rid="table2">Table 2</xref> and <xref ref-type="table" rid="table3">Table 3</xref>).</p><p>The etiologies were dominated by malaria (67%), Sickle cell anemia (9%), hepatitis A (7%) and hepatitis B (4%). Other etiologies such as bile duct atresia, hepatic abscess and pneumonia were found but in very low proportions (<xref ref-type="fig" rid="fig1">Figure 1</xref>).</p><table-wrap id="table2" ><label><xref ref-type="table" rid="table2">Table 2</xref></label><caption><title> Biological charateristics</title></caption><table><tbody><thead><tr><th align="center" valign="middle" >Parametres</th><th align="center" valign="middle" >Number</th><th align="center" valign="middle" >Percentage</th></tr></thead><tr><td align="center" valign="middle" >Total Bilirubin (n = 72)</td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >High</td><td align="center" valign="middle" >72</td><td align="center" valign="middle" >100</td></tr><tr><td align="center" valign="middle" >Normal</td><td align="center" valign="middle" >0</td><td align="center" valign="middle" >0</td></tr><tr><td align="center" valign="middle" >Conjugated Bilirubin (n = 72)</td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >High</td><td align="center" valign="middle" >21</td><td align="center" valign="middle" >29</td></tr><tr><td align="center" valign="middle" >Normal</td><td align="center" valign="middle" >51</td><td align="center" valign="middle" >71</td></tr><tr><td align="center" valign="middle" >Free Bilirubin (n = 72)</td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >High</td><td align="center" valign="middle" >56</td><td align="center" valign="middle" >78</td></tr><tr><td align="center" valign="middle" >Normal</td><td align="center" valign="middle" >16</td><td align="center" valign="middle" >22</td></tr><tr><td align="center" valign="middle" >AST (n = 33)</td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >Normal</td><td align="center" valign="middle" >6</td><td align="center" valign="middle" >18</td></tr><tr><td align="center" valign="middle" >High</td><td align="center" valign="middle" >27</td><td align="center" valign="middle" >82</td></tr><tr><td align="center" valign="middle" >ALT(n = 33)</td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >Normal</td><td align="center" valign="middle" >9</td><td align="center" valign="middle" >27.3</td></tr><tr><td align="center" valign="middle" >High</td><td align="center" valign="middle" >24</td><td align="center" valign="middle" >72.7</td></tr><tr><td align="center" valign="middle" >Alkaline Phosphatase (n = 15)</td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >Low</td><td align="center" valign="middle" >5</td><td align="center" valign="middle" >14</td></tr><tr><td align="center" valign="middle" >High</td><td align="center" valign="middle" >10</td><td align="center" valign="middle" >86</td></tr><tr><td align="center" valign="middle" >Gamma Glutamine Transferase (n = 18)</td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >Normal</td><td align="center" valign="middle" >4</td><td align="center" valign="middle" >8</td></tr><tr><td align="center" valign="middle" >High</td><td align="center" valign="middle" >14</td><td align="center" valign="middle" >92</td></tr><tr><td align="center" valign="middle" >Prothrombin time (n = 17)</td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >Normal</td><td align="center" valign="middle" >17</td><td align="center" valign="middle" >100</td></tr><tr><td align="center" valign="middle" >Collapsed</td><td align="center" valign="middle" >0</td><td align="center" valign="middle" >0</td></tr><tr><td align="center" valign="middle" >Thick Drop (n = 99)</td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >positive</td><td align="center" valign="middle" >67</td><td align="center" valign="middle" >68</td></tr><tr><td align="center" valign="middle" >negative</td><td align="center" valign="middle" >32</td><td align="center" valign="middle" >32</td></tr><tr><td align="center" valign="middle" >Serology hepatitis A (n = 9)</td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >Positive</td><td align="center" valign="middle" >7</td><td