ObjectiveThe purpose of this article is to provide a systematic overview of the literature on adrenal suppression and Cushing's syndrome secondary to an interaction between inhaled/intranasal fluticasone and ritonavir. The clinical presentation, diagnosis and management will be discussed. MethodsA literature search using Medline and EMBASE and a search of abstracts of the three previous years of major HIV-related conferences were carried out. ResultsThere were 25 cases (15 adult and 10 paediatric) of significant adrenal suppression secondary to an interaction between ritonavir and inhaled fluticasone, and three cases involving ritonavir and intranasal fluticasone. Cases with other steroids were not reported; however, there were cases of adrenal suppression with itraconazole [also a potent cytochrome p (CYP) 3A4 inhibitor] and inhaled budesonide. Clinicians need to differentiate between antiretroviral-induced lipodystrophy syndrome and iatrogenic Cushing's syndrome secondary to glucocorticoid use. Long-term fluticasone and ritonavir should be avoided. If ritonavir is required, another inhaled steroid such as low-dose budesonide or beclomethasone can be used cautiously. Upon discontinuation of inhaled corticosteroids, close monitoring for symptoms of adrenal insufficiency is warranted. The need for steroid replacement therapy at physiological doses should be assessed. ConclusionsThe combination of ritonavir and fluticasone should be avoided. Budesonide, beclomethasone, triamcinolone and flunisolide appear to be safer options.
A significant proportion of HIV-infected subjects attending 5 infectious disease clinics in Canada are coinfected with HSV. Routine type-specific HSV-2 testing should be introduced to direct education regarding symptoms, signs, and transmission reduction of genital herpes and perhaps ultimately HIV-1. Knowledge of HSV serostatus would also provide an opportunity to consider antiviral therapy.
A 29-year-old man with type 1 diabetes presented to the emergency department with shortness of breath and chest pain that had lasted for one week. The patient initially reported no systemic symptoms. However, upon further questioning, he stated that he had felt generally unwell for the past year, with fevers, night sweats and weight loss. He had not been coughing and had not felt chest pain or shortness of breath before this presentation. He had no recent travel history or sick contacts. The patient was taking insulin and pantoprazole. In addition, he reported that he had been inhaling marijuana daily through a vapourizer for the past 18 months to relieve neuropathic pain secondary to his diabetes. The marijuana was street purchased and always from the same supplier. He did not use any other illicit substances, and he was not taking any narcotics at the time of admission, but he had used oxycodone periodically during the previous year to relieve neuropathic pain. The patient worked as a professional in an urban area.His diabetes had been diagnosed one year earlier and was heralded by a six-month history of neuropathy. He was also found to have diabetic retinopathy. Two months after the diagnosis, the patient had received treatment for community-acquired pneumonia with evidence of infiltrate in the left lower lobe on chest radiograph. A follow-up radiograph was not performed. Computed tomography of the patient's abdomen several months later, performed for unrelated reasons, had shown evidence of ongoing left basilar and pleural consolidation.On physical examination, the patient's temperature was 36.6°C, his heart rate was 80 beats/ min, his respiratory rate was 18 breaths/min and his blood pressure was 125/85 mm Hg. He had an oxygen saturation of 100% on room air. A respiratory examination showed decreased air entry to his left lung base. The rest of the examination was unremarkable.A radiograph of the patient's chest showed a left pneumothorax with air space disease in the left lower lobe (Figure 1). Computed tomography of the chest showed a left pneumothorax and left lower lobe consolidation with cavitation, likely communicating with the pleura (Figure 2). Despite treatment with a chest tube, the pneumothorax persisted. Video-assisted thoracoscopic surgery was done for diagnostic and therapeutic purposes. Diffuse pleural adhesions were found, which required decortication and a wedge resection of the superior segment of the left lower lobe.Tissue samples from the wedge resection grew Aspergillus rugolosa, confirmed by DNA sequencing, a Penicillium species and a nonsporulating fungus. Samples of the patient's pleural fluid grew Aspergillus fumigatus. Histopathologic examination of biopsy specimens confirmed parenchymal and pleural invasion by hyphal elements (Figure 3). The result of a serum galactomannan test was negative, as was an immunoglobulin E assay for A. fumigatus.The patient's immunoglobulins were normal, with the exception of a mildly low level of immunoglogulin G4. HIV serology was negative, lymphocyt...
ObjectiveIt is recommended that hepatitis B virus (HBV)-susceptible, HIV-infected persons be immunized for HBV. However, 44-76% of HIV-infected persons fail to respond to a standard series of recombinant HBV vaccine. Intradermal (i.d.) administration of HBV vaccine has been effective in nonresponders to intramuscularly administered vaccine among healthcare workers, haemodialysis patients and renal transplant recipients. We evaluated the immunogenicity of HBV vaccine given by the intradermal route in HIV-infected individuals who failed to respond to two series of HBV vaccine given intramuscularly. MethodsRecombinant HBV vaccine [10 mg HBV surface antigen (HBsAg)/mL] was administered as 0.25 mL i.d. every 2 weeks for four doses in 12 HIV-infected adults who failed to respond to six doses of HBV vaccine administered by the intramuscular route. Anti-HBs was tested at least 2 weeks following the fourth dose of i.d. administered vaccine, and if the anti-HBs titre was negative or o30 IU/L, a second series of four i.d. doses were administered every 2 weeks. Anti-HBs was measured at least 2 weeks following the second series of i.d. administered HBV vaccine and 6 and 12 months after the last dose. ResultsProtective levels of anti-HBs (410 IU/L) were achieved in six subjects (50%) after four doses. Administration of four additional i.d. doses to the six nonresponders did not result in any additional seroconverters. Five of the six responders had no detectable anti-HBs at 12 months after the last dose of i.d. administered vaccine. ConclusionsThe i.d. route of administration of recombinant HBV vaccine does not appear to be immunogenic in HIV-infected adults who fail to respond to six doses of intramuscularly administered vaccine. IntroductionBecause of shared routes of transmission of HIV and hepatitis B virus (HBV), individuals infected with one of these viruses are at increased risk for infection with the other. The rate of HBV coinfection in HIV-infected individuals is 6.3-9.7% [1][2][3][4]. HIV-infected individuals with chronic HBV infection experience significant morbidity and mortality related to liver disease. In the Multicenter AIDS Cohort Study, liver-related mortality among HBVcoinfected patients was 14.2 per 1000 person-years compared with 1.7 per 1000 person-years in HIV-monoinfected patients [3]. In EuroSIDA, mortality was significantly higher in the HBV-coinfected population [2,5]. Current guidelines recommend that HIV-infected 295 individuals be screened for infection or immunity to HBV and administered HBV vaccine if they are neither infected nor immune [6,7]; however, actual usage of HBV vaccine among HIV-infected patients is suboptimal [8,9]. The original HBV vaccine manufactured from plasma of HBV surface antigen (HBsAg)-positive subjects [10] has been discontinued and replaced with recombinant vaccines manufactured by expressing HBsAg in the yeast Saccharomyces cerevisiae. Recombinant HBV vaccines are licensed for intramuscular administration in a series of three doses administered at 0, 1 and 6 months. ...
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