Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 
Print this page Email this page Users Online: 127

  Table of Contents  
CASE REPORT
Year : 2018  |  Volume : 11  |  Issue : 2  |  Page : 171-174  

Dental implications of an adult jaundice patient: A rare case report


1 Private Practice, Jind, Department of Oral Medicine and Radiology, Haryana, India
2 Private Practice, Jind, Department of Prosthodontics, Haryana, India

Date of Web Publication18-May-2018

Correspondence Address:
Swati Phore
Department of Oral Medicine and Radiology, 1922A, Urban Estate, Jind, Haryana
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/MJDRDYPU.MJDRDYPU_75_17

Rights and Permissions
  Abstract 


The color of a lesion is due to its nature and to its histological substratum. To ease diagnosis, oral cavity lesions have been classified according to their color. In the oral cavity, jaundice is classified under yellow lesions as diffuse macular yellow lesions. This interpretation of the lesions by its color is the first step to diagnosis. It should be taken into account that, as happens with any other classification, the yellowish group of lesions includes items with different prognosis as well as possible markers of systemic disorders. In this case report, the author discusses the oral manifestations of a patient with icterus and its dental implications.

Keywords: Bilirubin, jaundice, yellow


How to cite this article:
Phore S, Panchal RS. Dental implications of an adult jaundice patient: A rare case report. Med J DY Patil Vidyapeeth 2018;11:171-4

How to cite this URL:
Phore S, Panchal RS. Dental implications of an adult jaundice patient: A rare case report. Med J DY Patil Vidyapeeth [serial online] 2018 [cited 2019 Jul 17];11:171-4. Available from: http://www.mjdrdypv.org/text.asp?2018/11/2/171/232650




  Introduction Top


The word “jaundice” comes from the French word “',” which means yellow. Jaundice is a yellowish staining of the skin, sclera, and mucous membranes by bilirubin, a yellow-orange bile pigment. Bilirubin is formed by a breakdown product of hemerings, usually from metabolized red blood cells (RBCs). The discoloration typically is detected clinically once the serum bilirubin level rises above 3 mg/dL (51.3 μmol/L).[1]

Jaundice is not a common presenting complaint in adults. When present, it may indicate a serious problem. This article discusses the evaluation of the adult patient with jaundice. A systematic approach is warranted to clarify the cause quickly so that treatment can begin as soon as possible.


  Case Report Top


A 38-year-old male patient [Figure 1] visited dental outpatient department with the chief complaint of pain and swelling in lower left premolar region of mouth since 1 week. He had a history of jaundice 10 years back, for which he was treated completely. The patient also had a medical condition of piles. He usually had bleeding while passing stool and was getting treatment for same. He had no deleterious habit of drinking alcohol or smoking. General physical examination revealed generalized yellow discoloration of skin, nasolabial fold, sclera [Figure 2], and palms [Figure 3]. Nails were pale and had platynychia [Figure 4]. Intraorally, labial [Figure 5] and [Figure 6], buccal mucosa [Figure 7], and palate [Figure 8] showed yellowish discoloration with pale floor of the mouth [Figure 9], gingiva and tongue [Figure 10]. 35 was carious. No abnormality was detected in the salivary secretion from the glands. After patient's informed consent, radiograph, and blood investigations were performed. Direct, indirect, and total serum bilirubin count were raised, as 1.4 mg%, 2 mg%, and 3.4 mg%, respectively. Hemoglobin was 4.8 gm%, and total RBC count was 1.6 ml/mm3. Aspartate transaminase, alanine transaminase, platelet count, clotting time, thrombin, and prothrombin time were normal indicating no hepatocellular injury. Alkaline phosphatase and Y-glutamyltransferase were also normal, thus excluding chances of cholestasis. Panel test for hepatitis A, B, and C were also normal. On the basis of above investigations, the provisional diagnosis of jaundice secondary to chronic blood loss due to piles was made. The patient was referred to physician for treatment of icterus and piles. Root canal treatment was done for 35.
Figure 1: Extraoral profile of the patient

Click here to view
Figure 2: Yellow discoloration of skin, nasolabial fold and sclera

