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Cells of the immune system synthesize prolactin and express mRNA and receptors for that hormone. Interleukin 1, interleukin 6, gamma interferon, tumor necrosis factor, platelet activator factor, and substance P participate in the release of prolactin. This hormone is involved in the pathogenesis of adjuvant arthritis and restores immunocompetence in experimental models. In vitro studies suggest that lymphocytes are an important target tissue for circulating prolactin. Prolactin antibodies inhibit lymphocyte proliferation. Prolactin is comitogenic with concanavalin A and induces interleukin 2 receptors on the surface of lymphocytes. Prolactin stimulates ornithine decarboxylase and activates protein kinase C, which are pivotal enzymes in the differentiation, proliferation, and function of lymphocytes. Cyclosporine A interferes with prolactin binding to its receptors on lymphocytes. Hyperprolactinemia has been found in patients with systemic lupus erythematosus. Fibromyalgia, rheumatoid arthritis, and low back pain patients present a hyperprolactinemic response to thyrotropin-releasing hormone. Experimental autoimmune uveitis, as well as patients with uveitis whether or not associated with spondyloarthropathies, and patients with psoriatic arthritis may respond to bromocriptine treatment. Suppression of circulating prolactin by bromocriptine appears to improve the immunosuppressive effect of cyclosporine A with significantly less toxicity. Prolactin may also be a new marker of rejection in heart-transplant patients. This body of evidence may have an impact in the study of rheumatic disorders, especially connective tissue diseases. A role for prolactin in autoimmune diseases remains to be demonstrated.

We performed prospective hormonal studies in 9 patients (5 active and 4 inactive) with systemic lupus erythematosus (SLE) during pregnancy (Weeks 10 to 37). Nine healthy pregnant women and 5 patients with rheumatoid arthritis (RA) were used for comparison. Serum prolactin (PRL), testosterone and estradiol (E2) levels were determined by RIA. The patients with SLE showed higher serum PRL levels, the difference being statistically significant at Week 20, and reaching the highest levels at Weeks 30 to 40 (p = 0.05 when compared to healthy pregnant women). The 5 patients with active SLE had the highest serum PRL levels; one of these had fetal wastage. In active SLE the serum testosterone and E2 levels were decreased significantly from Weeks 10 to 30 compared with controls (p = 0.001). In patients with RA serum PRL levels, although higher than in controls, did not differ significantly, nor did the lower testosterone and E2 levels. We conclude that gonadal hormones and PRL changes observed in SLE are present also during pregnancy and may be related to fetal wastage and reactivation of disease.

All 4 patients with transverse myelitis (TM) included in a prospective study of 500 patients with systemic lupus erythematosus (SLE) tested for anticardiolipin (aCL) antibodies were found to be positive. To determine if the apparently strong association between transverse myelitis and antiphospholipid antibodies (aPLA) in patients with SLE continued to hold, we chose 12 patients with SLE with transverse myelitis from 2 institutions. Eleven of the 12 patients with SLE were tested for aCL and all but one was positive. Most of them (n = 8) had both IgG and IgM isotype aCL. The one who was negative had had a positive VDRL and prolonged APTT 15 months earlier, coinciding with the episode of transverse myelitis. One patient died before she was tested for aCL but she also had a false positive VDRL. Thus, all 12 patients with SLE with transverse myelitis had evidence of aPLA. We conclude that there is strong association between transverse myelitis in SLE and the presence of aPLA.

HLA typing done in 10 Mexican mestizo patients with Behcet's syndrome revealed that 7 of them had HLA-B5 antigen as compared to a frequency of 31% in a Mexican mestizo control population. These findings are akin to those made in Japan and Turkey but differ from those made in Caucasian populations in the United States and Great Britain. Ethnic groups with a high frequency of HLA-B5 in Asia and America may belong to the same ancestral trunk. The occurrence of Behcet's syndrome in them may be more frequently HLA-B5 positive than in other ethnic groups.

The diversity of antibodies in patients with scleroderma, mixed connective tissue disease or "primary" Raynaud's phenomenon could be used as a laboratory aid in the clinical diagnosis. In serum samples of 75 patients we screened for antinuclear antibodies (HEp 2 cells), anti DNA, soluble nucleoprotein and extractable nuclear antigens (Sm, rRNP, U1-nRNP, SSA/Ro, SSB/La and Scl-70). Distinctive antinuclear antibodies pattern was identified in each group of patients. This immunologic profile is valuable for clinical diagnosis and the preferential association of certain autoantibodies with some diseases and not with others, suggest an antigen-driven stimulus for its production.

