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ID PMID Title PublicationDate abstract
17321482 Survival of TNF toxicity: dependence on caspases and NO. 2007 Jun 15 Tumor necrosis factor (TNF) is an endogenous pro-inflammatory cytokine, implicated in pathologies such as rheumatoid arthritis and septic shock. It was originally discovered as a factor with extraordinary antitumor activity, but its shock-inducing properties still prevent its systemic use in cancer. Clinical trials revealed hypotension as the major dose-limiting factor of TNF toxicity. When administered to mice, TNF provokes a lethal shock syndrome, where cardiovascular collapse is centrally orchestrated by nitric oxide (NO). Nevertheless, NO synthase (NOS) inhibition in animal models and septic shock patients could not improve and even aggravated outcome, suggesting a bivalent role for NO. Lymphocyte and enterocyte apoptosis has been described in septic, endotoxemic, or TNF-treated animals, as well as in septic patients. In this review, we describe our recent studies on the role of NO and caspases in TNF-induced shock in mice. In summary, we have found that both NO and caspases may exert unexpected and dual functions during TNF shock. Whereas excessive NO production provokes lethal hypotension, it also has an important anti-oxidant function, protecting organs from oxidative stress and lipid peroxidation. In addition, our results also indicate that caspases may exert an important endogenous negative feedback on oxidative stress as well.
17255558 Gene silencing in severe systemic inflammation. 2007 Apr 15 This critical care perspective appraises reprogramming of gene expression in inflammatory diseases as an emerging concept of clinical importance. We emphasize gene reprogramming that "silences" acute proinflammatory genes during severe systemic inflammation, wherein in the systemic inflammatory response syndrome (SIRS) exists as a continuum during severe sepsis, septic shock, and the multiorgan dysfunction and failure phenotypes without infection. In contrast, silencing of acute proinflammatory genes is not apparent in sites of localized inflammatory processes like rheumatoid arthritis. We discuss in three parts the clinical context and the translational basic science associated with gene silencing during the SIRS continuum of severe systemic inflammation: (1) reprogramming of acute proinflammatory genes; (2) a "nuclear factor-kappaB paradox," coupled with RelB expression, that combine to silence genes using an epigenetic (inherited and reversible) signature on the nucleosome; and (3) the potential clinical importance of compartmentalization in gene silencing. Our emergent understanding of these physiologic processes may provide a novel framework for developing treatments.
17245215 High plasma osteopontin levels in patients with inflammatory bowel disease. 2007 Feb BACKGROUND: Osteopontin (OPN) plays a key role in the progression of T(H)1-immune-mediated disease in models of multiple sclerosis and rheumatoid arthritis. AIM: To determine whether plasma OPN levels in patients with inflammatory bowel disease are associated with disease activity. METHODS: Plasma samples were obtained from patients with ulcerative colitis (UC, n=30), Crohn's disease (CD, n=30), and healthy volunteers (controls, n=30) and enzyme immunoassay was performed. RESULTS: Plasma OPN concentrations were significantly higher in patients with Crohn's disease than in controls (951.9+/-538.5 ng/mL and 659.0+/-163.7 ng/mL, respectively). OPN concentrations in patients with UC were also higher than in the controls (1149.6+/-791.0 and 659.0+/-163.7, respectively). There was a significant difference in plasma OPN level between active UC and inactive UC (2102.0+/-552.8 and 649.4+/-313.0, respectively). Moreover, a significant correlation was observed between plasma OPN concentration and disease activity, as determined by the clinical activity index in patients with UC. CONCLUSIONS: Our results indicate that the plasma concentrations of OPN are elevated in patients with UC and that OPN expression is correlated with clinical activity. These results provide insight into UC pathogenesis and suggest that OPN may be a useful tool for assessing disease activity.
17215861 Involvement of macrophage migration inhibitory factor gene in celiac disease susceptibilit 2007 Mar The MIF gene has been associated with several diseases with inflammatory and autoimmune background, such as ulcerative colitis, rheumatoid arthritis and systemic lupus erythematosus. We aimed at testing the influence of two functional MIF promoter variants in celiac disease (CD) susceptibility. A (CAAT)(5-8) tetranucleotide repeat at position -794 and a single-nucleotide polymorphism at -173G/C were analyzed in the Spanish population (531 patients and 887 healthy controls). chi(2) statistics or Fisher exact test were used for comparisons. The -173C allele significantly increased risk ((CC+GC) vs GG: odds ratio (OR) (95% confidence interval (CI))=1.41 (1.10-1.81); P=0.005), as did carriage of the (CAAT)(7) allele (OR (95% CI)=1.36 (1.02-1.82); P=0.03) and of the haplotype (CAAT)(7)//-173C (OR (95% CI)=1.33 (1.00-1.76); P=0.04). Our data evidence for first time the role of the MIF gene increasing predisposition to CD. A common effect of MIF variants seems to underlie the etiology of these complex conditions.