Click here to view
Figure 3: Yellow discoloration of palms

Click here to view
Figure 4: Pale and platynychia nails

Click here to view
Figure 5: Yellow discoloration of lower labial mucosa

Click here to view
Figure 6: Yellow discoloration of upper labial mucosa

Click here to view
Figure 7: Yellow discoloration of buccal mucosa

Click here to view
Figure 8: Yellow discoloration of palate

Click here to view
Figure 9: Yellow discoloration of floor of the mouth

Click here to view
Figure 10: Pale tongue

Click here to view



  Discussion Top


The classic definition of jaundice is a serum bilirubin level >2.5–3 mg/dL (42.8–51.3 μmol/L) in conjunction with a clinical picture of yellow skin and sclera. Bilirubin metabolism takes place in three phases – prehepatic, intrahepatic, and posthepatic. Dysfunction in any of these phases may lead to jaundice.[2]

In the oral mucosa, the yellow discoloration is more frequently found at the junction between hard and soft palate, ventral surface of the tongue and cheeks, due to the affinity of the elastic fibers for bilirubin.[3]

Patients with jaundice may present with no symptoms at all (i.e., the condition is found accidentally), or they may present with a life-threatening condition. The wide range of possibilities is based on the variety of underlying causes and whether disease onset is quick or slow moving. Patients presenting with acute illness, which is frequently caused by infection, may seek medical care because of fever, chills, abdominal pain, and flu-like symptoms. For these patients, the change in skin color may not be their greatest concern. Patients with noninfectious jaundice may complain of weight loss or pruritus.[4]

Abdominal pain is the most common presenting symptom in patients with pancreatic or biliary tract cancers. Even something as nonspecific as depression may be a presenting complaint in patients with chronic infectious hepatitis and in those with a history of alcoholism.[5]

Occasionally, patients may present with jaundice and some extrahepatic manifestations of liver disease. Examples include patients with chronic hepatitis and pyoderma gangrenosum and patients with acute hepatitis B or C and polyarthralgias.[6]

Alcohol has been shown to affect bile acid uptake and secretion, resulting in cholestasis. Chronic alcohol use may result in fatty liver (steatosis), hepatitis, and cirrhosis, with varying levels of jaundice. Fatty liver, the most common pathologic liver finding, usually results in mild symptoms without jaundice but occasionally progresses to cirrhosis. Hepatitis secondary to alcohol use typically presents with acute onset of jaundice and more severe symptoms. Liver cell necrosis is indicated by highly elevated serum liver transaminase levels.[7]

As per reports of Centers for Disease Control and Prevention published in 2009, 340/478 patients of jaundice had hepatitis C virus (HCV). Since most patients do not exhibit any symptoms, a majority of acute HCV infection cases are unrecognized. Typically, within 7–21 days after exposure, HCV RNA becomes detectable in serum.[8] The diagnosis of acute HCV infection is infrequently made, primarily because more than 70% of patients do not have symptoms associated with acute infection. Overall, approximately, 25% of all patients with acute HCV present jaundice and 10%–20% develop gastrointestinal symptoms (nausea, vomiting, abdominal pain). The patient infected with HCV may spontaneously clear the virus or develop chronic infection. The diagnosis of chronic HCV is based on detection of both HCV antibodies and HCV RNA test, in the presence of signs of chronic hepatitis, either by elevated aminotransferases or by histopathological examination.[9] In the end, we should affirm that in the clinical practice it is important to identify an acute HCV, observe and wait before deciding to apply the treatment. Using a mix of predictive factors, as a favorable score, could be one of the options, as well as strategy “wait and see.” We should avoid a useless and harmful treatment of the patients.

