Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature. Otolaryngologic Manifestations of HIV The human immunodeficiency virus, the virus that causes AIDS, was isolated in 1983 as the cause of the syndrome recognized in 1981. The virion is a human retrovirus, meaning that it uses the enzyme reverse transcriptase to form DNA templates from its RNA genome. The virus consists of an icosahedral structure studded by the membrane protein gp120, which is linked to the lipid bilayer by the protein gp21. It consists of an RNA genome bound tightly to the enzyme reverse transcriptase. The molecule binds to its high affinity receptor, the CD4 ligand, which is present on a subset of T-lymphocytes, which are important in cell mediated immunity and helper function, which is a critical stage of immunity for eliminating viruses, intracellular bacteria, and fungus. The HIV viral replication cycle begins with binding of the virion by its gp120 protein to its high affinity receptor, the CD4 molecule. There is the co-receptor, CCR5 or another cell line, CXCR4, which is required for this high affinity binding. The HIV RNA is then subsequently released into the cell and the enzyme reverse transcriptase creates a DNA template from the RNA genome. The viral protein integrates and then integrates the DNA into the host cell genome, and the host cell machinery is used to transcribe viral mRNA and viral genomic RNA. Free proteins are then translated from the viral mRNA and the enzyme protease, and HIV protein breaks down the proteins into their functional units. The RNA and the proteins are then butted into the host cell membrane including the gp120 and gp41 molecules and virion particles are released. The natural history of an HIV infection occurs first with exposure to HIV virus through blood, semen, or vaginal secretions. The virus is then isolated from the blood stream of the infected host and sequestered in the lymphoid organs such as the spleen and the reticuloendothelial system. There is then a rapid phase of viral proliferation, which leads to an acute viremia, and this correlates with what is known as the acute HIV syndrome, seen about three to six weeks after exposure and it consists of an Epstein-Barr like mononucleosis syndrome that lasts for approximately one week. The host then typically mounts a cytotoxic T-lymphocyte response to the virus, which results in a decrease in the viremia, but not complete clearing of the virus. There is then a variable period, but untreated, on average approximately a ten-year period to the final decrease in CD-4 count and increase in viral load to the clinical state known as AIDS, which is defined by a CD-4 count of less than 200 or any one of 26 opportunistic illnesses as defined by the CDC. In 1993, the CDC released a new classification system for surveillance of HIV infection, which was based upon CD-4 counts as well as symptoms of HIV. They broke the patients down into class A, B, or C. Class A patients are patients being documented HIV infected, which were asymptomatic or in the acute HIV syndrome or with PGL, the phenomenon of lymphadenopathy that we will shortly discuss. Class B patients are patients who begin to exhibit opportunistic illnesses such as oral thrush or herpes simplex ulcerations, but that are not defining of AIDS as defined by the CDC in their 26 AIDS-defining illnesses. Category C patients have met one of the 26 required AIDS-defining illnesses. So, by this classification system, all of the patient classes seen in white here would be defined clinically has having AIDS based on CD-4 count or symptoms. So, what is the state of the HIV epidemic? If you look worldwide, it is estimated that right now there are approximately 39-40 million cases of HIV and about 25 million of these cases are in sub-Saharan Africa alone. So, it has really reached the state of pandemic in terms of HIV throughout the world. If you look throughout the United States through 2002, there were over 880,000 total AIDS cases reported up through 2002 with a 4:1 male preponderance. There have been over 500,000 deaths due to AIDS in the United States. If you look since the beginning of identification of HIV and AIDS in the early 80s at the annual death rates in 1992 for people 25-44 years of age, AIDS was the leading cause of death. You will note, though, in this trend that there has been a significant improvement since that time, which reflects some of the successes we have had in HIV medicine. There have been a couple of key successful breakthroughs in HIV medicine as seen in this graphic, which reflects the percentage of AIDS patients that survive at least one year after their diagnosis. In the first bump, an improved mortality came with the onset of use of AZT for the treatment of HIV, as well as Bactrim and pentamidine prophylaxis for pneumocystis pneumonia. The mortality then leveled off until there was a second bump in improvement with the onset of the highly active antiretroviral therapy (HAART) in the late 90s. You can see here if you look at the mortality statistics the significant improvement that was achieved in overall mortality with the advent of HART. Perhaps one of the greatest stories in both the prevention and treatment of HIV relates to the prevention of vertically acquired HIV from mother to fetus in the perinatal period. This reflects the use of AZT in pregnant women for the prevention of HIV transmission to the newborn. You will see that beginning in 1993 there was a significant increase in the amount of AZT used to prevent this and that correlates beginning in 1993 with a significant dropoff in the number of vertically acquired cases. So, this is a major success in the treatment of HIV. In 2003, there were estimated to be between 8-900,000 Americans who