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A case of selective IgM deficiency with giant leiomyoma of the stomach in a 66-year-old male is reported. Peripheral blood mononuclear cells from the patient synthesized only a small amount of IgM in the presence of pokeweed mitogen (PWM) in vitro. Co-culture of counterpart lymphocytes from the patient and a disease-free individual revealed that increased activity of IgM-specific suppressor T lymphocytes led to a IgM deficiency in this case.

The significance of Oreactive protein (CRP) elevation in patients with systemic lupus erythematosus (SLE) in the pretreatment stage was assessed with reference to other laboratory data obtained simultaneously. Sixteen of 31 cases were CRP-positive, and the CRP-positive group contained significantly more cases with urinary cellular casts and with a high anti-DNA antibody titer, compared with the CRP-negative group. We suggest that CRP in patients with SLE, as measured at the time of the first consultation, reflects the severity of the disease. This includes those cases complicated by nephropathy.

To examine the temporal relationship between the DTH skin reaction to HBsAg and antibody response to HBsAg, serial skin tests for HBsAg were carried out on seven individuals immunized with HB vaccine. All cases developed both a skin reaction and antibody response. In many cases, the DTH skin reaction appeared four weeks before the antibody response. These data suggest that DTH skin reaction may be a more sensitive method than humoral antibody assessment for monitoring the success of vaccination.

In an attempt to find a reliable method to assess fever in patients with systemic lupus erythematosus (SLE), a multifactorial analysis was applied to the routine laboratory examinations, including white blood cell count (WBC) and serum globulin fraction concentrations. During 74 febrile episodes, 49 SLE patients showed increased disease activity and the remaining 25 febrile episodes were due to intercurrent infection. The two different groups of fever episodes were clearly separated by a principal component analysis using five variables from the routine laboratory tests, including WBC, serum alpha-1, alpha-2, beta, and gamma globulins. Discriminant analysis showed that 95% of 74 febrile episodes could be correctly classified as to the cause of fever when a combination of WBC and alpha-2 globulin level was used as variables. A simple discriminant formula which we calculated was considered to be of practical use for the differentiation of the two clinical entities.

We measured alpha 2-plasmin inhibitor-plasmin complexes (PI-PC) in plasma of patients with systemic lupus erythematosus (SLE) to examine the plasminogen activation in SLE. The plasma PI-PC level in 23 patients with SLE was significantly higher than that in 18 normal subjects (P less than 0.001) and the SLE patients with nephrotic syndrome had higher plasma PI-PC levels than those without nephrotic syndrome (P less than 0.01). In addition, the plasma PI-PC level was significantly correlated with the level of plasma C3 breakdown products (iC3b/C3dg) in the patients with SLE (r = 0.53, P less than 0.01). These results suggest that plasminogen is activated in plasma of patients with SLE and that the plasminogen activation may be associated with the activation of complement in SLE.

Angiotensin converting enzyme (ACE) is a carboxyl terminal dipeptidyl dipeptidase, which is known to convert angiotensin I to angiotensin II (Ang II) and to hydrolyze bradykinin and enkephalin. In the brain, ACE is located in endothelial cells of capillaries throughout the brain, in the subfornical organ, and in the brush border of choroidal epithelial cells in contact with cerebrospinal fluid [1]. Administration of Ang II into the brain ventricles induces thirst [2], a rise in arterial blood pressure, and secretion of vasopressin [3]. Recently, the specific binding of Ang II to the membrane fraction of canine brain microvessels was detected, suggesting the role of Ang II in regulation of the brain microcirculation and transport across the blood-brain barrier [4]. Since ACE in the brain microvessels might affect the brain microcirculation by modulating the local production of Ang II, we measured ACE activity in brain microvessels obtained from 13-week-old spontaneously hypertensive rats (SHR), Wistar-Kyoto rats, and SHR of the same age under antihypertensive therapy to clarify the effect of hypertension on the brain microvessels.

We studied the expression of an iC3b neoantigen (iC3b-NEO) in plasma from patients with systemic lupus erythematosus (SLE), by using a monoclonal antibody specific for iC3b/C3dg/C3d, to investigate the activation of the third component of complement in SLE. The plasma iC3b-NEO level in 40 untreated patients with active SLE was significantly higher than that in 36 normal subjects (mean +/- SD 31.5 +/- 13.9 micrograms/ml versus 12.3 +/- 3.3 micrograms/ml; P less than 0.001). The plasma iC3b-NEO level was highly correlated with clinical disease activity (tau = 0.62, P less than 0.0001), and it was the parameter most closely correlated with renal histologic activity in lupus nephritis (tau = 0.52, P less than 0.0001). Also, patients with diffuse proliferative lupus nephritis had the highest levels of plasma iC3b-NEO among all World Health Organization classes of lupus nephritis (P less than 0.01). We conclude that the plasma iC3b-NEO level is strongly associated with clinical disease activity and renal histologic activity in patients with SLE, and that plasma iC3b-NEO may be a sensitive and useful measure of complement activation in SLE.