17210529 The role of anti-endothelial cell antibody-mediated microvascular injury in the evolution 2007 Feb We encountered 16 patients with connective tissue disease in whom pulmonary fibrosis developed. Routine light microscopic, ultrastructural, and direct immunofluorescent analyses were conducted, and circulating antibodies, including those of endothelial cell derivation, were assessed using indirect immuno-fluorescence and Western blot assays. Underlying diseases were dermatomyositis, scleroderma, mixed connective tissue disease, sclerodermatomyositis, Sjögren syndrome, rheumatoid arthritis, and anti-Ro-associated systemic lupus erythematosus. Antibodies to one or more Ro, RNP, Jo 1, OJ, and/or nucleolar antigens were seen in all cases and antiphospholipid antibodies in half. All biopsies revealed microvascular injury in concert with intraparenchymal fibrosis; in some cases, there were corroborative ultrastructural findings of microvascular injury. Patterns of fibroplasia represented nonspecific interstitial pneumonitis and usual interstitial pneumonitis. We noted IgG, IgA, and/or complement in the septal microvasculature. In 6 cases with available serum samples, indirect immunofluorescent endothelial cell antibody studies were positive and Western Blot studies showed reactivity of serum samples to numerous endothelial cell lysate-derived proteins. Pulmonary fibrosis, a recognized complication of systemic connective tissue disease, develops in connective tissue disease syndromes with pathogenetically established immune-based microvascular injury at other sites. A similar mechanism of antibody-mediated endothelial cell injury may be the basis of the tissue injury and fibrosing reparative response.
17081761 Discovery and synthesis of new immunosuppressive alkaloids from the stem of Fissistigma ol 2007 Jan 15 Three new alkaloids (1-3) and twenty-one known compounds were isolated from the stem of Fissistigma oldhamii (Hemsl.) Merr. which was the ruler herb in an approved Traditional Chinese herbal formula used for treatment of rheumatoid arthritis in China and synthesis of one new immunosuppressive alkaloid was achieved. These compounds, including the crude extracts of this herb, exhibited strong activities in the inhibition of T and B cell proliferation.
17039308 Evaluation of Pneumocystis pneumonia infection risk factors in patients with connective ti 2006 We conducted a retrospective, clinical evaluation of connective tissue disease (CTD) patients who were tested for either sputum or bronchoalveolar lavage fluid Pneumocystis polymerase chain reaction (PC-PCR) and analyzed the risk factors that cause Pneumocystis pneumonia (PCP) susceptibility and fatality. PC-PCR was performed on 66 CTD patients who presented with symptoms, data, or radiological findings strongly suggesting respiratory infection. Patients with higher oral corticosteroid doses, use of oral methotrexate (MTX), bilateral lung findings, positive beta-D-glucan, and no prophylaxis use were more susceptible to PCP. They had significantly low immunoglobulin G and significantly high beta-D-glucan and lactate dehydrogenase. Survivors and nonsurvivors of PCP were also evaluated. Poor prognoses were observed with older age, elevated beta-D-glucan, rheumatoid arthritis (RA) patients using MTX, hypoxemia, bilateral lung findings, and mechanical ventilation use. Nonsurvivors had significantly lower lymphocytes, oxygen saturation, and significantly higher beta-D-glucan. In RA, poor prognoses were seen with those taking MTX. Disease duration, underlying pulmonary complications, and oral corticosteroid doses did not lead to poor prognoses in RA. Because PCP in CTD leads to abrupt onset of symptoms with poor survival rates, early diagnosis and initiation of treatment are critical, and it is essential for clinicians to recognize risk factors that predispose patients to PCP and its mortality.
