Name:
A 34-Year-Old with Yellow Eyes
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A 34-Year-Old with Yellow Eyes
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T00H11M51S
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Upload Date:
2022-02-28T00:00:00.0000000
Transcript:
Language: EN.
Segment:0 .
[upbeat intro music]
DR. HANDY: Hi, welcome to Harrison's Podclass where we discuss important concepts in internal medicine. I'm Cathy Handy.
DR. WIENER: And I'm Charlie Wiener and we're coming to you from the Johns Hopkins School of Medicine. Welcome to Harrison's Podclass. This is episode 50: A 34-Year-Old with Yellow Eyes. The question starts, a 34-year-old man presents to the physician complaining of yellow eyes. For the past week, he has felt ill with decreased oral intake, low grade fevers that he measured about a 100 Fahrenheit, fatigue, nausea, and occasional vomiting.
DR. WIENER: He noticed that his eyes became yellow about four days ago. And since that time he's noticed pain in his right upper quadrant. He currently uses marijuana and ecstasy recreationally and has a prior history of injection drug use with cocaine. He has not injected drugs in at least one year. He has no other past medical history but he was unable to donate blood for reasons that he cannot recall within the past year.
DR. WIENER: His social history is remarkable for working as a veterinary assistant. His only medication is over the counter ibuprofen on occasion. On sexual history, he reports five male sexual partners over the past six months and he does not consistently use condoms.
DR. HANDY: Let's stop for a minute and unpack that history because there's really a lot there. So from the beginning, it sounds like he's jaundiced. What you describe is scleral icterus which you start to see with a bilirubin of about three milligrams per deciliter. So I'm immediately starting to think, why does he have an elevated bilirubin?
DR. WIENER: So what are you thinking?
DR. HANDY: Well, there are a lot of things that can cause that. His social history suggests a lot of possible exposures that could be toxic to the liver or could be associated with something else. You mentioned he has illicit drug use which exposes him to infections like hepatitis, HIV, although the IV drug use that you mentioned is not recent. There was something else that prevented him from donating blood.
DR. HANDY: Who knows what that is? Maybe infection, tattoos possibly, possibly travel though presumably he would remember that. Maybe it's anemia from some other cause. And of course he also has to work as a veterinary assistant. Who knows what zoonotic infections he might be at risk of and that would really depend on any recent animal exposures. And he's also at risk of sexually transmitted infections given the unprotected sex that you mentioned.
DR. WIENER: Okay, well, I'm going to give you some help. So here's a physical exam and laboratory values. On physical examination, he appears ill and has obvious jaundice with scleral icterus. His temperature is a 100.4 Fahrenheit. His blood pressure is 110 over 70, heart rate is 105 per minute. And his respiratory rate is 16 with a room air saturation of 99%. His lung and his heart are normal other than tachycardia.
DR. WIENER: His liver is 15 centimeters to percussion and palpable six centimeters below the right costal margin. The liver edge is smooth and tender to palpation. His spleen is not enlarged and there are no stigmata of chronic liver disease and no peripheral edema.
DR. HANDY: Well, it sounds like he could have acute hepatitis, I would definitely want more lab studies to include electrolytes, liver function tests, and given the high likelihood, viral hepatitis testing.
DR. WIENER: Okay. His AST is 1,232. His ALT is 1,560. His alkaline phosphatase is 394. His total bilirubin is 13.4. And his direct portion of that is 12.2. His INR is 2.3 and his APTT is 52 seconds.
DR. HANDY: Well, he clearly has an acute hepatitis with notable liver injury and disruption of synthetic function. Acute hepatitis can have numerous etiologies. These include viruses, toxins, drug-induced hepatitis, auto-immune diseases, metabolic diseases, exposures like alcohol, ischemia can cause this. If this were a pregnant woman, you sometimes see it as well. And there are other infectious etiologies like rickettsial diseases and leptospirosis that can cause it too.
DR. HANDY: In this clinical scenario, the patient has risk factors for hepatitis A, B, and C infection including being a man who has sex with men and a prior history of injection drug use. So I would definitely want viral studies.
DR. WIENER: Okay, you got it. Here it goes. Hepatitis serologies reveal the following. His hepatitis A IgM is negative. Hepatitis A IgG is negative. Hepatitis B core IgM is positive. Hepatitis B core IgG is negative. His hepatitis B surface antigen is positive. His hepatitis B surface antibody is negative. His hepatitis B e-antigen is positive.
DR. WIENER: His hepatitis B e-antibody is negative, and is hepatitis C antibody is positive.
DR. HANDY: That's very helpful. What does the question ask?
DR. WIENER: The question asks what is the cause of the patient's current clinical presentation?
A: acute hepatitis A;
B: acute hepatitis B;
C: acute hepatitis C;
D: chronic hepatitis B; or E: drug-induced hepatitis.
DR. HANDY: All right, let's take this systematically. We think the patient has acute viral hepatitis and not drug-induced so we can rule out E off the bat. The presentation that you initially described does not really help distinguish because all present with a similar clinical pattern, although incubation periods vary after the exposure. The most common initial symptoms are fatigue, anorexia, nausea, vomiting, myalgias, and headache. And he had a lot of those.
DR. HANDY: These symptoms precede the onset of jaundice by about one to two weeks. Once jaundice develops, the prodromal symptoms regress. On physical examination, as we saw in this patient, there's usually obvious icterus with an enlarged and tender liver. Splenomegaly can also occur. On labs, we would see AST and ALT that are elevated with peak levels that are quite variable and can be between 400 and 4,000 international units per liter and alkaline phosphatase levels are increased to a much lesser degree.
