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Biomedical subjects

R Y Lin

Publications and source records attributed to R Y Lin.

At least 91 records · Page 5Linked to original sources

Hypocomplementemia and human immunodeficiency virus infection. Clinical correlates and relationships to circulating immune complex and immunoglobulin G levels.

The levels of C4 and C3 were measured and related to other immunological and clinical parameters in 44 patients with the human immunodeficiency virus (HIV) infection. Circulating immune complexes (C1q-CIC) as measured by an enzyme-linked immunosorbent assay employing monoclonal antibody with specificity for bound Clq, and serum immunoglobulin G (IgG) concentrations were assessed simultaneously. Clinical parameters assessed included: (1) the presence of specific anti-infective medications; (2) the presence of hypotension and fluid administration, and (3) bacterial and specific opportunistic infections. Hypocomplementemia was observed in 25 of 46 sera for C3, and in 8 of 46 sera for C4. Clq-CIC increases were seen in 26 of 46 sera and hyper-IgG was present in 25 of 46 sera. Lower C3 concentrations were significantly associated with elevated Clq-CIC levels (p less than 0.001). There were significant correlations between Clq-CIC levels and C3 concentrations (p = 0.0065, negative) and IgG levels (p = 0.0075, positive). Clq-CIC were significantly higher with serum p-24 antigen levels of 50 pg/ml or greater. These data demonstrate that elevated Clq-CIC and hypocomplementemia are both common in HIV-infected patients and may have significant relationships.

Acquired Immunodeficiency Syndrome↗

T cell immunophenotypes and DR antigen expression in intravenous drug users. Relationship to human immunodeficiency virus serology.

Thirty-six intravenous drug users were studied for peripheral blood mononuclear cell (PBMC) immunophenotypes and human immunodeficiency virus (HIV) serological profiles. This population has a high risk for developing HIV infection. Half (18/36) were HIV antibody (Ab) negative (-) and half were positive (+). Total T lymphocytes (CD3+ and CD2+) were not different between HIV Ab-negative and HIV-positive groups. Unactivated T(CD3+DR-) cells/mm3 were less (p = 0.003) in HIV Ab-positive patients (1,467 +/- 628) compared to HIV Ab-negative patients (2,190 +/- 695). T-helper (CD4+) cells/mm3 were also less in HIV Ab-positive patients (762 +/- 344 vs. 1,161 +/- 419, p = 0.005). The most significant difference was in activated T lymphocyte CD3+DR+) percentages where the mean was 9.6% in those HIV Ab-positive compared to 3.8% in seronegatives (p less than 0.001). Preliminary studies showed that in vitro naloxone treatment of PBMC had no effects on immunophenotypic expression except for CD3+DR+ lymphocytes, where a significant reduction was observed in the HIV Ab-positive group (p = 0.022) but not in the HIV ab-negative group. These findings suggest that in certain populations, activated T cells may be an early manifestation of HIV infection.

Adult↗

Reiter's syndrome and human immunodeficiency virus infection.

A 35-year-old Black male with a long history of intravenous drug abuse developed clinical manifestations of Reiter's syndrome, with significant joint and psoriasiform skin involvement. In addition, he had signs and symptoms compatible with human immunodeficiency virus (HIV) infection and had a positive HIV antibody test confirmed with Western blot testing. Although many dermatologic manifestations of HIV infection have been described, this is the first time that an association with Reiter's syndrome has been reported. Recently, the development of psoriasis in other patients with HIV infection has been described. Taken together, these occurrences suggest that the purported retroviral relationship with psoriasis and related dermatoses may warrant further examination.

AIDS-Related Complex↗

Chronic diffuse dermatitis and hyper-IgE in HIV infection.

Diffuse dermatitis and markedly elevated serum IgE concentrations were observed in three adult males who were seropositive for human immunodeficiency virus (HIV) antibody. The clinical features in common for these patients included 1) an adult onset of greater than 6 weeks' duration associated with pruritus, 2) T-helper (CD-4) cell depletion, 3) the lack of overt atopic disease, and 4) the lack of opportunistic infection (except oral thrush) and neoplasia. The mean serum IgE concentration was 5,959 (range: 4,930-6,260) IU/ml. Cutaneous involvement consisted of hyperpigmented papules with variable excoriations and lichenification. Zidovudine was administered to all 3 patients and was associated with cutaneous improvement. Serum IgE concentrations from 19 AIDS patients without cutaneous disease did not show significant elevations. These observations suggest that certain patients with HIV infection can manifest a unique hyper-IgE syndrome associated with diffuse cutaneous disease.

Adult↗

Hyper-IgE and human immunodeficiency virus infection.

A 39-year-old black male who is an intravenous drug abuser developed certain clinical manifestations that were consistent with the hyper-IgE syndrome. These included an extremely elevated IgE (greater than 2000 IU/mL), extensive eczematoid dermatitis, and recurrent soft tissue infections. He had no history of atopic disease as a child. Immunophenotypic analysis of peripheral blood mononuclear cells showed a significant decrease in helper (CD 4) cells with a normal concentration of suppressor (CD 8) cells. Human immunodeficiency virus (HIV) antibody was detected in his serum. Previous studies of patients with atopic dermatitis as well as of patients with the hyper-IgE syndrome characteristically show decreases in total suppressor lymphocyte concentrations in peripheral blood. These results led some investigators to postulate that high IgE concentrations in patients with atopic dermatitis result from defective IgE specific suppression. More recent evidence suggests that helper cell function may be the more critical impairment in these disorders. The development of a hyper-IgE syndrome in this setting of T-helper cell viral affliction lends further support to the hypothesis that helper lymphocyte defects may have a key role in the development of atopic dermatitis and the hyper-IgE syndrome.

