Pericardial involvement in human immunodeficiency virus infection

STUDY OBJECTIVES: Previous studies have showed that the pericardium is frequently involved in HIV infection. However, the characteristics and etiology of the pericardial abnormalities that have been found remained poorly defined. We analyzed the features of pericardial involvement in these patients and investigated the clinical variables associated with moderate and severe effusions. DESIGN: Prospective, clinical, and echocardiographic study. SETTING: The service of infectious diseases of a university hospital. PATIENTS: 181 consecutive patients at all stages of HIV infection. RESULTS: Only one patient (0.55%) had acute pericarditis. Seventy-five patients (41%) had an asymptomatic pericardial effusion; in 23 patients (13% of all patients), the effusion was either moderate or severe. Ten cases (5.5% of all patients) of moderate or severe effusions resulted in right atrium diastolic compression, and three of these cases (1.6% of all patients) required pericardiocentesis for the management of tamponade. Six patients (3%) presented with echogenic pericardial masses of undetermined etiology. A moderate or severe effusion was present in a greater number of patients with symptomatic HIV infection than was present in asymptomatic HIV-infected patients, respectively: 17 vs 2% (p = 0.015). The following are variables independently associated with moderate or severe pericardial effusions: heart failure (odds ratio, 20.3; p = 0.0001); Kaposi's sarcoma (odds ratio, 8.6; p = 0.01), tuberculosis (TB; odds ratio, 47.2; p = 0.0006); and other pulmonary infections (odds ratio,15.0; p = 0.02). CONCLUSIONS: Most of these moderate or severe effusions are clinically unsuspected, but they can lead to life-threatening tamponade. This fact seems to justify echocardiographic surveillance in HIV-infected patients, especially in those with heart failure, Kaposi's sarcoma, TB, or other pulmonary infections.     

Pancreatic involvement in human immunodeficiency virus infection

Involvement of the pancreas by human immunodeficiency virus (HIV) infection has not been adequately addressed and is the object of this review. I analyzed the English language literature, including single case reports of pancreatic involvement and larger series reporting detailed pathological findings of patients with HIV infection. Nonspecific pathological changes in the pancreas are frequently seen at autopsy of HIV-infected patients, but are not more common than in controls. Several types of infections (mainly cytomegalovirus, Cryptococcus neoformans, and Mycobacteria) and neoplasms (lymphoma and Kaposi's sarcoma) can involve the pancreas because they are usually disseminated. Although the serum amylase may be elevated, the patient remains asymptomatic. Occasional instances of severe and even fatal pancreatitis have been reported with HIV infections and attendant drug toxicity. Pentamidine has a predictable incidence of hypoglycemic episodes and 2',3'-dideoxyinosine provokes pancreatitis in a minority of treated patients. Such drug toxicity seems to deserve greater clinical concern than opportunistic infections or neoplasms.     

Rheumatic conditions in human immunodeficiency virus infection

Many rheumatic diseases have been observed in HIV-infected persons. We, therefore, conducted a comprehensive literature search in order to review the prevalence, presentation and pathogenesis of rheumatic manifestations in HIV-infected subjects. Articular conditions (arthralgia, arthritis and SpAs) are either caused by the HIV infection itself, triggered by adaptive changes in the immune system, or secondary to microbial infections. Muscular symptoms may result from rhabdomyolysis, myositis or from side-effects of highly active anti-retroviral therapy (HAART). Osseous complications include osteonecrosis, osteoporosis and osteomyelitis. Some conditions such as the diffuse infiltrative lymphocytosis syndrome and sarcoidosis affect multiple organ systems. SLE may be observed but may be difficult to differentiate from HIV infection. Some anti-retroviral agents can precipitate hyperuricaemia and are associated with arthralgia. When indicated, immunosuppressants and even anti-TNF-alpha agents can be used in the carefully monitored HIV patient. Thus, rheumatic diseases and asymptomatic immune phenomena remain prevalent in HIV-infected persons even after the widespread implementation of highly active anti-retroviral therapy.     

