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Biomedical subjects

H C Lane

Publications and source records attributed to H C Lane.

At least 181 records · Page 10Linked to original sources
PubMed1985

Cryptococcosis in the acquired immunodeficiency syndrome.

The clinical course and response to therapy of 27 patients with cryptococcosis and the acquired immunodeficiency syndrome were reviewed. Cryptococcosis was the initial manifestation of the syndrome in 7 patients, and the initial opportunistic infection in an additional 7. Meningitis was the commonest clinical feature (18 patients). Blood cultures and serum cryptococcal antigen were frequently positive. In patients with meningitis, leukocyte count, protein level, and glucose level in cerebrospinal fluid were frequently normal; cerebrospinal fluid India ink test (82%), culture (100%), and cryptococcal antigen (100%) were usually positive. Only 10 of 24 patients had no evidence of clinical activity of cryptococcal infection after completion of therapy; 6 of these 10 had relapses shown by clinical findings or at autopsy. Standard courses of amphotericin B alone or combined with flucytosine were ineffective. Cryptococcosis in patients with the syndrome is a debilitating disease that does not respond to conventional therapy; earlier diagnosis or long-term suppressive therapy may improve the prognosis.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Immunopathogenesis of the acquired immunodeficiency syndrome.

Many abnormalities of humoral and cellular immunity associated with the acquired immunodeficiency syndrome can be explained by the preferential infection of the T4 lymphocyte subset with the etiologic retrovirus. Severe alterations in specific T4 functions, such as inadequate immune responsiveness to specific antigen, result in devastating morbidity and mortality. On the basis of accumulated scientific knowledge, we outline the immunopathogenesis of this syndrome.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Immunologic reconstitution in the acquired immunodeficiency syndrome.

Although effective therapies are available for many of the infections and tumors that occur in patients with the acquired immunodeficiency syndrome (AIDS), no therapy exists for the underlying immunodeficiency. Three approaches used to treat this immunodeficiency have included wholescale immune replacement through lymphocyte transfers, bone marrow transplantation, and thymic implantation; immunologic enhancement with biologic-response modifiers, such as gamma interferon, interleukin-2, and some drugs; and antiretroviral therapy. Because of the persistence of the etiologic virus, both immune replacement and enhancement will probably be ineffective unless effective strategies are developed against the virus. Agents that have shown antiviral activity in vitro which are currently in clinical trials include suramin, heteropolyanion-23 (HPA-23), ribavirin, and alpha interferon. Foscarnet and monoclonal antibodies have yet to enter clinical trials in the United States. It is still too early to tell if any of the antiviral agents will prove of value in the management of patients with AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Therapeutic approaches to patients with AIDS.

The immune systems of patients with acquired immunodeficiency syndrome are characterized by a profound defect in the number and function of helper/inducer T-lymphocytes, particularly at the level of soluble antigen recognition. Due to this selective yet profound defect in the immune system, these patients are prone to recurrent severe opportunistic infections and Kaposi's sarcoma. While therapies exist for some of these complications of acquired immunodeficiency syndrome, no effective therapies exist for the underlying immune defect of this syndrome. Reviewed here are some of our recent attempts at immune reconstitution in acquired immunodeficiency syndrome, using either whole scale immune reconstitution through the use of lymphocyte transfers and bone marrow transplantation or enhancement of the remaining immune systems with the T-cell-derived lymphokines interleukin-2 or immune gamma-interferon. In addition, recent advances in the therapy of Pneumocystis carinii pneumonia and disseminated cytomegalovirus disease are discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Pharmacokinetics of lymphocyte-derived and recombinant DNA-derived interleukin-2 after intravenous administration to patients with the acquired immunodeficiency syndrome.

Intravenous infusions of 250,000 U of lymphocyte-derived or recombinant DNA-derived interleukin-2 (IL-2) were administered to patients with the acquired immunodeficiency syndrome, and sera were obtained for pharmacokinetic studies. A methodology was developed for the determination of serum levels of interleukin-2, which resulted in a coefficient of variation of less than 8% and a sensitivity 32-fold greater than that of the traditional methodology using probit analysis of half-maximal stimulation. In addition to the previously described rapid clearance of IL-2, a later phase of interleukin-2 clearance with a half-life greater than 90 min was observed; bioactive interleukin-2 remained in the circulation for several hours after infusion.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Interleukin 2 enhances the natural killer cell activity of acquired immunodeficiency syndrome patients through a gamma-interferon-independent mechanism.

