Biomedical subjects
Publications and source records attributed to R P Messner.
A 69 year old man presented with painful proximal muscle weakness which clinically simulated polymyositis. Further evaluation revealed normal muscle enzymes and hypophosphatemia which resulted from unsuspected antacid abuse. "Pseudo-myopathy" is one example of the myriad of rheumatic diseases which may be mimicked by hypophosphatemia.
Explore the source record for details and available documents.
The prevalence of lymphocytotoxic antibody was studied in 131 relatives of 10 patients with Hodgkin's disease. The study group contained nine families, five of which had two subjects with Hodgkin's disease. One hundred twenty-eight control family members were studied in parallel. Lymphocytotoxic antibody was present in 35.5% of all family members of patients with Hodgkin's disease, and in 8.6% of controls (P less than 0.01). Lymphocytotoxic antibody appeared primarily in consanguineous relatives irrespective of close personal household contact with the probands. The prevalence of the antibody was equal in both first- and second-degree relatives. These findings suggest at least a genetic and possibly an environmental influence in the genesis of lymphocytotoxic antibody among relatives of patients with Hodgkin's disease.
Nine individuals from four families of patients with systemic lupus erythematosus (SLE) were studied by sucrose density gradient fractionation and filter radioimmunoassay for the presence of 19S IgM and 7S IgG antibodies to DNA, poly rA, and poly rA-poly rU. One individual in each family was totally asymptomatic, and at least one had actively systemic lupus erythematosus (SLE). The results indicate: (1) a correlation between 7S antibody to DNA and RNA and active SLE, and (2) the presence of 19S antibody to RNA in the asymptomatic relatives. These findings suggest that SLE may be a disorder of immunological regulation. The distribution of antibodies between IgM and IgG is closely related to disease severity. the asymptomatic relatives may have a partial regulatory abnormality resulting in the limited production of IgM antibodies to RNA. SLE patients may have a more complex failure of regulation permitting the additional synthesis of IgG antibodies to DNA and RNA.
Pulmonary function was measured in a group of 28 patients with systemic lupus erythematosus (SLE) who were free of pulmonary involvement at the time of the study. When compared with age and sex matched controls, the SLE patients had a pattern of restriction with reduced lung volumes and vital capacity. Diffusing capacity was reduced in proportion to the reduction in lung volume. This is felt to be most compatible with inapparent pleural thickening resulting in impaired lung expansion. There was no evidence of airway obstruction on maximal expiratory flow-volume curves. The effect of cigarette smoking in the SLE patients was a reduction in flows at low lung volumes, which was indistinguishable from the effects in the control smokers. Both SLE and control smokers had a significant reduction in DL/VA when compared with control nonsmokers. Pulmonary function was not influenced by the presence of renal disease.
We encountered an unusual case of arthritis caused by Serratia marcescens, with both positive and negative birefringent crystals in the same inflammatory synovial fluid. This combination of events is most likely to occur in men over 40 years old who have a predisposing illness or are receiving immunosuppressive drugs. This case shows the need to consider multiple pathological processes occurring in the same joint.
The recent literature on CNS-SLE has been reviewed. An improved prognosis is noted that is thought to be due to the use of high-dose corticosteroids. The frequencies of the various neurologic and psychiatric findings are discussed, and a distinction is noted between organic psychoses and functional psychiatric complaints. The question of corticosteroids versus cerebral vasculitis as the cause of the neuropsychiatric symptomatology in SLE is examined, and the necessity of clear psychiatric diagnosis and treatment is stressed. Recent observations on HL-A antigens, complement, immunoglobulins, virus, and immunocomplexes suggest that the latter are prominent in CNS-SLE, but that an infectious agent may be etiologic in the genesis of SLE. Fifty-four patients not previously reported are discussed. Thirty-eight of them had neuropsychiatric manifestations. The treatment of CNS-SLE with cytotoxic agents, in addition to corticosteroids, is considered, and the experience of the authors with such treatment is presented.
Explore the source record for details and available documents.
57% of sera from 124 relatives of 28 patients with systemic lupus erythematosus (SLE) were found to have antibody directed against lymphocytes. The incidence in 60 members of 16 control families was 3%. Both consanguineous and nonconsanguineous relatives had the antibody in their sera. 68% of close household contacts of the SLE patients showed lymphocytotoxic antibody whereas only 23% of consanguineous relatives who had no household contact with the probands had this antibody. These data suggest that environmental factors may be important in the pathogenesis of SLE.
