Outpatient repair of superior semicircular canal dehiscence via the transmastoid approach.

OBJECTIVES/HYPOTHESIS: Superior semicircular canal dehiscence (SSCD) syndrome has been a topic of much interest since its first description a decade ago. The symptoms of vertigo, autophony, and Tullio phenomenon have been well described as has the utility of surgical repair. The standard approach described for surgical repair of this problem has been to perform a middle fossa craniotomy followed by plugging of the superior semicircular canal. Recently, a transmastoid approach has been described as another surgical option in cases of SSCD, an alternative that could avoid the known risks of a middle fossa craniotomy. Herein we present further data for validation of the transmastoid SSCD repair technique. Additional factors leading to the successful treatment of these patients in the outpatient setting, an approach not previously described, are detailed. STUDY DESIGN: Retrospective study of three separate operative procedures in two patients (one patient with bilateral SSCD) in an academic medical center is presented along with postoperative course and hearing status. METHODS: Three ears with radiographic evidence of SSCD confirmed with vestibular evoked myogenic potentials after symptomatic presentation were studied. Each ear had preoperative and postoperative audiometry and outpatient surgery. SSCD was repaired in each patient using a transmastoid approach with specific anesthetic and surgical precautions taken to minimize nausea and vertigo. RESULTS: Each patient was discharged from the outpatient unit with two cases returning home the day of surgery and one case after 23-hour observation. All had resolution of their SSCD symptoms and postoperative hearing testing revealed no evidence of sensorineural hearing loss and resolution of related conductive components. CONCLUSIONS: The advantages noted by others with regards to the transmastoid repair of SSCD related symptomatology appear genuine and reproducible. In addition, this approach appears to offer potential freedom from a prolonged hospital admission with the potential for outpatient surgery in some circumstances without compromised clinical outcomes.

Paranasal sinus melanoma masquerading as chronic sinusitis and nasal polyposis.

Malignant melanoma of the nose and paranasal sinuses can be a devastating disease, typically presenting at an advanced stage, with a 5-year survival rate ranging between 20 and 30%. It is an uncommon process, often misdiagnosed both clinically and pathologically. We present the case of an 80-year-old man who had a 2-month history of progressively worsening left-sided epistaxis and nasal obstruction. Radiographic evidence indicated the presence of soft tissue in the left maxillary sinus and nasal cavity resembling massive nasal polyposis and chronic fungal sinusitis. Magnetic resonance imaging was not performed because the patient had a pacemaker. After endoscopic debridement of the soft-tissue mass, frozen-section analysis detected no evidence of tumor. The final pathologic diagnosis was malignant melanoma. Otolaryngologists should be familiar with the difficulties inherent in the diagnosis and management of sinonasal melanomas.

Human immunodeficiency virus type 1 (HIV-1)-specific CD8+-T-cell responses for groups of HIV-1-infected individuals with different HLA-B*35 genotypes.

Human immunodeficiency virus type 1 (HIV-1)-infected individuals with HLA-B*35 allelic variants B*3502/3503/3504/5301 (B*35-Px) progress more rapidly to AIDS than do those with B*3501 (B*35-PY). The mechanisms responsible for this phenomenon are not clear. To examine whether cellular immune responses may differ according to HLA-B*35 genotype, we quantified HIV-1-specific CD8(+)-T-cell (CTL) responses using an intracellular cytokine-staining assay with specimens from 32 HIV-1-positive individuals who have B*35 alleles. Among them, 75% had CTL responses to Pol, 69% had CTL responses to Gag, 50% had CTL responses to Nef, and 41% had CTL responses to Env. The overall magnitude of CTL responses did not differ between patients bearing B*35-Px genotypes and those bearing B*35-PY genotypes. A higher percentage of Gag-specific CTL was associated with lower HIV-1 RNA levels (P = 0.009) in individuals with B*35-PY. A negative association between CTL activity for each of the four HIV antigens and viral load was observed among individuals with B*35-PY, and the association reached significance for Gag. No significant relationship between CTL activity and viral load was observed in the B*35-Px group. The relationship between total CTL activity and HIV RNA among B*35-Px carriers differed significantly from that among B*35-PY carriers (P < 0.05). The data are consistent with the hypothesis that higher levels of virus-specific CTL contribute to protection against HIV disease progression in infected individuals with B*35-PY, but not in those with B*35-Px.

Discontinuation of antiretroviral therapy commenced early during the course of human immunodeficiency virus type 1 infection, with or without adjunctive vaccination.

Sixteen subjects were treated with highly active antiretroviral therapy within 120 days of the onset of symptoms of newly acquired human immunodeficiency virus type 1 (HIV-1) infection. Eleven of the 16 participated in an adjunctive therapeutic vaccine trial. After a mean of 3.2 years of treatment, they elected to discontinue therapy. Virus rebound occurred in all subjects and was followed by a spontaneous, transient although significant reduction in log plasma HIV-1 RNA level, ranging from 0.3 to 3.1 log(10) copies/mL. Despite evidence of the induction of HIV-1-specific cell-mediated immune responses, plasma viremia was not persistently suppressed to <500 copies/mL in any subject. The magnitude and dynamics of virus rebound were similar in both vaccinated and unvaccinated subjects. Nevertheless, given the transient suppression of viremia observed in nearly all subjects after treatment has been discontinued, further investigations of adjunctive vaccination with optimized antiretroviral therapy in treating HIV-1 infection are warranted.

Safety and immunogenicity of ALVAC vCP1452 and recombinant gp160 in newly human immunodeficiency virus type 1-infected patients treated with prolonged highly active antiretroviral therapy.

In order to boost immune responses in persons in whom highly active antiretroviral therapy (HAART) was initiated within 120 days of the onset of symptoms of newly acquired human immunodeficiency virus type 1 (HIV-1) infection, we administered vaccines containing a canarypox virus vector, vCP1452, with HIV-1 genes encoding multiple HIV-1 proteins, and recombinant gp160. Fifteen HIV-1-infected subjects who achieved sustained suppression of plasma viremia for at least 2 years were enrolled. While continuing antiretroviral therapy, each subject received at least four intramuscular injections of the vaccines on days 0, 30, 90, and 180. Adverse events were mild, with the most common being transient tenderness at the vCP1452 injection site. Of the 14 patients who completed vaccination, 13 had significant increases in anti-gp120 or anti-p24 antibody titers, and 9 had transient augmentation of their T-cell proliferation responses to gp160 and/or p24. HIV-1-specific CD8(+) T cells were quantified using an intracellular gamma interferon staining assay. Among 11 patients who had increased CD8(+) T-cell responses, seven had responses to more than one HIV-1 antigen. In summary, vaccination with vCP1452 and recombinant gp160 appears safe and immunogenic in newly HIV-1-infected patients on HAART.