Patients with the acquired immunodeficiency syndrome (AIDS) exhibit a variety of disorders of cellular immunity, including a deficient ability to generate cytotoxic T cells and depressed levels of natural killer (NK) cell activity. Interleukin 2 (IL 2) in vitro can markedly augment these depressed immune functions. Because IL 2 can induce the release of interferon-gamma (IFN-gamma) from normal peripheral blood lymphocytes (PBL), and because IFN-gamma may play a role in the regulation of NK cell activity, this study was performed to determine if the IL 2 enhancement of the NK cell activity of patients with AIDS was an IFN-gamma-dependent effect. PBL from eight healthy heterosexual donors and from nine patients with AIDS were studied for their ability to release IFN-gamma in response to IL 2 at a concentration of 100 U/ml. After 60 hr of culture, the PBL of all eight healthy donors produced IFN-gamma with a mean titer of 113 U/ml (range 40 to 320 U/ml). In contrast, the PBL from only two of nine patients with AIDS released measurable amounts of IFN-gamma (40 U/ml each) in response to IL 2 with a mean titer of 13.5 U/ml for all nine. Although the PBL from patients with AIDS were deficient in their capacity to produce IFN-gamma in response to 100 U/ml of IL 2, significant enhancement of NK cell activity could be obtained after only 1 hr of PBL treatment with 10 U/ml of IL 2, with an optimal NK enhancing effect occurring at doses of 50 to 100 U/ml of IL 2. The use of an anti-IFN-gamma monoclonal antibody resulted in complete neutralization of the IFN released from the normal PBL cultured with IL 2, but failed to inhibit the IL 2 enhancement of NK cell activity. Exogenous IFN-gamma exhibited different kinetics of enhancement of NK cell activity when compared to IL 2, requiring substantially more than 1 hr of pretreatment of PBL. These results indicate that the PBL from patients with AIDS usually do not release IFN-gamma when cultured with IL 2, and that IL 2 enhancement of the depressed NK cell activity of these patients may be an IFN-gamma-independent event. These results may have important implications for the therapy of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Transmission of HTLV-III infection from human plasma to chimpanzees: an animal model for AIDS.

Two of three chimpanzees given plasma from patients with acquired immune deficiency syndrome (AIDS) or pre-AIDS showed serum antibodies to type III human T-cell leukemia virus (HTLV-III) 10 to 12 weeks after transfusion. One animal also developed lymphadenopathy, transient depression of the ratio of T4 to T8 lymphocytes, and impaired blastogenic responses. No opportunistic infections occurred. Adenopathy persisted for 32 weeks, and antibody to HTLV-III persisted for at least 48 weeks. This transmission of HTLV-III by lymphocyte-poor plasma confirms the potential risk of such plasma or plasma derivatives to recipients. The susceptibility of the chimpanzee to HTLV-III infection and the ability to simulate the human lymphadenopathy syndrome in this animal makes it a valuable model for further study of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Nucleoside triphosphate changes during the peripheral life-span of erythrocytes of adult rainbow trout (Salmo gairdneri).

Determinations of nucleoside triphosphates (NTP) were made on rainbow trout erythrocytes segregated into age classes following velocity sedimentation at unit gravity. The NTP content of young cells was lower than that of mature cells, whereas it was significantly higher in the oldest cell population. Thin-layer chromatography of erythrocyte cell extracts showed that both ATP and GTP were present and that the former dominated in all age groups. Potassium cyanide was significantly more effective than iodoacetate in lowering NTP levels in the cells of the young age class whereas in the oldest cells the reverse was true.

Adenosine Triphosphate↗
PubMed1984

Ophthalmic involvement in acquired immunodeficiency syndrome.

Forty patients with acquired immunodeficiency syndrome (AIDS) were examined for ocular abnormalities. Twenty of these patients died and the eyes were obtained for culture and histopathologic examination. These patients have multiple opportunistic infections and neoplasms as the result of a severe depression of cellular immunity. Fifty percent of all patients with AIDS and 75% of the autopsy group have ocular signs attributable to AIDS. Ocular findings were confined to four major categories: cytomegalovirus retinitis (10 patients), retinal cotton wool spots (11 patients), conjunctival Kaposi's sarcoma (2 patients) and neuro-ophthalmic motility abnormalities (3 patients). Cytomegalovirus retinitis was a significant cause of visual loss. Seven of 40 autopsy eyes had hand motion or worse visual acuity prior to the patients' death because of CMV retinitis. This necrotic retinitis showed minimal inflammation and progressed to involve the entire retina in three to six months, resulting in a gliotic retinal membrane. Therapy with antiviral agents was not effective. Recognizing the ocular signs of AIDS may facilitate the diagnosis. The ophthalmologist also has a major role in the observation of progression or regression of these ocular manifestations, and can assist in the evaluation of therapy in patients with AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Persistence of Pneumocystis carinii in lung tissue of acquired immunodeficiency syndrome patients treated for pneumocystis pneumonia.

