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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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Test Results
Assessment
All patients who present for initial evaluation of HIV should have a set of routine lab
evaluation tests to determine the need for prophylactic medications and determine prognosis. T-
cell subsets (CD4 count) are the primary indicator for the need to initiate antiretroviral therapy
and for making decisions about prophylactic medications. CD4 count tells us what diseases the
patient is at risk for now, and it is the major clinical marker of the immunocompetence of the
patient.
Viral load testing tells us how aggressive a person’s disease is, i.e., the magnitude of
replication of the virus in the body. A high viral load implies a more aggressive disease in
which the CD4 count will drop more rapidly. Viral load testing gives a numerical value to the
amount of HIV in the patient’s blood. Viral load is like a glucose level in a diabetic patient:
Higher viral load implies the need for more medication. The viral load is the most important
test to monitor response to therapy. The aim of therapy is to have an undetectable HIV viral
load in the serum after 6–12 mos of therapy (<50 copies/µL).
Chemistries
Pap smear
Chest x-ray
Hepatitis A, B, and C serology
Rapid plasma reagin or venereal disease: normal
Toxoplasmosis antibody test: normal
CBC: normal
Chemistries: normal
Pap smear: normal
Chest x-ray: normal
Hepatitis A, B, and C serology: negative
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The other routine tests in HIV—syphilis serology, toxoplasmosis serology, TB skin testing with
PPD, and Pap smear—determine the likelihood of common opportunistic infections. This
patient’s PPD is considered positive because the induration is >5 mm in diameter (erythema
without induration is not considered a positive test).
Further Diagnostic Plan Results
Repeat viral load testing 150,000
Treatment Plan
Induration of ≥15 mm is considered positive for the general population that is at low risk of
developing active TB
Cutoff ≥5mm is considered for those patients at the highest risk of disease, e.g., HIV-
positive patients, recent contact of TB patients, patients with fibrotic changes on chest x-ray
consistent with prior disease, and organ transplant recipients or immunosuppressed patients
Cutoff ≥10 mm is used for those at intermediate risk of the disease, e.g., recent immigrants
from endemic countries [within 5 years], health care personnel, injection drug users and
mycobacteriology laboratory personnel, children age <4, and infants/children/adolescents
exposed to adults with active TB
Pneumocystis jirovecii (formerly carinii) pneumonia prophylaxis with
trimethoprim/sulfamethoxazole
1.
Mycobacterium avium complex prophylaxis with azithromycin weekly
2.
Antiretroviral therapy with 2 nucleosides and either 1 protease inhibitor (PI) or a non-
nucleoside reverse transcriptase inhibitor (NNRTI)
3.
Isoniazid 300 mg/d for 9 mos with pyridoxine (vitamin B6) to prevent peripheral
neuropathy associated with isoniazid
4.
Pneumococcal pneumonia vaccination
5.
Hepatitis A and B vaccination
6.
Influenza vaccination yearly
7.
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Discussion
Pneumocystis pneumonia prophylaxis must be initiated in all patients with <200 CD4 cells/mL.
The most effective therapy is trimethoprim/sulfamethoxazole. If the patient is allergic to sulfa
drugs, dapsone or atovaquone may be used as an alternative. Aerosolized pentamidine is only
used in patients who cannot tolerate either trimethoprim/sulfamethoxazole or dapsone.
Pentamidine is less efficacious than trimethoprim/sulfamethoxazole, dapsone, or atovaquone
and is rarely used. For treatment of pneumocystis in patients with sulfa allergy, the options
include IV pentamidine, clindamycin with primaquine, or atovaquone. Pentamdine has many
side effects including, hypoglycemia, hyperglycemia, acute pancreatitis, ATN, hepatotoxicity.
M. avium complex prophylaxis is indicated in all patients with <50 CD4 cells/mL.
Azithromycin or clarithromycin are the best medications. Because azithromycin is used only
1x/week, it is easier to take than clarithromycin, which is used 2x/day. Rifabutin is less
efficacious than either of these and has frequent side effects, such as uveitis. In addition,
rifabutin has numerous interactions with other medications that are metabolized through the
hepatic p450 system. Treatment of MAC is macrolide with ethambutol with or without
rifabutin.
The starting regimen is a combination of 2 nucleoside medications and at least 1 protease
inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). Nucleoside medications
are zidovudine, lamivudine, abacavir, didanosine, emtricitabine, stavudine, DDC, or tenofovir.
