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Biomedical subjects

A J Pinching

Publications and source records attributed to A J Pinching.

At least 127 records · Page 7Linked to original sources
PubMed1988

Upper gastrointestinal Kaposi's sarcoma in patients positive for HIV antibody without cutaneous disease.

Six patients with antibodies to the human immunodeficiency virus (HIV) and with persistent gastrointestinal symptoms of HIV infection but without cutaneous lesions of Kaposi's sarcoma underwent endoscopy. Four also underwent barium meal examination. In all six cases small lesions were seen in the stomach at endoscopy, and histological examination of biopsy specimens taken from the lesions confirmed the diagnosis of Kaposi's sarcoma. The barium meal examinations were reported as normal in three patients and showed oesophageal candidiasis in the fourth. These findings suggest that Kaposi's sarcoma of the upper gastrointestinal tract is common in patients positive for HIV antibody, even those without cutaneous lesions. Endoscopy, with biopsy of suspicious lesions, is necessary to make the diagnosis and is recommended in all HIV antibody positive patients with persistent upper gastrointestinal symptoms.

Adult↗
PubMed1988

Damage to jejunal intrinsic autonomic nerves in HIV infection.

Jejunal biopsies from 11 HIV-infected male homosexuals, without secondary enteropathogen infection, were examined at ultrastructural and light microscope level. Subjects were clinically categorized into four groups: asymptomatic (3), AIDS-related complex (4), persistent generalized lymphadenopathy (1), and AIDS (3). All 11 biopsies, including the three from asymptomatic HIV-infected individuals, showed extensive damage to autonomic nerve fibres in the lamina propria. These findings show that HIV infection damages the enteric autonomic nerves. Since asymptomatic HIV-infected individuals had similar damage, this appears to be an early event in the course of HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Lung function abnormalities in patients infected with the human immunodeficiency virus with and without overt pneumonitis.

Pulmonary function was measured in 169 male patients seropositive for the human immunodeficiency virus (HIV). The transfer factor for carbon monoxide (TLCO) in symptom free patients and patients with persistent generalised lymphadenopathy was normal (greater than 83% of predicted values). Patients with the AIDS related complex, non-pulmonary Kaposi sarcoma, and non-pulmonary non-Kaposi sarcoma AIDS (that is, opportunist infections affecting other organs) had lower mean values for TLCO (77%, 70%, and 70% of predicted respectively). These values were significantly lower than values for symptom free patients. Lower mean values of 50% and 63% predicted TLCO were observed in patients during the acute and recovery phases of Pneumocystis carinii pneumonia. TLCO was also low in patients with lung mycobacterial infection and in a patient with lung Kaposi sarcoma. Forced expiratory volume in one second, peak expiratory flow, and maximal expiratory flow at 50% of vital capacity were significantly reduced only in patients with acute pneumocystis pneumonia. This study shows that abnormalities in the results of pulmonary function tests, particularly TLCO, although greatest in patients with pulmonary complications of AIDS, are also present in patients with AIDS but without other evidence of pulmonary disease, and in patients with the AIDS related complex. The predictive and prognostic implications of these findings require further investigation.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Factors affecting the natural history of human immunodeficiency virus infection.

Human immunodeficiency virus (HIV) establishes latent infection in CD4 lymphocytes and macrophages. It can destroy CD4 cells by direct virus cytotoxicity, indirectly through the host response against HIV-infected cells, or by both means. Cells of the macrophage lineage are generally not destroyed but can serve as a reservoir of virus. HIV also causes functional impairment in remaining infected and uninfected cells. After exposure to infection by sexual, blood or maternofetal contact, about half the contacts become infected with HIV. Factors influencing the inoculum derived from the infected person include type of contact, phase of infection and local factors enhancing HIV replication or excretion. In the exposed person, genetic factors and systemic or local events such as infection or inflammatory injury may influence relative susceptibility. After infection with HIV, a number of outcomes may be seen, including symptomless carriage, with or without lymphadenopathy, or symptomatic disease, including the AIDS-related complex, acquired immune deficiency syndrome and HIV encephalopathy. Infection, multiple pregnancy and infancy are associated with increased or more rapid progression to symptomatic disease; malnutrition and immunosuppressive drugs may exert a similar effect. Genetic factors appear to affect disease susceptibility. Mechanisms influencing progression can be divided into those affecting the rate of HIV replication, those that determine the host response to HIV, and those mediated by other immunosuppressive influences. The host's balance with HIV thus resembles that of a tightrope walker, any force tending to tip him towards a catastrophic and irretrievable decline.

AIDS-Related Complex↗
PubMed1988

Peripheral blood dendritic cells in persons with AIDS and AIDS related complex: loss of high intensity class II antigen expression and function.