Hormonal abnormalities have been suggested to play a role in the pathogenesis of systemic lupus erythematosus (SLE). In order to define the regulatory mechanism involved, the pituitary reserve for gonadotropins secretion was investigated in eight untreated SLE patients with normal menstrual cycles. Serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were determined on the fifth day of the menstrual cycle before and after intravenous administration of 25 micrograms synthetic luteinizing hormone-releasing hormone (LH-RH). The pulsatile LH and FSH resting values in SLE were not significantly higher than those found in the controls; after LH-RH stimulation no difference was observed between the SLE group and controls. The LH and FSH response to exogenous LH-RH administration in SLE demonstrate the integrity of the hypothalamic-pituitary-ovary axis that explains normal menses and fertility in this disease.

We studied one hundred consecutive patients with rheumatoid arthritis from the cardiological point of view through non invasive methods to detect the frequency of cardiovascular complications. Seventy three (73%) were females and twenty seven (27%) males. Mean age, 48.6 years. Mean age of presentation of the disease, 34.2 years. Mean age of duration of the illness, 21.8 years. Fifty seven per cent had some type of cardiopulmonary complication. Clinically 52 per cent referred some type of cardiopulmonary symptoms. The physical examination was abnormal in 27 per cent. Rheumatoid factor (Waaler-Rose) was positive in 82 per cent. The cardiac X ray series was abnormal in 33 per cent, the resting electrocardiogram in 48 per cent and the M mode echocardiogram in 52 per cent of the cases. The complications detected were: pericardial effusion (21%); pleural effusion (9%); pulmonary fibrosis (6%) which represents a higher incidence of previously reported in the literature; congestive heart failure (10%); valvular lesion (9%) among those are included six patients with valvular heart disease of non detectable etiology; ischemic heart disease (8%); myocarditis (6%); rythm disturbances (22%) and conduction defects (20%) including a 46 year old female patient who developed a complete AV block during an exacerbation of her illness, requiring the insertion of definitive pacemaker. Our results showed that some of the detected lesions are in part more frequent and severe than those reported in the literature, probably due to, that on one hand their search was intentional and on the other, our group was constituted by with severe and long standing rheumatoid arthritis.

Human peripheral blood mononuclear cells showed increased synthesis and secretion of protein in response to stimulation by mitogens. Protein secretion in response to concanavalin A (Con A) correlated with cellular proliferation and originated from the proliferating cells. Selective depletion of either B lymphocytes or monocytes did not lead to a reduction in the total protein secreted, suggesting that the T lymphocyte was the cell contributing most of the synthetic activity. It is concluded that the measurement of newly synthesized and secreted protein by Con A activated mononuclear cells is a measurement of the T-lymphocyte response.

One case of the association of primary biliar cirrhosis and systemic sclerosis progressive (SSP) is described (Reynold's syndrome). This association has been reported in 21 patients. In our case the signs of liver disease precede two years the appearence of SSP. A review of the patients with Reynold's syndrome reported is done and compared with the present case. Diagnostic approach and management of this association is also discussed.

The hypothalamic-pituitary-gonadal axis was studied in 8 male patients with systemic lupus erythematosus (SLE), both before and after intravenous administration of luteinizing hormone-releasing hormone (LH-RH). We provide evidence herein that resting serum levels of estrone are increased and that resting serum testosterone (T) and dihydrotestosterone (DHT) levels are decreased in male patients with SLE. The decreased serum T levels were observed even after the IV administration of 25 micrograms of LH-RH. The high basal serum prolactin (PRL) levels observed in these patients with SLE is a novel finding not previously reported that could explain why serum T and DHT levels are low in this syndrome. We observed a decrease in the pituitary response to LH-RH stimulation; this low response could also be a hormonal manifestation of hyperprolactinemia. Furthermore, it has been suggested that PRL plays a role in immunocompetence, and therefore it could have influence either directly or indirectly in the altered immunoregulation observed in SLE.