Liver involvement in human immunodeficiency virus infection

The advances in management of patients with acquired immunodeficiency syndrome (AIDS) with highly effective anti-retroviral therapy (HAART) have resulted in increased longevity of patients with human immunodeficiency virus (HIV) infection. AIDS-related illnesses now account for less than 50 % of the deaths, and liver diseases have emerged as the leading cause of death in patients with HIV infection. Chronic viral hepatitis, drug-related hepatotoxicity, non-alcoholic fatty liver disease, and opportunistic infections are the common liver diseases that are seen in HIV-infected individuals. Because of the shared routes of transmission, co-infections with hepatitis B virus (HBV) and hepatitis C virus (HCV) are very common in HIV-infected persons. Hepatitis C is the most common viral hepatitis seen in HIV-infected patients. With the availability of directly acting agents, treatment outcome of HCV is comparable to that seen in non HIV-infected patients. Careful monitoring is required for drug interactions and drug-induced hepatotoxicity and modification of drugs should be done where necessary. The results of liver transplantation in select HIV-infected patients can be comparable with those of HIV-negative patients.     

Diastolic dysfunction in human immunodeficiency virus infection

AIMS: We sought to determine the prevalence and characteristics of echocardiographic abnormalities (systolic and/or diastolic dysfunction, pericardial effusion) in patients with human immunodeficiency virus infection (HIV) with no symptoms or previous history of cardiac disease, and compare them with a healthy control group. PATIENTS AND METHOD: Transthoracic echocardiography was performed in 125 patients (73% male, mean age 33.2 +/- 6.6 years) with HIV infection without cardiac involvement and 47 age and sex-matched healthy volunteers (78% male, 31.6 +/- 7.3 years). The immunologic situation was determined by CD4 lymphocyte counts. RESULTS: Abnormal left ventricular relaxation and filling patterns (E/A relation 1.31 +/- 0.35 in HIV group, 1.66 +/- 0.38 in control group, p < 0.001; pressure half-time 57.5 +/- 13 in HIV group, 50.6 +/- 6.6 in control group, p < 0.001), segmental wall-motion abnormalities (15%) and pericardial effusion (7.2%) were found in patients with HIV infection. Systolic function (EF 64.8 +/- 8.3) and left ventricular dimension (diastolic diameter 4.94 +/- 0.55, systolic diameter 3.17 +/- 0.51) showed normal patterns and did not significantly differ from those of the control group. CONCLUSIONS: Silent echocardiographic abnormalities in patients with HIV infection are frequent suggesting a direct myocardial effect of the virus. The development of diastolic dysfunction is directly related to a worse immunologic situation. Prospective studies are needed to clarify the clinical prognosis of these asymptomatic abnormalities.     

Tuberculosis and human immunodeficiency virus infection

Because of the abnormalities of host defenses caused by the human immunodeficiency virus (HIV), persons with HIV infection are vulnerable to tuberculosis. Inferential data from several parts of the country indicate increases in tuberculosis case rates, probably occurring in patients with HIV infection. In a person infected with both HIV and Mycobacterium tuberculosis, attack rates of tuberculosis seem to be very high. In general, the disease tends to occur earlier in the course of HIV infection than other opportunistic processes that serve to define the acquired immunodeficiency syndrome (AIDS), presumably because M tuberculosis is more pathogenic than Pneumocystis carinii or Mycobacterium avium complex, for example. The clinical features of tuberculosis in this patient population seem to vary depending on the stage of the HIV infection. Late in the process, tuberculosis usually has atypical features with chest films showing diffuse infiltration, no cavities, and intrathoracic adenopathy. Tuberculin skin tests commonly are negative. At earlier stages of HIV infection, the clinical findings are similar to those in HIV-seronegative persons. Response to treatment is generally good; however, it is recommended that the standard duration be at least 9 months, using isoniazid and rifampin usually supplemented by pyrazinamide in the first 2 months. The use of isoniazid for preventive therapy is recommended for all HIV-seropositive persons who have tuberculin skin test reactions greater than or equal to 5 minutes. Those implementing infection-control measures for HIV-infected patients who have pulmonary findings should take tuberculosis into account until the disease is excluded. Medical personnel providing care for patients with tuberculosis should use universal blood and body substance precautions because of the possibility of undetected HIV infection in patients with tuberculosis.     