The antigen-specific immune response in HIV sero-positive individuals is depressed or absent. This may be due in part to abnormal co-operation between T lymphocytes and antigen presenting cells (APC). We have isolated from the peripheral blood of healthy heterosexuals and patients with persistent generalized lymphadenopathy (PGL) and AIDS, cells of low density (LDC) with dendritic morphology. These cells are known to be potent APC. The expression of two cell surface antigens on these cells, namely 63D3 (a monocyte related antigen) and Class II antigens was examined. LDC from controls and patients with benign, non-progressive PGL (type A) were found to show biphasic expression of Class II antigens. By contrast, the high intensity Class II expression seen on a small proportion of 63D3 negative cells from controls and patients with PGL type A was absent in patients with PGL type B (showing subtle signs of progressive immunodeficiency) and AIDS. The loss of this population of dendritic cells was reflected in the absence of stimulator activity in autologous and heterologous mixed lymphocyte reactions. Thus, it is possible that the loss of these dendritic cells may contribute to the profound immunological abnormalities seen in AIDS.

AIDS-Related Complex↗
PubMed1988

Jejunal mucosal architecture and fat absorption in male homosexuals infected with human immunodeficiency virus.

Diarrhoea and weight loss are common features of human immunodeficiency virus (HIV) disease. The mechanism of diarrhoea occurring in the absence of known enteropathogens is currently unknown. We have measured fat absorption, using the 14C triolein breath test, and quantitatively assessed jejunal villous architecture in 20 male homosexuals at various clinical stages of HIV disease. Enteropathogens were not detected in any subject at the time of jejunal biopsy in stool or jejunal mucosa. Partial villous atrophy was the sole histological abnormality and was detected at any clinical stage of HIV disease. The 14C triolein breath test quantitatively correlated with the degree of jejunal villous atrophy. In addition subjective presence of diarrhoea was related to the detection of fat malabsorption. Thus diarrhoeal disease in HIV infected patients in the absence of enteropathogens may be due to jejunal enteropathy and may be present at early clinical stages of HIV disease.

Acquired Immunodeficiency Syndrome↗
PubMed1987

HIV testing: changing trends at a clinic for sexually transmitted diseases in London.

Trends in human immunodeficiency virus (HIV) counselling and antibody testing at a London clinic for sexually transmitted diseases showed substantial changes over a 12 month period. From around 100 a month in the summer of 1986 the numbers of people attending rose substantially to 276 in October 1986 and 475 in November at the time of the campaign in the popular press. They rose further still, to 700, at the time of AIDS (acquired immune deficiency syndrome) week in March 1987. In April they fell to the levels seen six months previously. Apart from this increase in overall numbers the proportions of women and heterosexual men who were seen increased.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Atopic manifestations in the acquired immune deficiency syndrome: response to recombinant interferon gamma.

Six patients with the acquired immune deficiency syndrome (AIDS) had exacerbations or recurrences of previously quiescent atopic disease when they developed immunodeficiency. Four developed a different atopic illness from that suffered previously. Atopic symptoms developed within three months after the patients developed AIDS or during prodromal illness. Two of the patients were treated with recombinant interferon gamma: both showed a striking improvement in symptoms and cellular immunity. These results indicate that cellular immunity, through interferon gamma, may have a role in regulating atopic disease.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Association of different allelic forms of group specific component with susceptibility to and clinical manifestation of human immunodeficiency virus infection.

The distribution of phenotypes of the group specific component (Gc) was examined in 203 homosexuals at risk of infection or infected by the human immunodeficiency virus and compared with that in 50 randomly selected homosexuals and 122 healthy male heterosexual seronegative controls. 30.2% of patients with the acquired immunodeficiency syndrome (AIDS) were homozygous for Gc 1 fast (Gc 1f) compared with 0.8% of controls (p less than 0.0001); patients with other clinical manifestations of HIV infection were also more likely than controls to have Gc 1f. By contrast, seronegative symptomless homosexual contacts of AIDS patients (AH-p) lacked this phenotype but were more likely than controls to be homozygous for Gc 2 (25% vs 9%, p less than 0.05). AIDS patients lacked the homozygous Gc 2 phenotype altogether. A chi 2 trend test showed that progression to AIDS had a strong positive association with the Gc 1f allele (p less than 0.0001) and a negative one with Gc 2 (p less than 0.05). It is proposed that Gc may be involved in viral entry into host cells, the ease of which varies with different allelic forms of Gc, according to their sialic acid content.

AIDS-Related Complex↗
PubMed1987

Identity cards for patients infected with HIV?

Dr A C Srivastava has written to us to describe a case that raises the suggestion that people infected with the human immuno-deficiency virus (HIV) should carry identity cards. We asked two physicians, a general practitioner working with patients with the acquired immune deficiency syndrome (AIDS), and a general practitioner with a special interest in medical ethics to respond to the broad issues raised by Dr Srivastava's letter.

Acquired Immunodeficiency Syndrome↗