Antiretroviral therapy initiation is now recommended with the diagnosis of HIV irrespective
of CD4 count.
In pregnancy, always treat with combination therapy, even if CD4 >500, to prevent perinatal
transmission. Start treatment immediately, i.e., do not wait for second trimester, and always
use at least 3 drugs.
Never use efavirenz in pregnancy.
Give the baby zidovudine during delivery and for 6 weeks after.
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Protease inhibitors are indinavir, ritonavir, nelfinavir, saquinavir, amprenavir, and
lopinavir/ritonavir, fosamprenavir, atazanavir, tipranavir and darunavir. Notice that all of the
protease inhibitors end in -navir.
The NNRTIs include efavirenz, etravirine rilpivirine, and nevirapine.
Second line agents that are used if there is resistance to the first line agents include:
CLINICAL PEARL
HIV patients with CD4 count >200 can get any vaccination.
Most protease inhibitors are now ‘boosted’ with ritonavir, another protease inhibitor.
Ritonavir by itself is not an effective antiretroviral because of poor efficacy and side effects.
However, when given in low doses with other protease inhibitors, it boosts serum levels by
inhibiting patients’ metabolism by inhibiting on the cytochrome P450 system. This allows for
higher serum levels of the boosted protease inhibitor, which decreases the probability of the
HIV virus developing resistance. In addition, a lower dose of the boosted protease inhibitor
can be given, which decreases adverse effects and improves compliance, also contributing to
the decreased likelihood of developing resistance.
HIV-positive patients should be treated at any age if their PPD is >5 mm in size. The usual
length of therapy in an HIV-negative patient is 9 months. Patients with HIV are treated for 9
months as well. Pneumococcal vaccination is indicated for most patients with significantly
Integrase inhibitor raltegravir
Entry inhibitors
Enfuvirtide(penetration) and maraviroc (attachment)
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compromised immune systems, such as HIV-positive patients. Vaccination is indicated
whenever you encounter the patient, regardless of T-cell count.
Let’s say a 19-year-old man is evaluated in the emergency department for a 10-day history of
fever, cervical lymphadenopathy, malaise and fatigue, sore throat, headache, and nausea, but no
vomiting, diarrhea, abdominal pain, nasal congestion, or cough. He had a rash a few days ago
that has resolved. He is sexually active with both men and women, and does not use condoms.
What is the next step?
The next step is the HIV nucleic acid amplification test. These symptoms may represent
infectious mononucleosis or syphilis, but this may also be acute HIV syndrome. It presents
within 2–4 wks of infection and lasts for a few weeks. Symptoms usually resolve without
treatment.
HIV nucleic acid amplification test is the test of choice. The ELISA/Western blot will be false
negative at this point because antibodies have not yet formed.
CCS NOTE
On the CCS, knowledge of preventive medicine in an ambulatory setting is more
important than knowledge of complex exotic diseases. Similarly, knowing when to start
prophylaxis in HIV is more important than knowing specific antiretrovirals.
Final Diagnosis
Acquired immunodeficiency syndrome (AIDS)
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Basic Science Correlate
Presumptive diagnosis is made with ELISA (sensitive, high false-positive rate and low
threshold, rule out test); results are then confirmed with Western blot assay (specific,
high false-negative rate and high threshold, rule in test).
HIV PCR/viral load tests determine the amount of viral RNA in the plasma.
ELISA/Western blot tests look for antibodies to viral proteins; these tests often are
falsely negative in the first 1–2 months of HIV infection.
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Case 7
Chief Complaint
Elevated liver enzymes
History and Physical Examination
A 39-year-old man with a history of IV drug use 20 years ago presents for evaluation of
elevated liver enzymes. He offers no complaints and feels well. He has no history of
anorexia, nausea or vomiting, malaise, fatigue, dark urine, or upper abdominal discomfort.
He denies blood transfusions or alcohol intake. He denies light-colored stools. He is
taking isoniazid for treatment of positive PPD. He went for routine screening tests and his
doctor told him that he has elevated liver enzymes.
His temperature is 37.4° and BP 150/80 mm Hg. Physical examination shows no scleral
icterus or jaundiced skin. The liver is non-palpable and non-tender; the spleen is not
palpable. There is no right upper quadrant tenderness.
Differential Diagnosis
Chronic viral hepatitis (B or C)1.