align="center" valign="middle" >78</td></tr><tr><td align="center" valign="middle" >Negative</td><td align="center" valign="middle" >2</td><td align="center" valign="middle" >22</td></tr><tr><td align="center" valign="middle" >Ag Hbs (n = 5)</td><td align="center" valign="middle" ></td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >Positive</td><td align="center" valign="middle" >4</td><td align="center" valign="middle" >80</td></tr><tr><td align="center" valign="middle" >Negative</td><td align="center" valign="middle" >1</td><td align="center" valign="middle" >20</td></tr></tbody></table></table-wrap><table-wrap id="table3" ><label><xref ref-type="table" rid="table3">Table 3</xref></label><caption><title> Distribution of patients according to jaundice classes</title></caption><table><tbody><thead><tr><th align="center" valign="middle" >Class jaundice</th><th align="center" valign="middle" >Number</th><th align="center" valign="middle" >Percentage</th></tr></thead><tr><td align="center" valign="middle" >Infectious jaundice</td><td align="center" valign="middle" >126</td><td align="center" valign="middle" >75</td></tr><tr><td align="center" valign="middle" >Cholestatic jaundice</td><td align="center" valign="middle" >18</td><td align="center" valign="middle" >10.7</td></tr><tr><td align="center" valign="middle" >Constitutional hemolytic jaundice</td><td align="center" valign="middle" >16</td><td align="center" valign="middle" >9.5</td></tr><tr><td align="center" valign="middle" >Isolated jaundice</td><td align="center" valign="middle" >8</td><td align="center" valign="middle" >5.4</td></tr><tr><td align="center" valign="middle" >Total</td><td align="center" valign="middle" >168</td><td align="center" valign="middle" >100.0</td></tr></tbody></table></table-wrap><p>A cure had been observed in 139 patients, 12 were discharged against medical advice, 9 were deceded and 8 are being followed up.</p></sec></sec><sec id="s4"><title>4. Discussion</title><p>Jaundice in infants and children has been a little studied in Africa. As a result, few references have been found in Mali and Africa to discuss our findings.</p><p>The frequency of 1.8% was relatively high given the different etiologies likely to cause jaundice in children in our context of malaria-endemic countries.</p><p>The average age was 6 years and 3 months and the most common age group was 1 to 5 years with 39.5% (66 patients). Given that infectious etiologies were the most common, the high frequency (39.5%) of the 1 - 5 year age group could be explained by their vulnerability to infection. The average age of 6.3 of our series was close to that of the study carried Morocco in 2010 on the febrile icteres of the child who found an average age of 6.1 &#177; 3 year, with a median age of 5.5 years (extreme: 1 - 15 years) and children under the age of six were the most affected with 51.7% [<xref ref-type="bibr" rid="scirp.106291-ref4">4</xref>] [<xref ref-type="bibr" rid="scirp.106291-ref5">5</xref>]. The sex ratio was 1.6 in our study, this predominance of the male sex had been reported by several authors [<xref ref-type="bibr" rid="scirp.106291-ref2">2</xref>] [<xref ref-type="bibr" rid="scirp.106291-ref5">5</xref>].</p><p>Anemia and fever were the most common reasons for consultation with 26.7% and 23.8% respectively, and jaundice was the reason for consultation for 13% of patients. The association of icterus with fever is much found in infectious diseases such as malaria which the etiology the most common in our searching. Anemia can be explained by hemolysis, which is due to infectious pathologies, in this case malaria, and to certain constitutional pathologies such as drepanocytosis (sickle cell disease).</p><p>At the entrance clinical examination, 81% of the patients had a fever, 42.8% had digestive problems and 20.8% had abdominal pain. All of these signs are found in the infectious syndrome, which remains the most common etiological group in our study.</p><p>Feces were discoloured in 5.3% of patients and dark urine in 6.5%. The association of jaundice with coloured feces and dark urine evokes a cholestatic jaundice.