Chronically elevated billirubin of 2.3 or higher dismissed as benign?
Hi everyone :)
I hope I can get someone to explain this to me but I found out last summer that my bilirubin levels are elevated and not just by a small amount. It seems they're pretty high at 2.3 and sometimes even higher.
My doctor ran some basic tests and found my AST, ALT, and other liver enzymes to be normal. The only thing that was elevated was bilirubin at 2.3. My bilirubin levels are always elevated. Since last summer I've had multiple tests done to see if anything was changing and everything is always normal except bilirubin its always chronically elevated at 2.3 or greater. My doctor has dismissed this as a benign condition called Gilbert's syndrome.
I would be completely fine with this diagnosis if I didn't feel sick. I've been dealing with health problems at the same time and have the following symptoms:
- Chronic fatigue
- Occasional low grade fevers 99.8 - 100.2+
- Frequent urination at night
- Generally not feeling well like I have a flu
So I'm just confused as to how my doc concluded my elevated bilirubin was benign? Shouldn't a chronically elevated level of bilirubin of this amount be perused further before labeling it benign? Or am I missing something.
Anyway thank you for reading this :D. I just wanted to know if elevated bilirubin is part of the puzzle as to why I'm not feeling good.
a complete hep panel to check for hepititus a,b or c. a cbc to check for anemia, a lipid panel, glucose and a abdominal ultrasound would be a good place to start. i wouldnt be comfortable with a possible gilberts syndrome. i would want to rule out any form of liver disease
I was looking at your profile and I read your post that said you have Lyme Disease. Lyme Disease can cause an elevated Bilirubin.
Lyme Disease can cause elevated Bilirubin, Loss of appetite, nausea, vomiting, abdominal pain, diarrhea, jaundice, enlarged liver and/or spleen, and elevated ALT level.
Here is something I found about Lyme Disease:
"Lyme disease is the most common vectorborne infec-
tion in the United States. It is caused by the spirochete
Borrelia burgdorferi and is transmitted by Ixodid ticks
(by Ixodes scapularis in northeastern and midwestern
states and by Ixodes pacificusin western states), generally
during the months of May through October.
Gastrointestinal signs and symptoms are common in the early
stages of Lyme disease. In a study of 314 patients with early Lyme
disease, the predominant clinical findings included anorexia (in 23% of patients), nausea (in 17%), vomiting(in 10%), abdominal pain (in 8%), right upper-quadrant tenderness (in 8%), hepatomegaly (in 5%), splenomegaly (in 6%), and diarrhea (in 2%) . Approximately 10% of the patients had symptoms that were suggestive of hepatitis. Subclinical hepatitis occurred in 27% of patients during the early stages of disease, according to one study . Abnormal liver function test (LFT) findings generally indicate mild hepatocellular injury. Patients with early disseminated Lyme disease
are more likely to have abnormal LFT findings than are patients with localized disease . The results of 3 different studies that evaluated abnormal LFT findings in patients with Lyme disease are compared in table 2. However, elevations in aspartate aminotransferase and alanine aminotransferase levels may indicate Lyme disease–associated myositis in some patients and may not be related to underlying hepatic injury.
The prognosis for patients with Lyme disease–associated hepatic dysfunction is excellent with appropriate antimicrobial
treatment . LFT elevations usually decrease or resolve within
3 weeks after starting treatment. Hepatitis has not been reported
as a late complication of the disease. In 1 case report, liver
function abnormalities occurred late in the course of Lyme
disease; however, recurrence of Lyme disease could not be dis-
tinguished from relapse in that case .
Pathogenesis and histopathologic findings:
The pathogenesis of liver injury in patients with Lyme disease includes
an interplay of direct hepatic invasion by the spirochete and
B. burgdorferi has been shown to pen-
etrate through vascular endothelial cells in vitro , and it is
this invasive capacity of the organism that is responsible for its
tissue colonization in vivo . Cellular and humoral immu-
nologic mechanisms also contribute to the abnormal LFT find-
ings commonly observed in the early stages of Lyme disease.
Lyme disease can result in a variety of histologic abnormalities
in the liver—in particular, sinusoidal infiltration by a mixed
inflammatory infiltrate . Kupffer cell hyperplasia, microves-
icular fat, and hepatocyte ballooning are less commonly ob-
served . Spirochetes have been identified within hepatic si-
nusoids and parenchyma [4, 7]. This is most common in early,
disseminated infection. Rarely, B. burgdorferi infection can re-
sult in a granulomatous hepatitis, which suggests that Lyme
disease should be included in the differential diagnosis of febrile
granulomatous hepatitis .
The diagnosis of Lyme disease should be
considered for any patient from an area of endemicity who
presents with a nonspecific illness and abnormal LFT findings,
regardless of the presence of a rash. The abnormal LFT findings
are usually mild and generally improve or resolve within 3
weeks after the initiation of appropriate therapy  "
The FIRST test to have is a FRACTIONALIZED BILIRUBIN.
TOTAL BILIRUBIN = DIRECT BILIRUBIN + INDIRECT BILIRUBIN.
A fractionalized bilirubin test breaks the total bilirubin down so you can see whether your direct bilirubin is elevated or your indirect bilirubin is elevated.
Elevated direct (conjugated) bilirubin would indicate a LIVER PROBLEM.
Elevated indirect (unconjugated) bilirubin would indicate Gilbert's Syndrome or hemolytic anemia WHICH ARE NOT LIVER PROBLEMS.
When bilirubin is elevated and all other liver tests are normal, bilirubin needs to be fractionated to look for the predominant component of bilirubin that is elevated (direct versus indirect). Liver diseases must be considered in cases where the contribution of direct-reacting bilirubin is significant (>10%), even if the other liver tests are normal.
This is not actually a disease, and is the most common cause of mild bilirubin elevation. The other liver tests are normal and ≥90% of bilirubin is indirect-reacting. A fasting bilirubin test is rarely needed but demonstrates an elevation of bilirubin with 48 hours of fasting, with return to normal within 24 hours of eating a normal diet. A urine test for bilirubinuria is negative. The major differential diagnosis of indirect hyperbilirubinaemia is haemolysis. Therefore, FBC, reticulocyte count, and blood smear are performed. A genetic test demonstrating homozygosity of TATA gene A(TA7)TAA alleles, instead of A(TA6)TAA, can confirm the diagnosis. 
In patients with predominant indirect bilirubinaemia (>90% indirect), the most common causes are associated with increased haemolysis. Blood tests should include haemoglobin, RBC count, reticulocyte count, blood peripheral smear, and Coombs test. Haemoglobin electrophoresis is also performed in patients with an ethnic background that increases the risk of disorders of haemoglobin (e.g., thalassaemia). These patients may also have increased risk for gallstones, and an imaging study of the abdomen may be required in appropriate clinical settings.
Large biliary duct obstruction
The most common initial imaging study is an abdominal ultrasound. Based on the history, physical examination, and subsequent laboratory and ultrasound tests, further imaging studies may be required. A contrast imaging study (CT/MRCP) is usually diagnostic in extrahepatic obstruction. ERCP can be therapeutic...."
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