Anti-RNA antibodies were found in 82% of 28 systemic lupus erythematosus (SLE) probands and in 16% of 124 of their family members. The incidence in 76 control family members was only 5%. In the SLE family members, the antibodies were found exclusively in 21% of the 94 close household contacts of the probands. The incidence of anti-native DNA (nDNA) antibodies was 68% for the SLE probands. The incidence of anti-nDNA antibodies in close household contacts of the probands was 6%, which was not significantly different from the 1% incidence found in control families. Lymphocytotoxic antibodies occurred in 57% of the SLE family members as a whole and in 68% of the close household contacts. In the SLE probands, lymphocytotoxic antibodies correlated with anti-single-stranded RNA (poly A) and anti-nDNA but not with anti-double-stranded RNA (poly A-poly U). On the other hand, lymphocytotoxic antibodies in the household contacts correlated with anti-double-stranded RNA (poly A-poly U) but not with anti-poly A or anti-nDNA. The anti-RNA antibodies were present in consanguineous household contacts but not in nonconsanguineous household contacts. These findings strengthen the hypothesis that both an environmental agent, possibly a virus, as well as the genetic response are important in the pathogenesis of SLE. Family members may therefore be a logical population in whom to search for specific antibodies to a viral agent.
Six patients are described in whom panniculitis was a major manifestation of systemic lupus erythematosus. These patients were seen in a combined-clinics population of 270 patients with systemic lupus erythematosus for an incidence of approximately 2%. Panniculitis was the first symptom of systemic lupus erythematosus in three of these patients indicating that systemic lupus erythematosus should be considered as an underlying cause in patients with panniculitis or Weber-Christian's disease. Analysis of these six cases and those previously reported suggests that the addition of hydroxychloroquine to the treatment regimen may be beneficial in lupus panniculitis.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Peripheral blood lymphocytes from normal subjects as well as patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and active tuberculosis were studied for the relative distribution of bone marrow-derived lymphocytes (B-cells) and thymic-derived T-cells. B-cells were identified by direct immunofluorescence of surface Ig markers; T-cells were studied using rabbit antisera to pooled human fetal thymocytes absorbed with chronic lymphatic leukemia lymphocytes as a source of B-cells. In normal subjects, the sum of percentages of peripheral blood lymphocytes staining for surface Ig (B-cells) plus the percentage of cells staining with the absorbed antithymocyte antiserum closely approximated 100%. The mean value for percent B-cells among 51 normals tested was 22.9%+/-7.1; mean T-cells value was 75.3+/-13.95%. T-cell-specific antiserum stained 18% of normal human bone marrow lymphocytes, 42.5% of lymphocytes from normal spleens, and 98% of cells obtained from thoracic duct drainage of patients with RA. Specificity of antihuman thymocyte antiserum appeared to depend on the use of living cells. When patients with RA were examined, a wide range (14-98%) of peripheral blood T-cell values was found. Values for low percentages of peripheral blood T-cells appeared to correlate to some extent with severe clinical disease. In 11 of 36 RA patients, the sum of identifiable B- plus T-cells accounted for only 34-55% of peripheral blood lymphocytes. The identity of the remaining "null" cells could not be identified.3 of 24 SLE patients studied showed low percentages of peripheral blood T-cells, but no correlation could be drawn between T- to B-cell ratios and clinical disease activity. Among 21 patients with active tuberculosis, one had a low value for identifiable T-cells. No significant differences from normals in range or proportion of B-cells was identified in patients with active tuberculous infection.
Peripheral blood lymphocytes from 23 patients with active systemic lupus erythematosus (SLE) were serially studied. Changes in bone marrow-derived lymphocytes (B cells), as measured by surface Ig receptors and C3 receptors, and in thymus-derived cells (T cells) measured by rabbit T-cell-specific antiserum and E-binding techniques, were correlated with fluctuations in clinical disease activity and treatment. In normal controls B- and T-cell percentages remained relatively stable, although the situation in SLE was much more labile. A relative and absolute decrease in T lymphocytes and cells bearing a receptor for C3 was found in active lupus. Absolute numbers of cells bearing surface Ig were decreased to a lesser extent, whereas the proportion of these cells was increased. It is postulated that the increase in autoantibody formation and diminished delayed hypersensitivity seen in systemic lupus may be due to a loss of T-lymphocyte function.
Explore the source record for details and available documents.
Explore the source record for details and available documents.