17038928 Temporomandibular joint cyst presenting as trigeminal neuropathy and middle fossa mass: ca 2006 Oct OBJECTIVE: We describe the case of a temporomandibular joint cyst eroding into the middle fossa, initially causing compression of the trigeminal nerve and trigeminal neuropathy, and ultimately causing destruction of the second division of the nerve with facial numbness. CLINICAL PRESENTATION: A 50-year-old woman with rheumatoid arthritis on prednisone developed right-sided, initially lancinating facial pain that ultimately became dull in nature in the maxillary division of the trigeminal nerve. This change in pain was associated with the development of numbness in the same distribution. The facial pain gradually resolved, but the facial numbness persisted. Imaging revealed a heterogeneously enhancing mass in the middle fossa lateral to Meckel's cave. INTERVENTION: During surgery, the dura was elevated, and a smooth, firm lesion with several thinly encapsulated, cystic areas containing viscous, white fluid was identified. The mass had eroded through the floor of the middle cranial fossa. The thick, fibrous capsule was freed from the bone edges and was sectioned sharply extracranially. Pathological evaluation was consistent with a cyst originating from the temporomandibular joint. CONCLUSION: Extracranial mass lesions involving the middle fossa structures are uncommon and typically arise from the parotid gland. This case represents the first example of a middle fossa mass originating from an abnormal temporomandibular joint and a unique cause of trigeminal neuropathy. After excision, there has been no recurrence after 2 years of follow-up.
16967610 [Polymyalgia rheumatica and giant cell arteritis--first results of a year-long study]. 2006 Jul INTRODUCTION: Due to ageing of population, gerontorheumatology becomes more and more important. Both polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) typically develop in later life and they have many other common features. The aim of our study was to explore diagnostic and prognostic markers and, prospectively, establish diagnostic and therapeutic algorithm for patients with PMR and GCA. SAMPLE AND METHODS: We examined 27 patients with suspected PMR or OBA. The diagnosis was verified in 22 patients. Three of them were in a long-term clinical remission. Besides examination for basic clinical and laboratory parameters, all other patients were subjected to ultrasonography of temporal artery and peripheral joints to detect any exudates. Also, they were examined for T-cell subpopulations in peripheral blood and HLA antigens. RESULTS: Exudate was confirmed in 7 patients; some of them had exudate in multiple joints. Puncture of synovial fluid was done in 4 patients. Increased resistance index of temporal artery was found in 2 patients with GCA and 4 patients with PMR. GCA patients showed lower level of T-cells and increased activation of CD8-cells. Decreased count of CD8+ T-cells was observed in 56 % of PMR patients. Analysis of HLA antigens indicates that GCA, rheumatoid arthritis and, probably, PMR are associated with HLA-DR4 antigen in Slovak population. CONCLUSION: The importance of assessment of disease activity and its prognosis in PMR or GCA patients via ultrasonographic evaluation of exudate in peripheral joints and resistance index of temporal artery as well as the analysis of T-cell distribution in peripheral blood and incidence of HLA-antigens has not been proved yet. Practical significance of monitoring the above-mentioned parameters can be verified only by further prospective study performed with a larger sample of patients.
16943108 Hepcidin is not a marker of chronic inflammation in atherosclerosis. 2006 Sep OBJECTIVE: To investigate the relationship between atherosclerosis, an inflammatory disease and hepcidin, which is reported as an indicator of inflammation. METHODS: A total of 75 subjects between 40 and 70 years of age were included in the study. The patient group consisted of 40 stable patients who had previously experienced an atherosclerotic event (18 women, 22 men; mean age 56.4+/-7.1 years). There were two control groups. The first control group consisted of 19 healthy subjects (11 women, 8 men; mean age 52.6+/- 7.4 years), while the second group included 16 patients (11 women, 5 men; mean age 56.5+/-9.3 years) with rheumatoid arthritis and anemia (diseased control group). Hepcidin measurement was performed using Hepcidin Prohormone ELISA (Solid Phase Enzyme-Linked Immunosorbent Assay) test kit. RESULTS: Mean serum hepcidin levels were 243.2+/-48.8 ng/ml, 374.5+/-86.4 ng/ml, and 234+/-59.9 ng/ml in the patient group, in diseased controls, and in healthy controls, respectively. Hepcidin levels were higher in diseased controls compared to the patient group and healthy controls (p=0.001). There were no significant differences between the patient group and healthy controls. CONCLUSION: These findings did not support the hypothesis that hepcidin levels could be increased in atherosclerotic cardiovascular diseases as a marker of chronic inflammation.