We measured U1-RNP: anti-U1-RNP immune complexes (U1-RNP ICs) in patients with mixed connective tissue disease (MCTD) and systemic lupus erythematosus (SLE) to examine the clinical significance of circulating U1-RNP ICs. The level of U1-RNP ICs in 11 patients with MCTD was significantly higher than that in 22 normal subjects and there was a close correlation between the level of U1-RNP ICs and the clinical disease activity index of MCTD. In contrast, the level of U1-RNP ICs in 31 patients with SLE was not significantly higher than that in normal subjects and that was not correlated with the clinical disease activity index of SLE or the renal histologic activity index of lupus nephritis. We conclude that U1-RNP ICs are present in sera of patients with MCTD and SLE, and that the level of U1-RNP ICs may be closely associated with clinical disease activity in patients with MCTD.

Intracellular pH in platelets from spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY) was measured using a pH-sensitive fluorescent dye, 2',7'-bis(carboxyethyl)carboxyfluorescein tetraacetoxy methyl ester (BCECF). Intracellular pH in platelets was significantly higher in SHR than in WKY (7.12 +/- 0.04 versus 7.06 +/- 0.02, P less than 0.01; n = 10). There was a close correlation between intracellular pH and systolic blood pressure (r = 0.66, P less than 0.01). Addition to platelets of 1-(5-isoquinolinesulphonyl)-2-methylpiperazine (H-7), a specific inhibitor of protein kinase C, produced a significantly larger decrease in intracellular pH in SHR than in WKY (0.06 +/- 0.02 versus 0.03 +/- 0.00, P less than 0.01, n = 5). These results suggest that protein kinase C may play an important role in the increased intracellular pH in SHR.

We developed a solid-phase radioimmunoassay for complement (C)-fixing nuclear ribonucleoprotein (nRNP):anti-nRNP immune complexes (nRNP ICs). The assay was based on the ability of the C-fixing nRNP ICs to bind strongly to immobilized F(ab')2 anti-C3. The extent of binding was quantified by incubating the C-fixing nRNP ICs bound to anti-C3 with 125I-labeled anti-nRNP-specific IgG. The interaction between anti-C3 and C-fixing nRNP ICs was rapid, time- and concentration-dependent and sensitive over a broad range of nRNP IC concentrations in an antigen-antibody ratio of 8 : 1 (9.8-5000 ng of human aggregated IgG equivalent per ml). We found that the assay also detected an immunoreactive U1-RNP antigen in Sm : anti-Sm immune complexes but did not detect SSA : anti-SSA immune complexes. The assay was preliminary applied for serum samples obtained from patients with mixed connective tissue disease (MCTD), and elevated concentrations of nRNP immune complexes were found in 3 out of 5 patients with MCTD. This assay appears to be applicable to the detection and quantification of circulating nRNP ICs in patients with MCTD.

Serum concentrations of interferon alfa, interleukin 1, and tumour necrosis factor alpha were measured in 25 untreated patients with systemic lupus erythematosus (SLE). A close correlation was found between serum concentrations of interferon alfa and the degree of fever, while no significant correlations were found between fever and interleukin 1 or tumour necrosis factor alpha. These results suggest the possible involvement of interferon alfa in the pathogenesis of fever in SLE.

• The relationship between the renal pathologic activity of systemic lupus erythematosus (SLE) and serum lactate dehydrogenase (LDH) was examined in 28 patients with active SLE involving only the kidney. Serum levels of total LDH, LDH1, and LDH2 were significantly higher in the patients with diffuse proliferative lupus nephritis (World Health Organization class IV) than in those with milder renal disease (classes I through III and V). Total LDH levels showed good correlations with the activity index and the total pathologic score of the renal pathologic scoring system, and with the glomerular hypercellularity and overall deposits. The elevated level of LDH was mainly due to elevated levels of its isozymes LDH1 and LDH2. These results suggest that the elevation of serum LDH levels in patients with SLE reflects the renal pathologic changes due to lupus nephritis. (Arch Intern Med1986;146:548-552)

Examination of 27 patients with systemic lupus erythematosus (SLE) before treatment showed an elevation of the serum level of lactic dehydrogenase (LDH) in 15 patients. In these patients, the LDH level fell to normal in response to corticosteroid therapy. In six of 27 patients, steroid myopathy with elevation of the LDH level developed during corticosteroid therapy. At the same time, there was no or only a slight increase in the creatine phosphokinase level, while the SGOT and aldolase levels remained normal. The elevated LDH levels gradually returned to normal as the corticosteroid dosages were reduced and the myopathic symptoms disappeared. We suggest that the measurement of LDH levels is useful for diagnosis and the subsequent treatment of patients with steroid myopathy in SLE. ( Arch Intern Med 1981;141:1176-1179)