</p><p>A hepatomegaly is most often a sign of hepatic suffering, its discovery most often leads to an infectious or cholestatic jaundice and requires an etiological assesment. It was found in 29% of our patients.</p><p>The predominance of infectious jaundice (75%) could be expalained by the poor hygienic conditions and especially by the fact that the study site is a malaria endemic zone.</p><p>The anemia found in 95% of patients could be explained by a high prevalence of martial deficiency in the pediatric population where the microcytosis (62%). According to Demographic and health survey-Mali V, 82% of children aged 6 to 59 months suffer from anemia [<xref ref-type="bibr" rid="scirp.106291-ref6">6</xref>].</p><p>The low rate of realisation of serum bilirubin (72/168) could be explained by the low income of the parents, free bilirubin was increased in 56/72 and conjugated bilirubin was increased in 21/72. Transaminases were carried out in 33/168 patients with high asparate aminotransferase in 27/33 and increased alamin aminotransferase in 24/33 explaining hepatic suffering due to hepatocyte damage. GGTs were increased in 14/18 patients and PALs were elevated in 10/15. This increase in GGTs points towards a cholestatic ictere.</p><p>The thick drop was the complementary examination aimed at the most requested diagnosis and was positive in 67% of patients, in our context every feverish patient is given a thick drop to confirm or rule out malaria. The etiologies were dominated by malaria (67%) followed by drepanocytosis (9%), hepatitis A (7%) and hepatitis B (4%). Other aetiologies such as biliary (tract) atresia, hepatic abscess and pneumonia were found but in very low proportions. In Morocco the etiologies are dominated by G6PD (glucose 6 phosphatase deshydrogenase) deficiency (18%), Wilson’s disease (18%) and hepatitis A (15%) [<xref ref-type="bibr" rid="scirp.106291-ref7">7</xref>]. Other studies carried out on the etiologiy of febrile jaundice had found hepatitis A as the first etiology with 91.5% [<xref ref-type="bibr" rid="scirp.106291-ref5">5</xref>] [<xref ref-type="bibr" rid="scirp.106291-ref8">8</xref>] [<xref ref-type="bibr" rid="scirp.106291-ref9">9</xref>] [<xref ref-type="bibr" rid="scirp.106291-ref10">10</xref>]. These results show a difference in the etiology of the jaundice between these two regions in Africa. In Mali, malaria is the first cause of death and death among children under 5 years, which represent 40% of the first cause of consultation in public health facility according to the health facility system data and its national prevalence is estimated to 52% [<xref ref-type="bibr" rid="scirp.106291-ref6">6</xref>].</p></sec><sec id="s5"><title>5. Conclusion</title><p>Jaundice is a frequent sign in infants and children, the infectious etiologies are more frequent and dominated by malaria. Other etiologies such as sickle cell anemia and cholestatic jaundice (Bile duct atresia) should not be forgotten. The treatment is especially etiologic and the progress beneficial if the etiological support is premature and fitted.</p></sec><sec id="s6"><title>Conflicts of Interest</title><p>The authors declare no conflicts of interest regarding the publication of this paper.</p></sec><sec id="s7"><title>Cite this paper</title><p>Sacko, K., Diakit&#233;, A.A., Traor&#233;, F., Maiga, B., Togo, P., Coulibaly, O., Guindo, G., Konat&#233;, D., Doumbia, A.K., Konar&#233;, H., Sagara, S., Demb&#233;l&#233;, A., Tour&#233;, A., Diakit&#233;, F.L., Sidib&#233;, L.N., Diall, H., Traor&#233;, M., Coulibaly, Y.A., Ciss&#233;, M.E., Sangar&#233;, A., Ibrahim, A., Dicko, F.T., Sylla, M. and Togo, B. (2020) Etiology of Pediatric Jaundice: Observation in the Pediatric Ward of the Gabriel Toure University Hospital. Open Journal of Pediatrics, 10, 759-768. https://doi.org/10.4236/ojped.2020.104077</p></sec><sec id="s8"><title>Enquiry Form</title><p>1) Identity:</p><p>File number:</p><p>Date of entry: /___/___/______/</p><p>Release Date: /___/____/_______/</p><p>Last name and First name:</p><p>Age:</p><p>Sex: □M □F</p><p>Tribe:</p><p>Address:</p><p>2) Medical background</p><p>a) Personal:</p><p>Gestational age: Childbirth: □Medicalized □Non-medicalized</p><p>Birth weight: psychomotor development:</p><p>Feeding mode: □artificial breastfeeding □breastfeeding □mixed breastfeeding</p><p>Expanded Program on Immunization (EPI): □correct □Incorrect □Not done</p><p>Educated: □Yes □No</p><p>Known pathology:</p><p>Transfusion: □Yes □No</p><p>Hospitalization antecedent: ________________</p><p>Jaundice Antecedent: □Yes □No</p><p>b) Familial:</p><p>Sibling: Consanguinity: □1<sup>st</sup> degree □2<sup>nd</sup> degree</p><p>Family history of jaundice: □Yes □No</p><p>3) Reason for consultation: _________________________________</p><p>4) History of the disease:</p><p>Start date: /___/___/_______/</p><p>Installation mode: □Brutal □Progressive</p><p>Associated signs: ________________________________________________</p><p>Urine appearance: □Dark □clear</p><p>Feces appearance: □discoloured □normal</p><p>Fever: □yes □no</p><p>Asthenia: □yes □no</p><p>Weight loss: □yes □no</p><p>Abdominal pain: □yes □no</p><p>Digestive disorders: □yes □no</p><p>pruritus: □yes □no</p><p>5) Admission examination:</p><p>a) General examination:</p><p>Weight (kg): _______</p><p>Size (cm): _________</p><p>Cranial perimeter (cm):_______</p><p>Temperature (˚C): _______________</p><p>Heart beat frequency:</p><p>Breathing frequency:</p><p>General condition: □good □fair □bad</p><p>Skin rash: □yes □no</p><p>Mucocutaneous pallor: □yes □no</p><p>Conjunctive: □jaundice □subicterus</p><p>Generalized jaundice (mucous membrane and teguments): □yes □no</p><p>Discolored stools: □yes □no</p><p>Dark urine: □yes □no</p><p>Pruritus: □yes □no</p><p>b) Examen abdominal:</p><p>Hepatomegaly: □yes □no</p><p>Splenomegaly: □yes □no</p><p>Abdominal mass: □yes □no</p><p>Ascites: □yes □no</p><p>Collateral venous circulation: □Yes □No</p><p>c) Other:</p><p>Psychomotor delay: □yes □no</p><p>Failure to thrive: □yes □no</p><p>Associated malformation: __________________________________________</p><p>Neurological signs: ________________________________________________</p><p>Other associated signs: _____________________________________________</p><p>6) Complementaryexamination:</p><p>a) Biological:</p><p>Blood count:</p><p>Red Blood Cells (RBC) HbHemoglobin</p><p>White Blood Cells (WBC) Polynuclear neutrophils platelets</p><p>Lymphocyte</p><p>Monocytes</p><p>Reticulocyte</p><p>Mean corpuscular volume</p><p>Average Corpuscular Hemoglobin Concentration</p><p>Gamma glutamyl transpeptidase (GGT)</p><p>Alkaline phosphatase (ALP)</p><p>LDH PRTotal BIL</p><p>Conjugate BIL</p><p>Free BIL</p><p>Aminotranferase: ALT AST</p><p>Serology</p><p>Ac anti HAV Ac anti HCV Ac anti HBc</p><p>AgHBs TPHA-VDRL CMV</p><p>Leishmaniasis Toxoplasmosis Rubella</p><p>Cytobacteriological study of urine Blood culture</p><p>Blood smear</p><p>Electrophoresis of Hemoglobin EPP</p><p>Rate of G6PD</p><p>Myelogram</p><p>THS</p><p>Liver function Liver biopsy puncture</p><p>Ascite puncture Other:</p><p>b) Radiologiques:</p><p>Chest X-ray Abdominal ultrasound</p><p>Echocardiography Abdominal CT</p><p>Digestiveendoscopy Cholangiography</p><p>CT cholangiography Cholecystography</p><p>Other:</p><p>7) Diagnostic selected:</p><p>_______________________________________________________</p><p>8) Complications:</p><p>_______________________________________________________</p><p>9) Care:</p><p>Symptomatic:</p><p>Etiologic:</p><p>Medical: ________________________________________________</p><p>Surgical: ________________________________________________</p><p>10) Duration of hospitalization:</p><p>______________________________________________________</p><p>11) Evolution:</p><p>Full recovery: □yes □No</p><p>Chronic evolution and secondary complication:</p><p>Cholestasis: □decreased □aggravated □stabilized</p><p>Edema-ascitic Syndrome: □HTP Portal hypertension □IHC Hepatocellular insufficiency □Infection □Cirrhosis</p><p>Sequelae:</p><p>Death:</p></sec></body><back><ref-list><title>References</title><ref id="scirp.106291-ref1"><label>1</label><mixed-citation publication-type="other" xlink:type="simple">Smahi, M.C., Rahmoun, L., Ghomari, S.M., Benmansour, S., Sendani, H., Bendaddouche, A.S. and Gendrel, D. 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