Pseudojaundice can occur with excessive ingestion of foods rich in beta-carotene (e.g., squash, melons, and carrots). Its clinical presentation is as a yellowish pigmentation in the palate and occasionally, in palms, soles and nasolabial fold. Unlike true jaundice, carotenemia does not result in scleral icterus or elevation of the bilirubin level.[10],[11]

We should be aware of the most frequent problems associated with liver disease in clinical practice. There are risks of viral contamination on the part of the dental professionals and rest of patients (cross infection), the risk of bleeding in patients with serious liver disease, and alterations in the metabolism of certain drug substances leading to drug toxicity. A thorough medical and dental history are mandatory.[12]

Consultation with a hematologist and hepatologist is suggested before beginning dental treatment when any abnormal levels are discovered; special attention should be emphasized in minimization of trauma to the patient during any minor oral surgical procedures. If the risk of bleeding increases, local hemostatic agents may be advised (oxidized and regenerated cellulose), as well as antifibrinolytic agents (tranexamic acid), and Vitamin K. All oral surgical procedures with potential tend to cause bleeding when performed on a patient with multiple or a severe single coagulopathy are to be hospitalized before the procedure.[13]

Patients with liver disease may show a significant decrease in hepatic drug metabolism, resulting in an increased or unpredictable effect at normal doses. The dental clinician should avoid or reduce the use of drugs metabolized by liver.[14]


  Conclusion Top


The day-to-day dental practice involves the administration of common drugs irrespective of the patient's health status. Extreme caution and modifications are to be given paramount importance while dealing with patients with hepatic disorders. Reassurance and follow-up of the patient are mandatory.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Modolell I, Guarner L, Malagelada JR. Vagaries of clinical presentation of pancreatic and biliary tract cancer. Ann Oncol 1999;10 Suppl 4:82-4.  Back to cited text no. 1
[PUBMED]    
2.
Pashankar D, Schreiber RA. Jaundice in older children and adolescents. Pediatr Rev 2001;22:219-26.  Back to cited text no. 2
[PUBMED]    
3.
Wheatley M, Heilpern KL. Jaundice: An emergency department approach to diagnosis and management. Emerg Med Pract 2008;10:1-24.  Back to cited text no. 3
    
4.
Pyrsopoulos NT, Reddy KR. Extrahepatic manifestations of chronic viral hepatitis. Curr Gastroenterol Rep 2001;3:71-8.  Back to cited text no. 4
[PUBMED]    
5.
Buskila D. Hepatitis C-associated arthritis. Curr Opin Rheumatol 2000;12:295-9.  Back to cited text no. 5
[PUBMED]    
6.
Blitz NM, Rudikoff D. Pyoderma gangrenosum. Mt Sinai J Med 2001;68:287-97.  Back to cited text no. 6
[PUBMED]    
7.
Tung BY, Carithers RL Jr. Cholestasis and alcoholic liver disease. Clin Liver Dis 1999;3:585-601.  Back to cited text no. 7
[PUBMED]    
8.
Lohia P, Raxitkumar J, Elizabeth M. Profound jaundice in a patient with acute hepatitis C. BMJ Case Rep 2013;2013:1-10.  Back to cited text no. 8
    
9.
Alexandra FR, Carlos F, Rui Tato M, Jose V. Spontaneous cure of acute hepatitis C. Curr Health Sci J 2015;41:1-4.  Back to cited text no. 9
    
10.
Pierach CA. Hypercarotenemia. N Engl J Med 2002;347:222-3.  Back to cited text no. 10
[PUBMED]    
11.
Fico AA, Petrela E, Zajmi E, Sinani N, Dobi D, Dobi F. Secondary carotenemia: Case report. Med Res Chron 2016;3:203-5.  Back to cited text no. 11
    
12.
Greenwood M, Meecham JG. General medicine and surgery for dental practitioners. Part 5: Liver disease. Br Dent J 2003;195:71-3.  Back to cited text no. 12
    
13.
Balatandayoudam A, Karthigeyan R, Sathyanarayanan R, Saravana Kumar B, Selvakumar R. Dental considerations for patients with hepatic dysfunction. JIDENT 2012;1:1-7.  Back to cited text no. 13
    
14.
John Firriolo F. Dental management of patient with end stage liver disease. Mosby's Drug Consult. 15th ed. St. Louis, MO: Mosby; 2005.  Back to cited text no. 14
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10]



 

Top
   
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
   Abstract
  Introduction
  Case Report
  Discussion
  Conclusion
   References
   Article Figures

 Article Access Statistics
    Viewed2237    
    Printed38    
    Emailed0    
    PDF Downloaded84    
    Comments [Add]    

Recommend this journal