Management of Psychiatric Disorders with HIV and Dermatological Disorders.

Addressing HIV-1 latency with Flow-FISH: Finding, characterizing and targeting HIV-1 infected cells.

Increased CDK5 Expression in HIV Encephalitis Contributes to Neurodegeneration via Tau Phosphorylation and Is Reversed with Roscovitine

Current Use and In-Hospital Outcomes of Mechanical Circulatory Support in HIV-Infected Patients: A Friend or a Foe?

To review the clinical features and current knowledge on the treatment of psychiatric symptoms and disorders in patients with human immunodeficiency virus (HIV) infection. We searched the PubMed database combining HIV/AIDS with different keywords for psychiatric diagnoses and symptoms (e.g. depression, mania, anxiety, psychosis, dementia, substance abuse) and for psychopharmacological treatment. The years covered by these searches included 1980 to 2008. Patients with HIV infection are at an increased risk of psychiatric illness. Major depressive disorder and subsyndromal depressive symptoms, as well as anxiety disorder and substance abuse are more prevalent among HIV infected individuals than among the general population. HIV-associated neurocognitive disorders (HAND) are common among HIV patients, and HIV-associated dementia (HAD) is a serious condition during the acquired immune deficiency syndrome (AIDS) stage of HIV disease. Secondary mania and psychosis might be the first clinical symptom of HIV dementia. The introduction of highly active anti-retroviral therapy (HAART) has resulted in significant decreases in morbidity and mortality for HIV infected patients. HAART has also decreased the incidence of HAD, but does not give complete protection from this condition. The utility of psychotropic medications in HIV patients has not been studied sufficiently as a basis for guidelines, and more controlled trials are needed. Psychiatric illness is common in HIV infected individuals, and underlines the importance for screening not only for cognitive impairment but also for co morbid mental disease in HIV-positive patients. Further studies of the neuropsychiatric complications during HIV disease and the use of psychotropics under these circumstances are clearly needed. A better understanding of the pathogenesis of HAD is essential to identify additional therapeutic strategies for prevention and treatment of this neurodegenerative disease. Studies are also needed for optimizing effective utilization of antiretrovirals into the CNS. Mania and psychosis secondary to HAD may be used as an indicator to initiate HAART, irrespective of CD4 count. Further research on the utility of HAART in the treatment of such acute neuropsychiatric symptoms associated with HIV infection should be initiated.

Combined antiretroviral therapy (cART) attenuates hepatic fibrosis in hepatitis C virus and HIV coinfected patients. However, the role of HIV or cART on hepatic fibrosis in HIV monoinfection is discussed controversially. During liver fibrosis, matrix metalloproteinases (MMPs) degrade extracellular matrix (ECM) proteins into small soluble fragments, which reflect hepatic remodeling processes. This study used these novel biomarkers to investigate the effect of HIV and cART on hepatic fibrosis remodeling. In 249 patients with HIV monoinfection and 55 healthy controls, the serum levels of MMP-degraded collagen type III (C3M), biglycan (BGM), elastin (ELM), as well as the formation marker 7S (P4NP 7S), and MMP-degraded collagen type IV (C4M) were determined using specific ELISAs. Sixty-eight patients underwent a follow-up visit 3 years later including assessment of ECM markers and fibrosis using transient elastography (Fibroscan). C3M, BGM, C4M and P4NP 7S were significantly elevated in HIV patients compared to controls and correlated to HIV viral loads and inversely to cART duration. C4M, P4NP 7S and ELM were lower in patients under cART therapy and in patients without HIV viremia, indicating that lowering of the HIV load by cART attenuates remodeling of ECM. The levels of C3M, C4M, P4NP 7S and ELM correlated significantly with the progression of fibrosis in these patients. Specific therapy of patients with HIV monoinfection also beneficially influences liver fibrosis. These novel markers of liver fibrosis remodeling may help to monitor the hepatic effects by HIV therapy.

Nerological Soft Signs in HIV-associated Neurocognitive Disorder: a Clinical Marker?