16720637 Towards a pro-inflammatory and immunomodulatory emerging role of leptin. 2006 Aug Leptin is a 16 kDa adipocyte-secreted hormone that regulates weight centrally and links nutritional status with neuroendocrine and immune function. Since its cloning in 1994, leptin's role in regulating immune and inflammatory response has become increasingly evident. Actually, the increase of leptin production that occurs during infection and inflammation strongly suggests that leptin is a part of the cytokines loop which governs the inflammatory-immune response and the host defence mechanism. Indeed, leptin stimulates the production of pro-inflammatory cytokines from cultured monocytes and enhances the production of Th1 type cytokines from stimulated lymphocytes. Several studies have implicated leptin in the pathogenesis of autoimmune inflammatory conditions such as type 1 diabetes, rheumatoid arthritis and chronic bowel disease. Obesity is characterized by elevated circulating leptin levels which might contribute significantly to the so called low-grade systemic inflammation, making obese individuals more susceptible to the increased risk of developing cardiovascular diseases, type II diabetes or inflammatory articular degenerative disease such as osteorathritis (OA). As a matter of fact, a key role for leptin in OA has been recently demonstrated since leptin exhibits, in synergy with other pro-inflammatory cytokines, a detrimental effect on articular cartilage cells by promoting nitric oxide synthesis. This review will focus prevalently on the complex relationships existing among leptin, inflammatory response and immunity, trying to provide surprising insights into leptin's role and to discuss challenges and prospects for the future.
16622723 A case of interstitial pneumonia caused by bucillamine: a study using serological markers. 2006 The patient was a 61-year-old man diagnosed with rheumatoid arthritis (RA) in 2001. He initially received treatment at a nearby clinic, but his condition could not be satisfactorily controlled. He subsequently consulted our hospital during the same year. Although his symptoms improved in response to treatment at our hospital, slight fever, cough, and then high fever and dyspnea subsequently developed. A diagnosis of interstitial pneumonia was made on the basis of findings of diagnostic imaging. The time course of changes in serological markers, including surfactant protein A (SP-A), surfactant protein D (SP-D), and KL-6, as well as markers of inflammatory reaction and lactate dehydrogenase was examined to determine the clinical significance of serological markers in the management of interstitial pneumonia.
16597207 Probiotics: their role in the treatment and prevention of disease. 2006 Apr A probiotic is a "live microbial food ingredients that, when ingested in sufficient quantities, exerts health benefits on the consumer". Probiotics exert their benefits through several mechanisms; they prevent colonization, cellular adhesion and invasion by pathogenic organisms, they have direct antimicrobial activity and they modulate the host immune response. The strongest evidence for the clinical effectiveness of probiotics has been in their use for the prevention of symptoms of lactose intolerance, treatment of acute diarrhea, attenuation of antibiotic-associated gastrointestinal side effects and the prevention and treatment of allergy manifestations. More research needs to be carried out to clarify conflicting findings on the use of probiotics for prevention of travelers' diarrhea, infections in children in daycare and dental caries, and elimination of nasal colonization with potentially pathogenic bacteria. Promising ongoing research is being conducted on the use of probiotics for the treatment of Clostridium difficile colitis, treatment of Helicobacter pylori infection, treatment of inflammatory bowel disease and prevention of relapse, treatment of irritable bowel syndrome, treatment of intestinal inflammation in cystic fibrosis patients, and prevention of necrotizing enterocolitis in premature infants. Finally, areas of future research include the use of probiotics for the treatment of rheumatoid arthritis, prevention of cancer and the treatment of graft-versus-host disease in bone marrow transplant recipients.
16549141 Outcome of kidney transplantation for renal amyloidosis:a single-center experience. 2006 Mar The aim of this retrospective study was to investigate the results of kidney transplantation in patients with renal amyloidosis. We analyzed the results of renal transplantation in 13 amyloidotic transplant recipients compared with those in a control group of 13 nonamyloidotic patients. While the etiology of amyloidosis was rheumatoid arthritis in one patient, in all of the others it was secondary to familial Mediterranean fever. Acute rejection episodes developed once in six and twice in one patient. The renal function in these patients was improved by antirejection treatment. Chronic rejection did not develop in any patient. However six patients (46%) died due to various complications despite functional grafts. The others are still being followed with well-functioning grafts. Among the control group, acute and chronic rejection were diagnosed in three and two patients, respectively: one patient returned to hemodialysis after 26 months of transplantation, while the others are still alive with functional grafts. There was no death in the control group. The 5- and 10-year actuarial patient survival rates of the amyloidosis and control groups were 52.2%, 26.6%, and 100%, 100%, respectively (P = .002). However, the graft survivals of the amyloidosis versus control groups were 100%, 100%, versus 87.5%, 87.5, respectively (P = .47). In conclusion, we observed a high rate of early mortality among recipients with amyloidosis associated with infectious complications. Moreover, patient survivals were lower among amyloidotic renal recipients.
