Ethical attitudes related to problems of managing patients with acquired immunodeficiency syndrome

We evaluated, with a questionnaire, ethical attitudes towards the clinical attention of patients with AIDS in 88 physicians. Most of the surveyed were residents and all were working in two mexican hospitals with experience managing patients with AIDS: The National Institute of Nutrition and the National Institute of Respiratory Diseases. None of the questions was answered similarly by all physicians and some of them considered ethically unquestionable, behaviours that traditionally are immoral or even illegal. Reproducibility of the results, evaluated in 10 doctors 5 months later, was acceptable. Ethical attitudes were heterogeneous and inconsistent in the surveyed. This can be the results of a poor or absent training in Medical Ethics in medical schools and during residencies. We believe this deficiency helps maintaining discriminatory attitudes against patients with AIDS and may decrease the quality of medical services to the group.     

Effect of a non-viral fraction of acquired immunodeficiency syndrome plasma on the vulnerability of lymphocytes to cortisol

We have observed previously that the rate of cortisol catabolism by lymphocytes (CCL) was indicative of the vulnerability of these cells to cortisol. We attempted to ascertain whether cortisol-sensitive lymphocytes (e.g. thymocytes) metabolize cortisol at a different rate from cortisol-resistant cells and whether lymphocytes in which cortisol catabolism is inhibited become cortisol sensitive. The work was facilitated by the observation that an ethanol extract plasma from patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) had the capacity to inhibit CCL. The capacity of thymocytes to metabolize cortisol was found to be 11 times lower than that of peripheral lymphocytes. Inhibition of CCL with an ethanol extract of plasma from AIDS/ARC patients made the cells vulnerable to cortisol, causing them to die at a rate seven times greater than that of control samples. It is suggested that these findings may have important implications with regard to the nature of lymphocyte depletion in AIDS/ARC patients or in people at risk of developing the syndrome.     

Human T-cell leukemia virus in lymphocytes of two hemophiliacs with the acquired immunodeficiency syndrome

Fresh and cultured peripheral blood cells from two patients with hemophilia A and the acquired immunodeficiency syndrome were examined for markers of infection with human T-cell leukemia virus (HTLV) type 1. Neither patient had antibody to membrane antigens of HTLV-infected cells at the time of culture. Electron microscopy of peripheral blood cells from Patient 1 and cultured cells from Patient 2 showed type C retrovirus-like particles. Examination of peripheral blood lymphocytes showed other smaller virus-like particles in circulating mononuclear cells from both patients. Indirect immunofluorescence of peripheral mononuclear cells from both patients and of cultured cells from Patient 2 showed staining with antibodies to purified HTLV and to HTLV core proteins p24 and p19.     

Plasma platelet-activating factor acetylhydrolase activity in human immunodeficiency virus infection and the acquired immunodeficiency syndrome

Platelet-activating factor (PAF) acetylhydrolase (PAF-AH) catalyzes the hydrolysis of PAF, a mediator of inflammation, as well as other biologically active oxidized phospholipids. In humans, plasma PAF-AH activity is bound to low-density lipoprotein (LDL) and high-density lipoprotein (HDL). Higher levels of plasma PAF-AH activity have been found in a variety of diseases, and are thought to be a defense mechanism against the toxic effects of PAF and oxidized phospholipids. We studied plasma PAF-AH activity in patients with human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS), a disease characterized by chronic HIV infection and a systemic host response. Plasma PAF-AH activity was significantly greater in AIDS patients compared with control subjects (25.2 +/- 2.0 v 17.0 +/- 0.8 nmol/min/mL, P < .001). The higher levels of plasma PAF-AH activity were found in LDL (28.2 +/- 2.2 v 18.3 +/- 1.0 nmol/min/mL for AIDS v controls, respectively, P = .0005), but not in HDL. Plasma PAF-AH activity in AIDS correlated with circulating interferon alfa (r = .575, P = .005) and plasma triglycerides (r = .556, P < .0025). The presence of secondary infection in AIDS did not significantly change plasma PAF-AH activity. The initiation of a new antiretroviral regimen with either a protease inhibitor or the nucleoside analog lamivudine did not significantly decrease plasma PAF-AH activity, despite successful suppression of HIV RNA levels. Plasma PAF-AH activity may be a sensitive marker of the host response to infection, and the higher levels of plasma and LDL-associated PAF-AH activity in patients with HIV infection and AIDS may be a physiological response to protect the host against oxidative injury from PAF and oxidized phospholipids.     