are HIV positive. That includes both patients infected HIV and with the syndrome AIDS. This data identifies some of the leading challenges that we face in the future in the United States. If you look at new cases, African Americans and Hispanics constitute three-fourths of the cases of new diagnosed HIV, such as our patient, but they represent only one-fourth of the total U.S. population. Since 1986, there has been a steadily increasing incidence in AIDS cases among racial and ethnic minorities. So, why is HIV important to the otolaryngologist? Well, it is estimated that as high as 85% of HIV positive patients will present with head and neck pathology. They represent a diverse spectrum of disease ranging from the common complaints that the otolaryngologist treats such as sinusitis and otitis media to unique presentations. Finally, it is important because early manifestations may present in the head and neck in patients who do not have an established diagnosis of HIV. HIV Head and Neck Now we will begin to look at some of the specific head and neck considerations in the HIV patient. We will begin with our patient, the patient who presents with a neck mass and a diagnosis of HIV. The differential would include a differential for neck mass in, of course, any patient, but there are special considerations, which include lymphadenopathy, parotid masses, Kaposi’s sarcoma, lymphoma, and infection. Persistent generalized lymphadenopathy (PGL) is defined as a syndrome of two or more extra inguinal nodal sites with lymphadenopathy for more than three months. This is a very frequently seen presentation in early HIV and is seen in up to 70% of HIV patients. In the pediatric population, it is even more common with as high as 83% of children being reported with lymphadenopathy. This table is from a study in the Annals of Internal Medicine, which sort of cataloged all the sites of lymphadenopathy and the most common site in PGL is posterior cervical adenopathy. Another important consideration in the HIV patient is non-Hodgkin’s lymphoma. These lymphomas are the second most common AIDS associated malignancy. In a new diagnosis of AIDS, they account for 15% of patients who present with a diagnosis of AIDS, but the lymphomas in HIV are not typical in that 70% are high grade and they tend to be very aggressive lymphomas. Up to one-third of patients who present with lymphoma will have central nervous system involvement at presentation; and their prognosis is related to 1) CD-4 count, 2)a prior AIDS diagnosis with the diagnosis of lymphoma, and 3)bone marrow or central nervous system involvement. It is also important to note that with non-Hodgkin’s lymphoma up to 89% of these patients present actually with lymphoma in extra-nodal sites. So, it is not just the neck mass in which lymphoma should receive consideration in the HIV patient, but with manifestations throughout the oral cavity, larynx, and head and neck. Benign parotid disease is a common problem seen in HIV patients and it ranges a spectrum. One end of the spectrum is what is referred to as the diffuse infiltrating lymphocytosis syndrome (DILS). This is a syndrome known as DILS caused by an expansion of CD8 lymphocytes similar to the lymphocytes that expand in response to the acute viremia seen with HIV infection. DILS has a predilection for the salivary glands and for the lung. With parotid involvement, you can see significant dry mouth and parotid enlargement as well as submucous nodules with minor salivary gland involvement. In the pediatric population, this is very common and parotid enlargement is seen in up to 30% of patients. Along the other end of the spectrum is the benign lymphoepithelial cyst, which our patient actually presented with. This is highly associated with the lymphadenopathy seen in early HIV and it is thought to be along the spectrum of DILS. The mechanism proposed is that due to the lymphoid expansion you get obstruction of lymphatic channels followed by squamous metaplasia and then cyst formation. These lesions are actually extremely specific to HIV, and, in the patient who presents with a characteristic parotid mass, HIV testing should be performed if the patient has not had one. FNA is diagnostic and therapeutic for these lesions. Early in the course of HIV medicine, parotidectomy was frequently used for these lesions, but it was seen that very rarely is malignancy associated with these lesions. Approximately 1% can have malignancy associated. It is important to notice that if the mass in an HIV parotid lesion is a solid mass, the incidence of malignancy jumps to 40%. Cyst aspiration is the treatment of choice, so recurrence is expected. For cosmetically deforming lesions or intractable lesions, therapy such as doxycycline sclerosis, low-dose radiotherapy, or even parotidectomy can be considered. This is a CT scan revealing multiple fluid-filled cystic structures within both parotid glands in the HIV patient. Kaposi’s sarcoma is seen in 14% of AIDS cases and it is the most common malignancy associated with HIV. The most common site for Kaposi’s sarcoma is in the head and neck. These consist of red, violaceous, non-itchy, painless, raised lesions; and if you look at the epidemiology of patients with Kaposi’s sarcoma, three-quarters of these patients will have no other risk factors for HIV than sexual transmission. It was thought early on that possibly there was an infective agent associated with Kaposi’s sarcoma and in 1994 the human herpes virus‑8 was isolated as an infective agent associated with KS. In 95% of Kaposi’s sarcoma specimens, you can see evidence of human herpes virus-8 RNA. Kaposi’s sarcoma also has a predilection for the oral cavity, and here is a characteristic lesion of KS. It most typically in the