Eleven patients with acquired immunodeficiency syndrome (AIDS) and Pneumocystis carinii pneumonia (PCP) were studied by repeat bronchoscopy during PCP treatment to assess histologic evidence of resolution of the pneumonia. Nine of 10 patients studied after 8 to 21 days of therapy demonstrated evidence of persistent PCP. Four of 6 patients studied after 22 to 35 days of therapy continued to demonstrate Pneumocystis carinii cysts on repeat examination, while only 1 of 4 patients studied after 35 days of therapy showed evidence of PCP pneumonia. The rate of resolution of PCP in patients with AIDS may be different from the rate of resolution of PCP in patients without AIDS. There was no apparent correlation between rate of clinical response and likelihood of histologic resolution on follow-up biopsy. The PCP in patients with AIDS may require more prolonged therapy for complete resolution of this pneumonic process.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Monocyte function in the acquired immune deficiency syndrome. Defective chemotaxis.

The ineffective immune response in patients with the acquired immune deficiency syndrome (AIDS) contributes to severe and widespread infections and unrestricted growth by certain tumors. To determine whether monocyte dysfunction contributes to this immunosuppressed condition, we investigated monocyte chemotaxis in patients with AIDS. Using three different chemotactic stimuli, N-formylmethionylleucylphenylalanine, lymphocyte-derived chemotactic factor, and C5a des Arg, we studied the chemotactic responses of monocytes from seven homosexual men with AIDS, three homosexuals with lymphadenopathy and an abnormal immunological profile, seven healthy homosexual men, and 23 heterosexual control individuals. Monocytes from each of the AIDS patients with Kaposi's sarcoma and/or opportunistic infection exhibited a marked reduction in chemotaxis to all stimuli compared with the healthy control subjects. The reduced chemotactic responses were observed over a wide range of concentrations for each stimulus. Monocytes from AIDS patients who had clinically apparent opportunistic infection(s) exhibited a greater reduction in monocyte migration to all three stimuli than monocytes from the AIDS patient with only Kaposi's sarcoma. Monocytes from each of three homosexuals with lymphadenopathy and an abnormal immunological profile exhibited decreased chemotactic responses that were intermediate between those of the AIDS patients and the healthy heterosexual control subjects. In contrast to these findings, monocytes from each of seven healthy homosexuals exhibited normal chemotactic responses to the same stimuli. In addition, monocytes from AIDS patients exhibited reduced chemotaxis to soluble products of Giardia lamblia, one of several protozoan parasites prevalent in AIDS patients. Thus the immune abnormality in AIDS, previously thought to involve only the T-, B-, and natural killer lymphocytes, extends to the monocyte-macrophage. Defective monocyte migratory function may contribute to the depressed inflammatory response to certain organisms and to the apparent unrestricted growth of certain neoplasms in patients with AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Kaposi's sarcoma of the head and neck in the acquired immune deficiency syndrome.

Since 1981 a new syndrome of acquired immune deficiency (AIDS) has been recognized. Male homosexuals, male and female intravenous drug abusers, and recipients of blood products (i.e., hemophiliacs) appear to be the populations at risk. The syndrome has been manifested by community-acquired opportunistic infections and/or Kaposi's sarcoma (KS). Otolaryngologic manifestations of AIDS are not infrequent. Thirteen AIDS patients at the National Institutes of Health with KS of the head and neck region are presented. All 13 patients were homosexual or bisexual males. Nine initially presented with KS, five with KS of the head or neck. As a group the patients demonstrated lesions involving the oropharyngeal, tracheobronchial, and gastrointestinal regions. Their clinical course and complications are presented in detail. The mortality rate in this subgroup of AIDS patients is extraordinarily high (62%), with an average longevity of 11 months following initial diagnosis.

Acquired Immunodeficiency Syndrome↗
PubMed1984

NIH conference. Acquired immunodeficiency syndrome: epidemiologic, clinical, immunologic, and therapeutic considerations.