S tudies published over the past 3 years have tracked the incidence and course of human immunodeficiency virus (HIV) infection in relation to cardiac illness in both children and adults. 1 These studies show that subclinical echocardiographic abnormalities independently predict adverse outcomes and identify high-risk groups to target for early intervention and therapy.The Joint United Nations Program on HIV/AIDS estimates that 36.1 million people were living with HIV infection at the end of the year 2000. 2 If 8% to 10% of patients develop symptomatic heart failure over a 2-to 5-year period, 3 then 3 million cases of HIV-related heart failure will present during that period. 1 Cardiovascular manifestations of HIV have been altered by the introduction of highly active antiretroviral therapy (HAART) regimens.On one hand, HAART has significantly modified the course of HIV disease, lengthened survival, and improved the quality of life of HIV-infected patients.On the other hand, the early data have raised concerns that HAART is associated with an increase in both peripheral and coronary arterial diseases. 1The HAART-associated changes are relevant only to the minority of HIV-infected individuals worldwide who have access to HAART.Thus, studies conducted before HAART became available remain globally applicable.In this review article, the principal HIV-associated cardiovascular manifestations will be discussed, with an emphasis on new knowledge about prevalence, pathogenesis, and treatment.

Exercise and the brain: a slap on the HAND

Expanding directly observed therapy: tuberculosis to human immunodeficiency virus

Belatacept Conversion in an HIV-Positive Kidney Transplant Recipient With Prolonged Delayed Graft Function.

Human Immunodeficiency Virus: The Initial Physician-Patient Encounter

With the development of effective therapies against human immunodeficiency virus (HIV), hepatitis C virus (HCV) infection has become a major cause of morbidity and mortality among patients with both infections (coinfection). In addition to the high prevalence of chronic HCV, particularly among HIV-infected injection drug users, the rate of incident HIV infections is increasing among HIV-infected men who have sex with men, leading to recommendations for education and screening for HCV in this population. Liver disease is the second leading and, in some cases, a preventable cause of death among coinfected patients. Those at risk for liver disease progression are usually treated with a combination of interferon (IFN) and ribavirin (RBV), which is not highly effective; it has low rates of sustained virologic response (SVR), especially for coinfected patients with HCV genotype 1 and those of African descent. Direct-acting antivirals might overcome factors such as immunodeficiency that can reduce the efficacy of IFN. However, for now it remains challenging to treat coinfected patients due to interactions among drugs, additive drug toxicities, and the continued need for combination therapies that include pegylated IFN. Recently developed HCV protease inhibitors such as telaprevir and boceprevir, given in combination with pegylated IFN and RBV, could increase the rate of SVR with manageable toxicity and drug interactions. We review the latest developments and obstacles to treating coinfected patients.

The prevalence and clinical correlates of body-focused repetitive behaviors in pediatric Tourette Syndrome

Eradication of human immunodeficiency virus-1 reservoir in the brain microglia.

To identify the main clinical and laboratory features of disseminated histoplasmosis (DH) in human immunodeficiency virus (HIV) patients and compare them with those of HIV patients with other opportunistic diseases. Retrospective study of HIV patients comparing the clinical and laboratory data of patients with and without DH. Univariate and multivariate analyses were performed to verify the risk factors related to DH. In total, 378 HIV patients were included, 164 with DH and 214 with other opportunistic diseases. Acute renal failure, respiratory insufficiency and septic shock were more frequent in DH patients, who also had a higher mortality (32%vs. 14%, P < 0.001). Independent risk factors for DH were: acute renal failure [odds ratio (OR) 5.2; 95% confidence interval (CI) 3.2-8.5; P < 0.001], splenomegaly (OR 3.4; 95% CI 1.19-9.9; P < 0.001), respiratory insufficiency (OR 2.7 95% CI 1.5-5.0; P < 0.001), proteinuria (OR 2.7; 95% CI 1.3-5.2; P = 0.03), hypotension (OR 2.5; 95% CI 1.2-5.0; P = 0.008), hepatomegaly (OR 2.4; 95% CI 1.2-4.8; P = 0.01), cutaneous lesions (OR, 1.9; 95% CI 1.0-3.3; P = 0.02) and weight loss (OR 1.8; 95% CI 1.0-3.1; P = 0.03). Our results suggest that DH is a severe opportunistic disease with high mortality rate, which should be promptly recognized in order to provide early specific treatment.