oral cavity presents on the hard palate. HIV and the Oral Cavity That brings us to some of the other important considerations in oral cavity lesions in HIV. The oral manifestations range from neoplasm, as we have discussed, to infectious complications and idiopathic or autoimmune complications. The number one infectious complication in the oral cavity in HIV patients is Candida infection. It is very frequently seen in HIV patients and it is even more frequent in children infected with HIV. Candida actually consists of several subtypes of infection, not just the typical thrush that is often associated with Candida. The first type is pseudomembranous candidiasis, which is classic thrush. This consists of cheesy, white plaques on any of the mucosal surfaces of the oral cavity, which are easily scraped off with an underlying erythematous base. The second type of candidal infection in the oral cavity in the HIV patient is erythematous candidiasis. This consists of erythematous, excoriated lesions, most typically presenting on the hard palate and the dorsum of the tongue. A third variant of candidal infection in the HIV patient is angular cheilitis. This consists of linear fissuring and ulceration at the oral commissures with or without associated hyperkeratosis along the fissure. Finally, the fourth type of candidal infection is hyperplastic candidiasis, which consists of very thick, non-removable white plaques throughout the oral cavity. These can frequently be misdiagnosed as another HIV associated condition, oral hairy leukoplakia. In any patient who presents with oral candidiasis, it is important to realize that there is a high rate of concurrent esophageal and pharyngeal candidiasis. So, if patients present with odynophagia, retrosternal chest pain, and oral candidiasis, that AIDS defining illness of esophageal candidiasis should be entertained. Oral hairy leukoplakia is another infectious lesion seen in the HIV patient in up to one-quarter of HIV patients. It consists of filiform white patches along the lateral border of the tongue and is highly associated with the Epstein-Barr virus. This lesion is important because it is highly prognostic for the subsequent development of AIDS in the patient. In one study, nearly half of patients with oral hairy leukoplakia went on to develop AIDS at 16 months, and nearly 85% had developed AIDS at 31 months. In contrast to oropharyngeal candidiasis, oral hairy leukoplakia is actually extremely uncommon in the pediatric population and this can be distinguished also from candidiasis in that these lesions are not removable by scraping with a tongue blade. Oral ulcers are an important manifestation seen in the HIV patient, and a very common cause of ulceration in these patients is the herpes simplex virus. This can present any where throughout the oral cavity as small vesicles, which then rupture and coalesce to form very painful ulcers surrounded by an erythematous halo. These should be distinguished from oral aphthous ulcers, which are actually an immunologically mediated phenomenon seen in HIV patients very similar to the aphthous ulcers seen in Behçet’s disease. These ulcers can be divided into categories of minor and major aphthous ulcers with minor aphthous ulcers being usually less than 5 mm with the typical appearance of the overlying pseudomembrane and surrounding erythema. Major aphthous ulcers are greater than 1 cm in diameter. They are very painful and they persist for long periods of time leading to significant problems with swallowing and speech. HIV Otology A number of otologic complaints can present to the otolaryngologist in the patient with HIV, and we will begin looking at some complaints of the external ear. Of course, Kaposi’s sarcoma can present on the auricle or any skin site really in the head and neck. In dealing with HIV patients, this should be kept in mind. Otitis externa is not seen with more frequency in the HIV patient, but these patients, because of their immunocompromised status, are more predisposed to osteomyelitis of the temporal bone or malignant otitis externa. Then finally, unique manifestations in HIV patients are external auditory canal polyps, which, when biopsied and stained with methenamine silver, reveal these crushed ping-pong ball appearing pneumatosis, which is characteristic of Pneumocystis carinii. So, these patients develop pneumocystis polyps in their external canal. Otitis media is the most common otologic manifestation of HIV, and serous otitis media is the most common. It is thought to result from the nasopharyngeal adenoidal hypertrophy that is seen with the early polyclonal expansion in HIV patients. Otitis media in the HIV patient tends to run longer courses and has more recurrence. In a study conducted here at Baylor by Dr. Stewart and colleagues at Texas Children’s, it was shown that pediatric patients with HIV actually had a fivefold increase in recurrence of otitis media. Now, otitis media in the HIV patient is usually caused by the common etiologic agent seen in the general population; strep pneumonia, H. flu, and Moraxella. But, in the patient that remains refractory to treatment, other agents including tuberculosis, pneumocystis, and Nocardia should be considered. Sensorineural hearing loss is an important complaint in the HIV patient and up to one-half of the patients with HIV will present with some degree of sensorineural loss. This loss is a sloping, high frequency loss and in patients with loss, up to one-third of these patients will have moderate to severe loss at more than three frequencies. Interestingly, sensorineural hearing loss does progress as HIV disease progresses. The mechanism of HIV associated sensorineural loss is thought to be multifactorial. One proposed theory is