The acquired immunodeficiency syndrome is a new disease whose cause is unknown but is almost surely due to a transmissible agent, most likely a virus. The disease is clearly spread by sexual contact, particularly homosexual activity. Blood-borne transmission constitutes the other major recognized form of spread of the disease, although it is highly likely that the disease is not readily spread through casual, nonsexual, non-blood-borne routes. Although the disease is still highly concentrated in the United States, it is now seen in several countries throughout the world. The common denominator of the disease is a profound suppression of cell-mediated immunity, specifically a quantitative and qualitative defect in the T4 inducer or helper subset of T lymphocytes. Hyperactivity of B lymphocytes is also characteristic. The clinical manifestations are those of severe and life-threatening opportunistic infections and unusual neoplasms, particularly Kaposi's sarcoma. The mortality may well approach 100%, making this one of the most extraordinary transmissible diseases in history.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Pneumocystis carinii pneumonia: a comparison between patients with the acquired immunodeficiency syndrome and patients with other immunodeficiencies.

Clinical features of 49 episodes of Pneumocystis carinii pneumonia in patients with the acquired immunodeficiency syndrome were compared with those of 39 episodes in patients with other immunosuppressive diseases. At presentation patients with the syndrome were found to have a longer median duration of symptoms (28 days versus 5 days, p = 0.0001), lower mean respiratory rate (23.4 versus 30, p = 0.005), and higher median room air arterial oxygen tension (69 mm Hg versus 52 mm Hg, p = 0.0002). The survival rate from 1979 to 1983 was similar for the two groups (57% and 50% respectively). Patients with the syndrome had a higher incidence of adverse reactions to trimethoprim-sulfamethoxazole (22 of 34 versus 2 of 17, p = 0.0007). Survivors with the syndrome at initial presentation had a significantly lower respiratory rate, and higher room air arterial oxygen tension, lymphocyte count, and serum albumin level compared to nonsurvivors. Pneumocystis carinii pneumonia presents as a more insidious disease process in patients with the syndrome, and drug therapy in these patients is complicated by frequent adverse reactions.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Thoracic manifestations of the acquired immune deficiency syndrome.

The acquired immune deficiency syndrome is characterized by the development of multiple recurrent opportunistic infections or unusual neoplasms in individuals with no prior history of immune suppression. This report summarizes the thoracic diseases encountered in such patients before after death and the role of diagnostic techniques currently used in the evaluation of thoracic disease in 15 patients with this syndrome. Efficacy of treatment was determined by correlation with postmortem findings in all patients. Pulmonary disease was present in all 15 patients and necessitated 23 transbronchial biopsies in 11 patients. Pneumocystis carinii pneumonia and cytomegalovirus pneumonia were the most common findings. Nine open lung biopsies in eight patients disclosed either Pneumocystis carinii pneumonia or Kaposi's sarcoma. Esophageal disease was present in four patients, and endoscopic evaluation demonstrated Candida esophagitis (two), esophageal Kaposi's sarcoma (one), and cytomegalovirus esophagitis and Kaposi's sarcoma (one). Mean time to death from diagnosis of acquired immune deficiency syndrome was 7.7 months, with respiratory insufficiency being the most common cause of death (9/15, 60%). Pneumocystis carinii pneumonia was successfully eradicated in 70% of the patients. Candida esophagitis was ameliorated in both patients with the disease. Unsuspected pulmonary Kaposi's sarcoma, cytomegalovirus pneumonitis, and other infectious pathogens were documented at autopsy. These data reveal that Pneumocystis carinii pneumonia and Candida esophagitis can be managed successfully in patients with acquired immune deficiency syndrome if appropriately diagnosed. The major cause of death in this series was pulmonary insufficiency, often the result of severe cytomegalovirus infection. Thoracic surgeons must continue to play an aggressive and important role in the early diagnosis and management of potentially treatable pulmonary and esophageal disease in these patients.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Use of interleukin-2 in patients with acquired immunodeficiency syndrome.

Twelve patients with acquired immunodeficiency syndrome were treated with a natural product, highly purified human interleukin-2. Doses ranged from 250 to 250,000 units. No clinical responses were seen. Minimal toxicity was noted and consisted of mild prolongation of partial thromboplastin time and proteinuria. Immunologic changes during the study included a decrease in the number of circulating T8 lymphocytes, increased skin test reactivity, and a decline in serum immunoglobulin levels.

Acquired Immunodeficiency Syndrome↗