Ritonavir-boosted atazanavir may be efficacious in HIV-infected patients concurrently receiving omeprazole.
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Biomedical subjects
Publications and source records attributed to Kirk M Chan-Tack.
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The combination of atazanavir (ATV) plus lopinavir/ritonavir (LPV/r) has been used in practice. However, clinical data supporting its use are limited. The objective of this study was to evaluate the efficacy and tolerability of regimens with ATV + LPV/r in protease inhibitor (PI)-susceptible and PI-resistant patients. A retrospective review of 2703 charts was performed to identify all patients who received ATV + LPV/r. From June 2003 to January 2005, 33 patients received ATV + LPV/r with nucleoside reverse transcriptase inhibitors (NRTIs) for 3 months or more. Virologic success (HIV-RNA < 400 copies per milliliter) was achieved in 30 patients (91%) in a median of 10 weeks (range, 2-68). Nineteen of the 23 patients (83%) who had ultrasensitive viral load (VL) assays were nondetectable. Among patients with 6 or more protease resistance (PR) mutations (PI-resistant), 11 of 14 (79%) achieved virologic success. Eleven of those received phenotypic testing (10 Virtual Phenotype, VircoLab, Baltimore, MD). Despite predicted phenotypic resistance to ATV (6 patients) and LPV/r (7 patients), virologic success was achieved in 4 of 6 (67%) and 4 of 7 (57%), respectively. The 3 PI-resistant patients who were virologic failures had extensive prior LPV/r use, 8-11 PR mutations, and predicted phenotypic resistance to LPV/r, but 2 of 3 had CD4 increases with ATV + LPV/r. Overall, 28 patients (85%) continue to tolerate ATV + LPV/r for a median of 32 weeks follow-up (range, 12-76). Combination ATV + LPV/r with NRTIs appears safe, tolerable, and efficacious in PI-resistant patients (>/=6 PR mutations) and predicted phenotypic resistance to ATV and LPV/r. Further studies of ATV + LPV/r in HIV-treatment are warranted.
Immune reconstitution inflammatory syndrome (IRIS) encompasses a variety of conditions that occur among HIV-infected patients in a temporal relationship with increases in CD4 cell count as a result of highly active antiretroviral therapy (HAART). Most conditions associated with IRIS are infectious. Malignancies, such as Kaposi's sarcoma, have also been reported. We report a case of sinusitis with presumptive inflammatory pseudotumor as a manifestation of IRIS that occurred 20 weeks after the initiation of HAART.
Amyloidosis is an uncommon cause of renal disease in HIV-positive patients. Diagnosis is challenging, treatment options are limited, and prognosis remains poor. We discuss an HIV-positive patient with acute renal failure and nephrotic range proteinuria. The differential diagnosis included nephropathy due to trimethoprim/sulfamethoxazole, tenofovir, HIV, hepatitis C, heroin, or multifactorial causes. Serum and urine study findings were inconclusive. Rapid clinical deterioration ensued and a renal biopsy was performed. Pathologic examination revealed eosinophilic, amorphous material in the glomerular tufts that stained red-orange with Congo red stain. Immunohistochemical analysis confirmed amyloid A (AA) amyloidosis. AA amyloidosis occurs as a complication of chronic infection or chronic inflammatory disease. It has been reported in intravenous or subcutaneous drug abusers, some of whom were HIV-positive. This case underscores the importance of tissue diagnosis to determine the cause of renal disease in HIV-positive patients. Clinical diagnosis, based on CD4 count, viral load, and degree of proteinuria, may not predict the pathological diagnosis in HIV-positive patients.
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West Nile virus (WNV) can cause severe central nervous system (CNS) illnesses including meningoencephalitis (MNE) and acute flaccid paralysis (AFP). Risk factors include advanced age, immunosuppression, cancer, and diabetes. In vitro studies show that tumor necrosis factor (TNF) has anti-WNV activity and is protective against WNV infection. Anti-TNF-a monoclonal antibodies may increase susceptibility to WNV by inhibiting an adequate TNF-a response, leading to prolonged viremia, viral penetration into the CNS, and fulminant WNV-CNS disease. We describe a fatal case of WNV with MNE and AFP after infliximab therapy. During WNV outbreaks, clinicians should encourage patients receiving anti-TNF-a drugs to take appropriate preventive measures because of the risk of severe WNV-CNS disease.
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Mucormycosis can cause fatal infections in immuno-compromised persons. Rhinocerebral and pulmonary disease predominate. Diagnosis is challenging, dissemination frequent, and mortality high. Positive blood cultures are rare. We report the first case of central venous catheter-associated mucormycosis fungemia (Mucor circinelloides). Early diagnosis and multi-modal therapy led to clinical and microbiological cure.
WNV infection can cause meningoencephalitis (MNE) and acute flaccid paralysis (AFP). Both syndromes are associated with high morbidity and mortality. Interferon alpha-2b (IFN-alpha-2b) inhibits WNV replication in vitro. To date, 5 patients with WNV-CNS disease have recovered neurologic function with IFN-alpha-2b. We report the first failure of IFN-alpha-2b in the treatment of WNV-MNE-AFP.
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An 83-year-old woman was transferred to our cardiac intensive care unit with an acute non-Q-wave myocardial infarction and pulmonary edema. Enoxaparin was one component of the treatment regimen used. Her hospital course was complicated by episodes of hypotension, as well as by recurrent left hip and left thigh pain. The defining event occurred when the patient became acutely hypotensive and developed abdominal distention, peritoneal signs, intense left flank pain, and a 3.3 g/dl hemoglobin decrease. Abdominal computed tomography showed a 9 x 6 x 20 cm left retroperitoneal hematoma. The hematoma was spontaneous, secondary to enoxaparin use. The patient died despite vigorous supportive care. Enoxaparin is being increasingly used in patients with acute coronary syndromes. Review of the medical literature revealed that this is the first reported case of a patient with an acute coronary syndrome who died as a result of an enoxaparin-induced, spontaneous retroperitoneal hematoma. This article reviews important clinical signs and symptoms, identifies high-risk patient populations, and discusses management strategies.