direct HIV infection either of the inner ear, the cochlear nerve, or the central nervous system. Other infections are also proposed etiologies including oto-syphilis. In the patient with HIV and concomitant syphilis, there is a rapid progression to oto-syphilis of between two and five years. This is significantly faster than in the patient with syphilis alone that typically presents with hearing loss after 15-30 years. Other potential nervous system infections and the demyelinating infection of progressive multifocal leukoencephalopathy can be the cause of sensorineural hearing loss as well as cryptococcal meningitis. Neoplasm of the central nervous system is an important consideration in sensorineural loss and finally, for the clinician, iatrogenic sensorineural loss is an important consideration in the HIV patient. These are just a list of a few of the medications that are commonly used in HIV patients that have been shown to have ototoxic properties. Facial paralysis is a common presentation in HIV patients with otologic complaints and is thought to be more prevalent in HIV than in the general population. If you look at endemic regions of Africa with HIV, a patient presenting with a unilateral facial paralysis has a 69% chance of being HIV positive. The prognosis for facial paralysis in HIV is excellent with most patients regaining function within three weeks to three months. The possible etiologies of the facial paralysis in the HIV patient include Bell’s palsy or Ramsey-Hunt syndrome due to viral reactivation, central nervous system demyelinating infections such as PML, AIDS encephalopathy, or other CNS infections or neoplasms. HIV Rhinology The nose and sinuses illustrate an important class of disease in the HIV patient in that HIV really, aside from being a disease of immunodeficiency of T-cell immunity, is also a disease of immune dysregulation leading to some of the complaints that otolaryngologists see. A good example is in the nose and sinuses. With the loss of T-cells, there is in HIV a polyclonal B-cell activation, which leads to both increased immunoglobulin secretion and hyperplasia of the lymphoid tissues. This subsequently results in a hyperactive allergic response amongst these patients as well as potential anatomic obstruction of the sinus ostia. So, in considering the HIV patient who presents with nasal congestion, anywhere from 20-68% of HIV patients have episodes of rhinosinusitis. It is important to note that as the CD-4 count falls below 200, chronic sinusitis becomes much more prevalent in these patients. Studies have looked at the development of allergic rhinitis in patients who seroconverted to being HIV positive, and the prevalence of allergic rhinitis after seroconversion reported in these patients doubled. The rhinitis seen in HIV has been dubbed “HIV rhinitis” and it is unique in that the secretions amongst these patients are extremely thick. So, it is important in dealing with these patients to remember to use mucolytics amongst their treatment regimen. Finally, in dealing with the HIV patient with sinusitis, it is critical to realize that as the CD-4 count falls to low levels below 50, it is really important to think of fungus in the differential of sinusitis. So, in summary, minority patients such as our patient represent an increasing proportion of HIV patients as well as an important target for prevention and therapies in the near future. HIV patients experience a diverse spectrum of disease throughout the head and neck, and these complaints range from the common otolaryngologic complaints seen to unique head and neck manifestations. Finally, improved HIV treatments will likely increase the number of HIV patients seen by the otolaryngologist and possibly offer new presentation in the future. Case Presentation: M.B. is a 44-year-old female who presented to the BTEC with one year of a fluctuating mass in the left neck, which has steadily grown over the past three months. It is non-tender and has had no drainage. The patient has reported a 15 pound weight loss over the past six months. She denies fevers, cough, headache, pain, GI complaints or facial weakness. Past medical history is notable for hypertension. In addition, the patient reports that approximately one year ago, she was told that she possibly had HIV. She is unsure why she was told this and does not know if she was tested. She takes no medications and has no allergies. She has no family history of malignancy. The patient currently lives with two roommates, and has been unemployed for two years. She denies alcohol or IV drug use. She currently smokes two packs of cigarettes per day and uses cocaine. Physical exam was notable for intact cranial nerves III-XII. Otherwise the exam was remarkable for a 7cm x 6cm x 4cm ballotable nontender mass in the region of the left parotid gland. The mass was soft, apparently cystic, and had no overlying erythema or drainage. Based on the presentation and history of possible HIV, a clinical diagnosis of benign lymphoepithelial cyst of the parotid gland was established. The cyst was aspirated in clinic to yield 60 cc of golden fluid with complete resolution of the mass after aspiration. M.B. was admitted by the internal medicine service for work-up of HIV, and discharged on hospital day one. 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Pathologic manifestations of Acquired Immunodeficiency Syndrome in the head and neck. Ear Nose Throat J 1990;69:406-415. Youngs R. Human immunodeficiency virus in otolaryngology. J Laryngol Otol 1997;111:209-211. Grand Rounds Archive | Department Home pageBCM Public | BCM Intranet | Privacy Notices | Contact BCM | BCM Site Map | ©2001-2006 Baylor College of Medicine
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