Cardiac manifestations of acquired immunodeficiency syndrome

Acquired immunodeficiency syndrome is a serious problem worldwide. Recent advances in the knowledge about human immunodeficiency virus (HIV) replication and the treatment of HIV infection have improved survival in HIV patients. Because of the longer survival in HIV patients, the more manifestations of late-stage HIV infection will be seen, including HIV-related cardiac diseases. The common cardiac manifestations in patients with the acquired immunodeficiency virus are pericardial effusion, myocarditis, dilated cardiomyopathy, endocarditis, pulmonary hypertension, malignant neoplasms, and drug-related cardiotoxicity. This review focuses on these cardiac manifestations in patients with the acquired immunodeficiency syndrome.     

Predictors of cardiac morbidity and related mortality in children with acquired immunodeficiency syndrome

OBJECTIVES: The aim of this study was to determine the prevalence of cardiovascular dysfunction and its predictors in children with acquired immunodeficiency syndrome (AIDS). BACKGROUND: Cardiovascular manifestations are common among children with AIDS but may be clinically occult. METHODS: We reviewed the medical records, echocardiograms, electrocardiograms, and Holter monitor studies of 68 children with AIDS. We tested clinical and demographic characteristics at the time of AIDS diagnosis for their ability to predict serious cardiac events, death, and cardiac death. RESULTS: The median time from AIDS diagnosis to death or end of follow-up was 1.0 year (range, 1 week to 7.9 years). Nineteen patients (28%) experienced serious cardiac events after AIDS diagnosis. Of 43 patients who died, 15 (35%) had cardiac dysfunction. Multivariable analyses revealed that recurrent bacterial infections, wasting, encephalopathy, male gender, and an earlier year of AIDS diagnosis were predictors of serious cardiac events (relative risk [RR] = 9.3, 6.9, 4.7, 4.1, and 0.76, respectively, p < 0.05). Wasting, encephalopathy, a low age-adjusted CD4 count, a low age-adjusted immunoglobulin G (IgG) level, and an earlier year of AIDS diagnosis increased the risk of all-cause mortality (RR = 8.9, 5.1, 2.7, 0.82, and 0.8, respectively, p 相似文献   

Granulocyte-macrophage colony-stimulating factor enhances neutrophil function in acquired immunodeficiency syndrome patients.

We conducted a clinical trial of human recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF) in leukopenic patients with acquired immunodeficiency syndrome (AIDS) and analyzed neutrophil function before, during, and after in vivo administration of rGM-CSF. Prior to GM-CSF infusion, AIDS patients' neutrophil superoxide generation and neutrophil antibody-dependent cell-mediated cytotoxicity were enhanced normally by in vitro exposure to GM-CSF. Neutrophil phagocytosis and intracellular killing of Staphylococcus aureus were also normal in the majority of these patients. Two patients, however, had discrete neutrophil functional defects: one in phagocytosis and one in intracellular killing. During the period of GM-CSF infusion, these abnormalities were corrected. The number of circulating neutrophils increased in all patients treated with GM-CSF in a dose-dependent manner. Neutrophils produced in vivo in response to GM-CSF administration functioned normally and there was evidence for neutrophil priming and activation in vivo. We conclude that GM-CSF treatment of AIDS patients leads to the production of functionally active neutrophils, suggesting therapeutic potential for GM-CSF in the treatment of patients with impaired host defense.     