Acquired Immunodeficiency Syndrome↗

Severe spirometric defects in systemic lupus erythematosus. A possible role for bronchoalveolar lavage and gallium scanning.

Two patients with systemic lupus erythematosus (SLE) developed progressive chronic pulmonary disease. Pulmonary bronchoalveolar lavage (BAL) and Gallium-67 scanning were performed and were consistent with alveolitis. In one patient, an open lung biopsy was performed and showed the presence of several immunoreactants as well as interstitial pneumonitis. Although mild pulmonary function abnormalities are common in SLE, some patients such as the two described in this report develop progressive and incapacitating pulmonary impairment. The need for developing standardized indices of pulmonary inflammation such as BAL and gallium scanning for the purposes of diagnosis, prognostication, and monitoring treatment responses in systemic lupus erythematosus is stressed.

Adolescent↗

Immunopathological changes after multiple spider bites.

Utilizing a panel of immune complex assays, antigen-antibody complex formation in a 29-year-old man shortly after a spider bite was documented. The clinical picture and laboratory parameters were consistent with a serum sickness reaction. Immune hyperactivity was evidenced by a detectable autoimmune serological response. This constellation of findings may be a common attendant to arthropod envenomation.

Adult↗

In vivo reduction of circulating C1q binding immune complexes by intravenous gammaglobulin administration.

Six patients with systemic lupus erythematosus were treated with high-dose intravenous gammaglobulin. Immunological parameters were studied and included solid-phase immune complex determinations, quantitative immunoglobulins G, A, and M, as well as C3 and C4 concentrations. Pretreatment values of circulating immune complex concentrations as measured by either C1q binding or anti-C3 binding assays were elevated in all patients. Posttreatment values showed reductions in all C1q binding immune complexes (p less than 0.01) and anti-C3 binding immune complexes also decreased in 5 out of 6 patients. These assays are described in detail and were also used to define in vitro interactions between the intravenous gammaglobulin preparation and heat-aggregated IgG or sera containing elevated circulating immune complexes. No reduction of immune complex levels were observed when IgG was incubated in vitro with either heat-aggregated IgG or sera with elevated immune complex concentrations. The duration of the in vivo effect and the patients' clinical responses are described. These findings show that high-dose intravenous gammaglobulin administration can reduce certain types of immune complexes in patients with elevated levels of these substances.

Adolescent↗

Human splenic Fc receptor function and dysfunction: definition by circulatory clearance rate compared to computerized kinetic scintigraphy.

In vivo reticuloendothelial Fc receptor function was studied in 14 individuals. To assess this function Tc-99m-labeled IgG-coated autologous erythrocytes were injected intravenously and circulatory clearance rates of radioactivity were determined. In 12 individuals [6 normals and 6 patients with systemic lupus erythematosus (SLE)], kinetic computerized scintigraphic imaging of various internal organs was compared to circulatory clearance rates. Both circulatory clearance rates and percentage splenic uptake (PSU) were significantly depressed in patients. The difference between patients and normals was more significant for PSU than for circulatory clearance. Splenic uptake curves showed significantly less linearity for patients, suggesting that splenic defects in SLE are not only quantitative, but also are qualitative. Understanding the nature of immune clearance defects in immune complex mediated diseases may allow for a more rational approach to treatment of patients with these disorders.

Adult↗

Serum sickness syndrome.

Numerous agents are known to cause serum sickness reactions. Although generally a benign disorder, serum sickness must be distinguished from various rheumatic and infectious disorders. The causative agent must be identified in order to avoid subsequent reactions. With the introduction of new drugs and biotechnically produced hormones and antibodies, new causes of serum sickness reactions are likely.

Anti-Bacterial Agents↗

Cold urticaria.

Cold urticaria is probably the most common form of physical urticaria. It is usually a chronic idiopathic disorder but may be secondary to another disease characterized by abnormal serum proteins with a cold-dependent property. In delayed cold urticaria, hives appear 24 to 48 hours after cold challenge. In addition to challenge testing, the physician should obtain serologic tests to exclude the presence of associated cold agglutinins, Donath-Landsteiner antibody, cryoglobulins and cryofibrinogen.

Cold Temperature↗

Fatal frontal sinusitis due to Neisseria sicca and Eubacterium lentum.

Infectious sinusitis may on occasion be associated with meningitis, subdural empyema, epidural empyema, brain abscess, or osteomyelitis. We report a 29-year-old male patient with frontal sinusitis who developed all of these intracranial complications due to two previously unreported causative organisms, Neisseria sicca and Eubacterium lentum. The fulminant and fatal course resulting from locally invasive disease underscores the importance of early diagnosis and proper treatment of these complications. Possible exacerbating factors in this patient were sickle cell disease and immune compromise due to intravenous drug abuse.

Adult↗

Multiple dermatofibromas and systemic lupus erythematosus.

We report on three black women with multiple dermatofibromas and systemic lupus erythematosus. In one patient occurrence of new dermatofibromas was definitely related to increases in corticosteroid dosage, but in another the dermatofibromas predated all treatment. Histopathologic, ultrastructural, and direct immunofluorescence studies of lesions of two of the patients showed characteristic changes of dermatofibroma but did not reveal a specific cause. This finding in patients with systemic lupus erythematosus is probably much more common than has previously been appreciated.

Adult↗