Septic bursitis in human immunodeficiency virus infection

Septic bursitis is a well described entity in immunocompromised patients. Common factors contributing to an immunocompromised state are alcoholism and corticosteroid therapy. We describe 2 patients with Staphylococcus aureus olecranon bursitis with evidence of human immunodeficiency virus (HIV) infection and no other contributing factors to immunodeficiency. The clinical course in these patients was refractory to conservative management. Such a persistent course of septic bursitis, especially in the absence of other contributing factors, should raise the possibility of HIV infection.     

Infectious diarrhea in human immunodeficiency virus infection

Gastrointestinal symptoms, particularly diarrhea, are common in patients with AIDS. Recent evidence indicates that enteric pathogens can be identified in most of these cases. Appreciating the clinical features caused by protozoal, fungal, bacterial, and viral pathogens will assist the clinician in effectively evaluating the gastrointestinal symptoms. Antimicrobial agents now are available for many of these pathogens.     

Tuberculosis and human immunodeficiency virus infection

Progressive human immunodeficiency virus infection eventually leads to activation and dissemination of a wide variety of microorganisms normally held in check by the cellular immune system. Mycobacterium tuberculosis is one of these pathogens, and the disease caused by it has become a common presenting infection in the patient with AIDS. Dr. Richard E. Chaisson and Dr. Gary Slutkin have studied tuberculosis in the United States and worldwide, respectively. In this AIDS Commentary they address the unique nature of this infection, its diagnosis, and its treatment in the patient with AIDS.     

Pseudo-SLE by human immunodeficiency virus infection

A 61-year-old woman was admitted for long-lasting fever and recurrent opportunistic infections during the treatment of SLE. She had been diagnosed as SLE and type-IV nephritis based on a renal biopsy and serological findings. A colonoscopy and liver biopsy revealed disseminated Mycobacterium avium complex infection. Human immunodeficiency virus (HIV) infection status was then examined and found to be positive. From the clinical course, the first symptoms were inferred to have been those of HIV infection.     

Tuberculosis in patients with human immunodeficiency virus infection

Tuberculosis (TB) is the major opportunistic infection of human immunodeficiency virus (HIV)-infected persons worldwide. Human immunodeficiency virus infection is the most potent known risk factor for reactivation of latent Mycobacterium tuberculosis infection, and TB disease appears to increase the rate of HIV progression. Pulmonary disease is seen in most patients, including a large proportion of those with extrapulmonary disease. Failure to suspect TB and to order the appropriate diagnostic tests is the most common reason for diagnostic delays. With advancing HIV infection, tuberculin skin test reactivity decreases along with reactivity to nonspecific antigens such as mumps, tetanus toxoid, and Candida; anergy testing need not be a routine component of tuberculosis screening of HIV-infected persons. The diagnosis depends on identifying the organism on smears or cultures; direct amplification tests may facilitate rapid identification of M. tuberculosis, but the relatively low sensitivity in smear-negative specimens limits their use. Also, these tests must be used in conjunction with the clinical assessment, and they must always be performed in conjunction with microscopy and standard culture. Shorter courses of combination preventive therapy of patients with latent tuberculous infection are effective, but the potential advantages of improved adherence and reduced costs of shorter courses should be balanced with an increased risk secondary to ongoing TB exposure in areas with a high TB prevalence. Six months of treatment for active tuberculosis is recommended, unless the response of a particular patient is slow or otherwise suboptimal. The use of highly active antiretroviral therapy (HAART) made a remarkable impact on the course or HIV disease, but raises several issues with respect to HIV-related TB. Drug interactions necessitate either a non-rifamycin-based regimen or a rifabutin-based regimen in patients on HAART treated for TB.