In 1960 Rabinowitz and Dameshek emphasized the close relationship between idiopathic thrombocytopenic purpura (ITP) and systemic lupus erythematosus (SLE) and suggested that ITP is often a prodrome of SLE. On the basis of tis observation, the present study was designed to investigate the prevalence of SLE in patients with the initial diagnosis of ITP, autoimmune hemolytic anemia (AIHA), Fisher-Evans' syndrome (F-E) and idiopathic aplastic bone marrow (IABM) and to investigate the salient clinical manifestations and prognosis of these patients. We studied 62 patients, 35 with ITP, 16 with AIHA, 9 with F-E and 2 with IABM. Seventeen developed four or more ARA criteria for SLE within 6 of 14 years after the initial hematologic manfestations (IHM). Mucocutaneous symptoms predominated in all groups. None developed renal failure and only 2 had central nervous system involvement. When these patients were matched by age, sex and duration of illness with 24 SLE patients without hematologic abnormalities, the everity and therapeutic indices of the former showed a significantly (p 0.001) milder course. Eight of the 9 patients that required splenectomy are at present without treatment. SLE patient with IHM have a more benign course which is not worsened by splenectomy.

Salmonella bacteremia is more frequently seen in hospitalized patients with systemic lupus erythematosus (SLE) than in hospitalized patients with other diseases. In our experience. Salmonella enteritidis septic arthritis is more common in SLE than in patients with others connective tissue diseases. We report that 4 of 7 patients with SLE with glomerulonephritis and history of Salmonella enteritidis septic arthritis were chronic carriers of this bacteria, since positive cultures were obtained from feces, bone marrow and bile fluid from 20 84 months after Salmonella arthritis developed. In contrast, none of 24 patients with SLE without a history of Salmonella arthritis were chronic carriers and only one of 12 patients with rheumatoid arthritis had positive bile culture to S. typhi while otherwise being asymptomatic. From our study we conclude that patients with active SLE who have gomerulonephritis are at increased risk of becoming chronic carriers of Salmonella enteritidis and of developing Salmonella arthritis once combined prednisone cyclophosphamide treatment has begun. A chronic Salmonella carrier state must be ruled out in patients with active SLE living in endemic zones, before initiating immunosuppressive therapy.

A case of a 44 years old man with the unique combination of polyarteritis nodosa (PAN) and the congenital absence of a kidney is presented. The clinical picture consisted of fever, general symptoms, hypertermia, peripheric neuropathy, subcutaneous nodules and renal damage. Laboratory findings included increased WBC, telescoped urinary sediment, renal insufficiency, positive rheumatoid factor, policlonal gammopathy and positive Australia antigen. A review of the pertinent literature and the etiopathogenic role of Australia antigen in PAN is discussed. Efficacy of immunosuppressive therapy was evident in this case.

Forty three patients with systemic lupus erythematosus (SLE) were divided into three groups, inactive, active without treatment and active on treatment with steroids. T lymphocytes from peripheral blood were determined and the results compared with those of twenty five normal individuals. In further experiments, the mitogenic capacity of SLE lymphocytes to Con A and the serum's activity of these patients upon normal lymphocytes were analized. Decreased T lymphocytes were found in all groups of patients with SLE. There were no difference between the mitogenic response of SLE patients and controls when the lymphocytes were incubated with normal human AB serum. When normal lymphocytes were incubated with serum from SLE patients with active disease, and inhibition of mitogenic response to Con A was observed. These results suggests that the decrease cellular immunity observed in SLE is due to serum factors rather than to intrinsic T cell abnormality.

We report the first case of systemic lupus erythematosus with hyperviscosity syndrome as the presenting manifestation. A polyclonal increase in all immunoglobulins was observed. Ultracentrifuge studies showed 17-19S intermediate immune complexes (IC) composed primarily of autoreactive IgG demonstrated at acid pH. This was confirmed by chromatographic fractionation of sera, since the intermediate IC eluted as did purified heat aggregated IgG. Small amounts of IgM and IgA in the intermediate IC were also demonstrated by more sensitive techniques, i.e., nephelometry, polyacrylamide gel electrophoresis, and electrophoretic blotting. The decrease of serum viscosity was associated with the decrease of circulating IC after plasmapheresis or combined treatment of prednisone and cyclophosphamide. Serum viscosity bore no relationship to the amount of dissociated immunoglobulins.

Avulsion of the quadriceps tendons with primary hyperparathyroidism has been reported twice before. We describe a patient with primary type 1 hyperparathyroidism who developed well defined rheumatic symptoms in both knees as a consequence of bilateral rupture of the quadriceps tendons.