Polymorphic expression of decay-accelerating factor in human colorectal cancer

BACKGROUND: We have previously shown that expression of decay-accelerating factor (DAF), a complement regulatory protein, is enhanced immunohistochemically on the luminal surface of cancer glands in human colorectal cancer and is detected in stool specimens of patients with colorectal cancer. The amount of DAF present in the stools might be influenced by the stability of DAF on the cell surface which is regulated by biochemical properties such as glycosylation of the protein. In the present study, to help elucidate the mechanism for the release of DAF from human colorectal cancers, we biochemically analyzed DAF expression by western and northern blotting by using surgically resected specimens of colorectal cancers. METHODS: Surgically resected colorectal cancer tissues were obtained from 10 patients. Expression of DAF was determined by western and northern blotting, and glycosylation of DAF protein was analyzed with glycosidase digestion. RESULTS: Northern blot analysis demonstrated that the expression of DAF mRNA in colorectal cancer was enhanced two- to threefold compared with normal tissues. In western blotting, expression of DAF protein in the cancer tissue was increased, and heterogeneity in the apparent molecular weight of DAF was observed among patients. When o-linked sugars were removed, this heterogeneity of DAF size diminished. CONCLUSIONS: The polymorphic expression of DAF in colorectal cancer is likely to reflect variability in the o-glycosylation of the protein. We speculate that this variability could affect the stability of DAF on the surfaces of cancer cells and, in turn, the amount of DAF shed into the stools of colorectal cancer patients.     

Altered sensitivity to antiviral drugs of herpes simplex virus isolates from a patient with the acquired immunodeficiency syndrome

Acyclovir (ACV)-resistant herpes simplex virus type 2 (HSV-2) was isolated from a patient with acquired immunodeficiency syndrome after long-term but intermittent ACV therapy. These thymidine kinase-defective isolates were sensitive in vitro to foscarnet. While combined therapy with ACV and interferon produced only partial clinical improvement, the in vitro effect of this combination against an ACV-resistant isolate from the patient was strongly synergistic. A short course (10-12 days) of intravenous foscarnet controlled severe ulceration, and clinical improvement lasted 6 months. After recurrence and further courses of foscarnet, however, the patient responded poorly, and subsequent HSV isolates were resistant to both ACV and foscarnet and hypersensitive to aphidicolin.     

Endocrine complications of the acquired immunodeficiency syndrome

Acquired immunodeficiency syndrome (AIDS) is a multisystem disorder characterized by defects in the immune system that result in opportunistic infections and neoplasms. While endocrine dysfunction has not been a prominent clinical feature of AIDS, all endocrine glands may be affected by the opportunistic infections and neoplasms or by agents used in their treatment. Adrenal cortical insufficiency related to cytomegalovirus and ketoconazole therapy, hypoglycemia related to pentamidine therapy, and hyponatremia secondary to diverse causes are the most serious endocrine abnormalities that commonly occur. As the numbers of patients with AIDS increase, the development of these and other endocrine complications will occur more often. Because the clinical manifestations of endocrine dysfunction may be nonspecific or subtle, they may be overlooked, particularly in the setting of chronically and severely ill patients. Recognition and prompt therapy for endocrine dysfunction is essential for optimal treatment of these patients.     

Pulmonary manifestations of acquired immunodeficiency syndrome.

In at least 65% of patients with acquired immunodeficiency syndrome (AIDS), the lung is the site for life-threatening illness. To establish a basis for understanding the pulmonary pathology of such illness, we first review briefly the effects of the human immunodeficiency virus on the immune system and then review the pathological pulmonary processes occurring in AIDS in terms of their various etiologies: infections, idiopathic processes, and neoplasia. In the section on each etiology, we discuss clinical manifestations, pulmonary pathology, diagnostic findings, and therapeutic options. In the last section, we outline our overall initial diagnostic approach to the patient with AIDS who presents with respiratory symptoms, and we discuss the integration of clinical, laboratory, and radiographic findings.