A patient with rheumatoid arthritis taking prednisone developed Blastocystis hominis acute diarrhoea, which was associated with increased inflammation and effusion of the left knee. B hominis organisms were found in synovial fluid from the left knee. The patient responded dramatically to metronidazole treatment. B hominis may become disseminated in immunosuppressed patients with diarrhoea and may cause infective arthritis. Abdominal examination disclosed tenderness in the lower abdomen. Rectal examination was normal. Sigmoidoscopy showed mild to moderate erythema and oedema of the rectal mucosa. Histology of the rectal mucosa was nondiagnostic, however. The haemoglobin concentration was 64 g/l with a hypochromic, microcytic blood film. The total leucocyte count was 81 -x I09 cells/l with 62% neutrophils, 36% lymphocytes, and 2% eosinophils. The erythrocyte sedimentation rate (ESR) was 150 mm in the first hour. Radiology disclosed unequivocal periarticular osteoporosis in the hands, and mild joint space narrowing of the metacarpophalangeal joints and hips bilaterally. There were marginal erosions of the proximal interphalangeal and right metacarpophalangeal joints. The rheumatoid factor, antinuclear factor, and antibodies to double stranded DNA were negative. The total serum complement level was 1-95 g/l (normal 1-22-1-66 g/l). The HIV test was negative. Joint fluid aspirated from the left knee was turbid and the leucocyte count was 38 x 109/1 with 100% neutrophils.Treatment was started with cefotaxime intravenously for presumed infectious arthritis of the knee pending results of joint fluid, blood, and stool cultures. There was no improvement after five days. Routine aerobic and anaerobic cultures of blood, synovial fluid, urine, and endocervical swab were all negative.Examination of synovial fluid (light microscopy, trichrome stain) from the left knee showed B hominis organisms. Stool specimens also disclosed large numbers of B hominis organisms (>5 per high power field). Culture for salmonella, shigella, campylobacter, and other parasites was negative.Drug treatment was switched to metronidazole 400 mg eight hourly for two weeks. The abdominal pain, diarrhoea, and left knee inflammation subsided over the next five to seven days. Repeat knee aspirate and stools were negative for B hominis. There was no recurrence of the knee inflammation at follow up four months after discharge from hospital.

The prevalence of HTLV-I antibodies was evaluated in Jamaica among persons with various malignant, infectious, autoimmune and hematologic disorders and in clinically normal persons. Results document that: (1) the prevalence of HTLV-I antibodies in this population increases with age; (2) overall, there is no significant difference in the antibody prevalence between males and females; (3) antibody-positive individuals are born in all major regions of the island and geographical variance in antibody prevalence by place of birth was not prominent; (4) there is further confirmation of the high prevalence of HTLV-I antibody-positive lymphomas in Jamaica; and (5) the prevalence of HTLV-I antibodies in hemophiliacs, patients with chronic lymphocytic leukemia (CLL), myelogenous leukemias, and patients with breast cancer is higher than in the age-matched population without malignancies, although none of these differences were statistically significant. The increased prevalence in hemophiliacs is most likely related to their frequent transfusion with blood products, but it has not yet been determined whether the prevalence in patients with other diseases is related to their diseases or other as yet undefined factors in common.

Background The abnormal biological activity of cytokines plays an important role in the pathophysiology of both systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). Several studies have highlighted the association of vitamin D and certain pro-inflammatory cytokines with disease activity in SLE. However, there are limited data on the association of vitamin D and antiphospholipid antibodies (aPL) with various proinflammatory biomarkers in these patients and their relative impact on clinical outcomes. Methods The serum levels of several aPL, 25-hydroxy vitamin D, pro-inflammatory cytokines including IFNα, IL-1β, IL-6, IL-8, IP10, sCD40L, TNFα and VEGF were measured in 312 SLE patients from the Jamaican (n-=45) and Hopkins (n=267) Lupus cohorts using commercial Milliplex and ELISA assays. Oxidized LDL/β2glycoprotein antigenic complexes (oxLβ2Ag) and their associated antibodies were also measured in the Jamaican cohort. Healthy controls for oxidative marker and cytokine testing were utilized. Results Abnormally low vitamin D levels were present in 61.4% and 73.3% of Hopkins and Jamaican SLE patients respectively. Median concentrations of IP10, TNFα, sCD40L and VEGF were elevated in both cohorts, oxLβ2Ag and IL-6 were elevated in the Jamaican cohort and IFNα, IL-1β and IL-8 were the same or lower in both cohorts compared to controls. IP10 and VEGF were independent predictors of disease activity, aPL, IP10 and IL-6 were independent predictors of thrombosis and IL-8 and low vitamin D were independent predictors of pregnancy morbidity despite there being no association of vitamin D with pro-inflammatory cytokines. Conclusions Our results indicate that aPL-mediated pro-inflammatory cytokine production is likely a major mechanism of thrombus development in SLE patients. We provide presumptive evidence of the role IL-8 and hypovitaminosis D play in obstetric pathology in SLE but further studies are required to characterize the subtle complexities of vitamin D’s relationship with cytokine production and disease activity in these patients.

Vitamin D has important effects on the immune system as it has been shown to exert antiproliferative and relative immunosuppressant effects. Low levels of this hormone may contribute to the immune activation in systemic lupus erythematosus (SLE) and other autoimmune diseases. Serum levels of 25-OH vitamin D were measured in 75 patients with SLE in Jamaica, using an enzyme-linked immunoassay. Correlations with clinical data and disease activity as determined by the BILAG index were determined. Of a total of 75 patients, 33 (44%) had vitamin D sufficiency with mean vitamin D level of 39.45 ng/ml (range, 30.35-58.16). Forty-two (56%) patients had either vitamin D deficiency or insufficiency, 30 (40%) had vitamin D insufficiency, mean 26.36 ng/ml (range, 20.26-29.88), and 12 (16%) had vitamin D deficiency, mean 16.07 ng/ml (range, 7.78-19.90). There was an overall negative relationship between the total disease activity score using the BILAG index and vitamin D levels, and this was influenced primarily by the relationship seen among the vitamin D-deficient subgroup. This was also impacted on by a patient population that was significantly skewed toward low disease activity. The negative association trended toward statistical significance. Vitamin D deficiency is prevalent among patients with SLE in Jamaica. A relationship between low serum levels of vitamin D and SLE activity may occur.

We examined CD4+ T cell TCRBV-CDR3 transcripts from 19 lupus patients and 16 controls to test the hypothesis that CD4+ TCRBV-CDR3 expression in SLE differs from normals. Within the disease group we also performed exploratory analyses to determine the association between risk of oligoclonality and HLA-DRB specificities and the duration of the CDR3 patterns. Oligoclonal patterns consistent with CDR3 restriction were three times more likely in SLE than in controls (OR = 3.7). TCRBV1, BV4, BV5.1, BV7, BV9, BV18 and BV22 gene segment CDR3 patterns of oligoclonality were seen exclusively among lupus patients. HLA-DRB3 increased the risk of oligoclonal expression in SLE. In four patients studied over time, the pattern of TCRBV-CDR3 expression was stable in a second sample obtained 6-14 months later. The increased frequency of CD4+ T cell TCRBV-CDR3 oligoclonal expression in SLE when compared to controls and the persistence of these patterns are consistent with an expanded pool of autoreactive CD4 T cells in SLE which recognize peptides derived from autoantigens. The association of HLA-DRB3 genes with increased risk of CDR3 oligoclonality among the SLE subjects is compatible with the hypothesis that molecules encoded by HLA-DRB3 may facilitate autoantigen recognition by CD4 T cells.