Drug-induced hepatitis2.
Wilson’s disease, hemochromatosis, autoimmune hepatitis3.
Choledocholelithiasis4.
Fatty liver5.
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Initial Diagnostic Plan Results
13.2 seconds (normal: <13 seconds)
Normal
Assessment
This patient has elevated liver enzymes which has many causes. Alcohol is not a likely factor
because the ratio of AST:ALT is not 2:1.
Acute hepatitis is not likely because he is asymptomatic and he has a mild elevation in his
transaminiases. The symptoms of acute hepatitis include malaise, anorexia, jaundice,
abdominal pain, and tenderness and they are all identical. In acute viral hepatitis the
transaminase would be very high, maybe over a thousand.
Hepatitis B and C are characterized occasionally by extrahepatic manifestations such as rash,
arthralgias, glomerulonephritis, cryoglobulinemia (hepatitis C), and polyarteritis nodosa
(hepatitis B) in a small number of cases.
Drug-induced or toxin-induced hepatic injury, such as from the patient’s isoniazid or other
medications, is also indistinguishable from acute viral hepatitis. Acetaminophen, halothane,
alpha-methyldopa, erythromycin, and allopurinol are among the most common causes of drug-
induced hepatitis. Wilson disease, hemochromatosis, primary biliary cirrhosis, and so-called
LFTs
Bilirubin (total)1.0 mg/dL;
AST (SGOT) 50 u/L (normal: 5–45 units);
ALT (SGPT) 150 u/L (normal: 5–45 units);
albumin 2.7 mg/dL (normal: 3.5–5.5 mg/dL)
PT
CBC
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“autoimmune” or lupoid hepatitis are other forms that can often only be distinguished by a liver
biopsy.
The initial step for determining the cause is to check hepatitis serologies. CT scan offers little
help. MRI scan shows increased iron and sonography shows fat infiltration.
This patient needs a workup for chronic hepatitis that includes transferrin saturation for
hemochromatosis, hepatitis serologies, anti-smooth muscle and anti-LKM for autoimmune
hepatitis. Wilson's is less likely due to the lack of CNS symptoms.
Further Diagnostic Plan/Results
CCS NOTE
As you advance the clock, you can use the “INTERVAL HISTORY” button at the top of
the physical examination screen to give you a progress report on the patient.
Treatment Plan
Tenofovir
Hepatitis serologies (including A, B, and C): Hepatitis A: IgM negative
Hepatitis B: anti-HB core: IgM negative anti-
HB core: IgG positive: HBsAg positive; HBe
Ag-positive; anti-HBs antibody-negative
Hepatitis C: Ab negative HBV DNA high
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Discussion
This patient has chronic active hepatitis B and should be treated. The goal of antiviral
treatment is ideally to convert hepatitis B surface antigen (HBsAg)–positive status to HBsAg-
negative status, though a more common goal is to induce suppression of viral replication
without necessarily obtaining clearance of virus. Diagnosis is made by HB core: IgG positive:
HBsAg positive with the surface antigen. The elevated HBV DNA and elevated liver enzyme
indicate that the hepatitis B is active and replicating.
Patients with chronic active HBV infection, defined by elevated hepatic aminotransferases or
active inflammation on liver biopsy, should receive antiviral therapy. Clinical outcomes are
improved in patients with chronic active HBV with effective viral suppression. For all forms
of acute viral hepatitis, there is no specific treatment; rest and avoidance of hepatotoxic
medications are generally recommended.
The HBe Ag is a measure of active viral replication and potential infectivity. These are the
patients that are most likely to benefit from treatment. The anti-hepatitis B IgM core is an
antibody that is also a measure of acute hepatitis B. Hepatitis B is treated with interferon or a
reverse transcriptase inhibitor, such as lamivudine, telbivudine, or adefovir. The limiting factor
with lamivudine is the development of high rates of resistance. Tenofovir and entecavir are
newer, preferred agents because of lower rates of resistance. Patients should also be monitored
for hepatocellular carcinoma (HCC) with regular liver U/S. Alpha-feto protein has poor
sensitivity and should not be used for HCC screening.
The major differences between hepatitis A and B are their sources, methods of transmission,
and incubation times.
Hepatitis A is predominantly food- and water-borne, with a 2–4 week incubation period. It
can be transmitted by sex.
Hepatitis B is transmitted by sex, transfusion, needle sharing, and vertically from mother to
child.
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