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The association of SLE with tuberculosis (TB) was studied in a group of 388 patients with SLE monitored between 1953-1994. TB was diagnosed in 14 patients (3.6%). The occurrence of septic fevers in SLE patients that did not respond to glucocorticoid therapy indicated the possibility of complication with TB. SLE-associated TB included miliary and far-advanced pulmonary and extrapulmonary forms. Three patients from our group died due to myco-bacterial infection and one patient died of active SLE and TB. The treatment was successful in nine patients. Early diagnosis and appropriate management are mandatory in SLE associated TB, which otherwise may have a potentially fatal outcome.

Prolonged repeated analyses of sera from 98 patients with systemic lupus erythematosus (SLE) and 76 patients with similar diffuse diseases of connective tissue by a radioisotope membrane binding method for the assessment of antibodies against double-stranded ribonucleic acid (anti-ds-RNA) revealed that these antibodies are most frequently encountered in patients with the evolutive form of SLE (53%), but also in approximately one fifth of patients with non- evolutive SLE and in patients with similar diffuse diseases of connective tissue. Anti-ds-RNA are not linked with stages of clinical activity; their occurrence is on the whole independent on the occurence of antibodies against ds-DNA and nuclear ribonucleoprotein. There is a very close association with the incidence of antibodies against denatured DNA and a substantially small association with antibodies against acid nuclear antigen (Sm). The occurrence of anti-ds-RNA is a favourable prognostic sign, as in the majority of patients who had such antibodies at any time in their serum, later the disease can be suppressed by treatment, while patients who never had anti-ds-RNA in serum remain for a long time in the active stage of the disease.

A family with hereditary C2 deficiency was discovered in Czechoslovakia. The proband is a 47-year-old female with a SLE-like syndrome and zero activity of the classical complement pathway. Functional CH50, C1, C2, and C4 estimations for all family members revealed a homozygous C2 deficiency in both the proband and her elder sister, and several heterozygotic C2-deficient individuals. The defect segregates with haplo-type HLA A25, B18, DR2.

A correlation was made between the severity of clinical symptoms of SLE and the results of the migration inhibitory factor (MIF) production test. For this purpose 10 patients with various manifestations of SLE were examined by MIF production test before and after the immunosuppressive therapy. A good correlation between the actual clinical stage and the results of the MIF production test was found. The successful immunosuppressive therapy turned the positive MIF production into the negative one in most of the observed patients. The MIF production test is therefore recommended as a good complementary test for the estimation of the actual state of the SLE.

The simultaneous occurrence of interferon and migration inhibitory factor was found in sera from 9 patients with systemic lupus erythematosus (SLE). Their clinical picture was characterized by a moderate course of the disease. In 7 patients the inflammatory tendoarticular manifestations were accentuated. Glomerulonephritis was found only in 3 patients and was successfully suppressed by immunosuppressive therapy. In the peripheral blood of most of these patients, normal or moderately increased levels of active E-rosettes were found. Therefore we consider these SLE patients as a group with characteristic signs of activated cell-mediated immunity (lymphokine release, active E-rosettes). Although the reason for this activation remains unknown, we suppose that some concomitant bacterial infection, perhaps mycobacterial, may contribute to this immunological phenomenon.

During a period of 4 years urine samples from 54 patients with systemic lupus erythematosus (SLE) were repeatedly analysed for the activities of lactate dehydrogenase (LDH), leucine aminopeptidase (LAP) and alanine aminopeptidase (AAP). Increased urinary enzyme levels were consistently found in 8 patients with severe lupus nephritis and the nephrotic syndrome, as well as in 9 patients with chronic lupus nephritis resistant to therapy. A further group of 9 patients with lupus nephritis responded favourably to immunosuppressive therapy with arrest of kidney-damaging processes; a concomitant normalization of urinary enzyme levels was observed, giving an accurate reflection of the progression of the disease. Another 14 SLE patients showed raised enzyme levels preceding the development of clinical signs of nephropathy. The last 14 SLE patients displayed neither nephropathy nor altered enzyme activities. The determination of urinary enzyme activities is, therefore, considered to be a useful supplement to the routine biochemical analyses performed on the urine in cases of SLE.