DR. HANDY: Hyperbilirubinemia with levels between about 5 to 20 can occur also with primarily an increase in levels of conjugated bilirubin. And in this case, we heard that he had a total bilirubin of 13 that was mostly conjugated.
DR. WIENER: Okay. So you mentioned he's at risk of hepatitis A, B and C. Which do you think he has? Tell me more.
DR. HANDY: Hepatitis A is an RNA virus that presents with acute hepatitis and is transmitted by the fecal oral route. In the acute state, the immunoglobulin or IgM is elevated, and we do not see that in this scenario, so we can rule out answer A.
DR. WIENER: Okay. He does not have acute hepatitis A because his IgM is negative. And his IgG being negative, does that suggest he was not vaccinated?
DR. HANDY: Yeah. So based on that, he has not been vaccinated for hepatitis A and has not had a history of hepatitis A. Based on the values you presented, he has acute hepatitis B.
DR. WIENER: Why do you say that? And you're going to have to explain to me why he's not been vaccinated against hepatitis B, also, as you come through with this explanation.
DR. HANDY: Hepatitis B virus is a DNA virus with three common antigens that are tested serologically to determine the time course of the illness. These antigens are the surface antigen, the core antigen, and the e-antigen which is a nuclear capsid protein produced from the same gene as the core antigen but immunologically distinct. Several distinct patterns can be observed. And that helps us figure out what we're dealing with here.
DR. HANDY: So in acute hepatitis B, the core IgM, the surface antigen, and the e-antigen are all positive, and that's what we see in this case. At this point, the patient is highly infectious and there's viral shedding in bodily fluids, including saliva usually. In the late acute infection, core IgG may be positive at the same time as surface and e-antigen positivity.
DR. HANDY: In chronic hepatitis B, the same pattern of serologies is seen. If a patient has a prior infection without development of chronic hepatitis, the core IgG and surface antibody are positive. However, when immunity is obtained via vaccination, only the surface antibody is positive. The e-antigen and surface antigen will be negative since the patient was never infected.
DR. WIENER: Okay. So I'm convinced he has acute hepatitis B. You made a very compelling case there. But why does he not have acute hepatitis C?
DR. HANDY: Hepatitis C is an RNA virus with at least six different genotypes causing the disease. The RNA virus can be detected in the serum. We did not report that result in this patient but he does have a positive hepatitis C antibody. He could have acute hepatitis C however, given his clinical history of prior injection drug use and inability to donate blood, this likely indicates a chronic hepatitis C infection and may have excluded him from previous blood donation.
DR. HANDY: In some instances, ecstasy has been reported to cause drug-induced hepatitis but given the viral serologies in this patient, I think that that's more likely than ecstasy causing his presentation.
DR. WIENER: How do you think he got the acute hepatitis B?
DR. HANDY: Probably from the sexual activity that you reported.
DR. WIENER: Okay. So there's a follow-up question. And that reads, in the patient described above, what would be the best approach to prevent the development of chronic hepatitis? And the options are A: administration of anti-hepatitis A virus immunoglobulin, or IgG;
B: administration of lamivudine;
C: administration of pegylated interferon alpha plus Ribavirin;
D: administration of prednisone beginning at one dose of one milligram per kilogram, daily; or E: do nothing and observe as 99% of individuals with this disease recover.
DR. HANDY: The answer in this case is E. No treatment is recommended for acute hepatitis B in most individuals because 99% of infected individuals will recover without any assistance. Therefore it would not be expected that an individual would derive any particular benefit from additional treatment. In severe acute hepatitis B nucleoside analogues including lamivudine have been used successfully, although there are no clinical trial data to support such an approach.
DR. HANDY: I would suggest following the patient for resolution of the acute infection. Now, this is in contrast to hepatitis C. So in typical cases of acute hepatitis C, recovery is not common, maybe about 15 to 20%. So progression to chronic hepatitis is generally the rule.
DR. WIENER: So if he had acute hepatitis C, would you recommend treatment?
DR. HANDY: Not usually in the acute setting but we do have a lot of treatments for chronic hepatitis C and there about a half a dozen different oral, generally brief duration, usually about 12 weeks. They're very well tolerated and they're highly effective with sustained virologic response rates that exceed 90 to 95%. And there are generally a combination of regimens which include polymerase inhibitors, protease inhibitors, and NS5A inhibitors.
DR. HANDY: And they're available again to treat patients with chronic hepatitis C. And just to note, this patient should also be tested for HIV.
DR. WIENER: Okay, so the teaching points in this case are that acute hepatitis may be caused by a variety of viral and non-viral causes that typically can not be distinguished clinically. Understanding the time course and the immunologic response to viral infections can help determine whether a patient is acutely infected, chronically infected, or vaccinated. Most patients with acute hepatitis B recover without treatment.
DR. HANDY: And if you want to read more about this, you can check out the Harrison's chapter on acute viral hepatitis. [outro music] [Mr. Shanahan] This is Jim Shanahan, publisher at McGraw Hill. Harrison's Podclass is brought to you by McGraw Hill's Access Medicine, the online medical resource that delivers the latest trusted content from the best minds in medicine.
DR. HANDY: Go to accessmedicine.com to learn more.