16540268 Low density multiparticulate system for pulsatile release of meloxicam. 2006 Apr 26 A blend of floating and pulsatile principles of drug delivery system would have the advantage that a drug can be released in the upper GI tract after a definite time period of no drug release. A multiparticulate floating-pulsatile drug delivery system was developed using porous calcium silicate (Florite RE) and sodium alginate, for time and site specific drug release of meloxicam. Meloxicam was adsorbed on the Florite RE (FLR) by fast evaporation of solvent from drug solution containing dispersed FLR. Drug adsorbed FLR powder was used to prepare calcium alginate beads by ionotropic gelation method, using 3(2) factorial design. Developed formulations were evaluated for yield, entrapment efficiency, image analysis, surface topography, mechanical strength, apparent density, buoyancy studies and dissolution studies. Entrapment efficiency of different formulations varied from 70% to 94%. Formulations show a lag period ranging from 1.9 to 7.8 h in acidic medium followed by rapid release of meloxicam in simulated intestinal fluid USP, without enzymes (SIF). Complete drug release in SIF occurred in less than 1h from the formulations. The size of beads varied from 2.0 to 2.7 mm for different batches. Prepared beads were spherical with crushing strength ranging from 182 to 1,073 g. Floating time was controlled by density of beads and hydrophobic character of drug. A pulsatile release of meloxicam was demonstrated by a simple drug delivery system which could be useful in chronopharmacotherapy of rheumatoid arthritis.
16529558 Cyclooxygenase inhibitory natural products: current status. 2006 Non-steroidal anti-inflammatory drugs (NSAIDs) are of huge therapeutic benefit in the treatment of rheumatoid arthritis and various types of inflammatory conditions. The target for these drugs is cyclooxygenase (COX), a rate-limiting enzyme involved in the conversion of arachidonic acid into inflammatory prostaglandins. COX-2 selective inhibitors are believed to have the same anti-inflammatory, anti-pyretic and analgesic activities as that of nonselective inhibitor NSAIDs with little or none of the gastrointestinal side effects. Thus, in the last 6-7 years several selective COX-2 inhibitors including coxibs were discovered and introduced into clinic. Recent reports evidence that selective COX-2 inhibitor such as rofecoxib, can lead to thrombotic cardiovascular events through inhibition of prostacyclin formation in the infracted heart. This has resulted in withdrawal of rofecoxib from the clinic in September 2004. Moreover, the COX-2/COX-1 selectivity ratio is vital in the design of COX-2 inhibitory drugs, as it is clear from rofecoxib, which is more than 50-fold COX-2 selective. After looking at all above mentioned facts, natural product-based compounds seem better as these compounds are generally supposed to be devoid of severe side effects. The literature indicates that natural product-based compounds are mainly COX-1 selective. Through minor semi-synthetic changes in the structures, their selectivity towards COX-2 can be increased. The present review article addresses natural product COX inhibitors of plant and marine origin, reported during last ten years and their advantages, possible leads for further development and current status. In addition we describe our experience in the characterization, design and synthesis of potential natural COX inhibitors.
15952187 Effects of fish oil treatment on bleomycin-induced pulmonary fibrosis in mice. 2006 Sep Bleomycin is an antibiotic used to treat a variety of neoplasms. A major side-effect of bleomycin therapy is the induction of an intense inflammatory response that develops into pulmonary fibrosis. Several studies have shown that certain polyunsaturated fatty acids found in fish oil reduce the inflammatory response in vivo. Fish oil has been employed for the treatment of several pathologies such as glomerulonephritis, cardiovascular diseases, rheumatoid arthritis, and even as an adjuvant in cancer therapy. This study examined the effects of fish oil treatment on the development of bleomycin-induced pulmonary fibrosis. Mice were intraperitoneally treated with bleomycin or with saline daily for 10 days, and 15 days after the last injection they started to receive fish oil by gavage for 14 days. The lungs were processed for light microscopy, biochemical and immunohistochemical investigations. Fish oil did not prevent the development of pulmonary fibrosis after the injury as shown by light microscopy, cytokines immunohistochemical analysis, TBARS content and protein levels in the lung. In addition however, fish oil itself induced a slight inflammatory process in the lung, as observed by the increase in cellularity, vasodilatation in the lung parenchyma, TBARS content, and a slight increase in the lung protein content.
18703106 STAT4: a risk factor for type 1 diabetes? 2008 Oct Genes and mechanisms involved in autoimmune diseases, affecting approximately 5% of human population, remain still obscure but there is accumulating evidence that common genetic factors might predispose to multiple autoimmune disorders. STAT4, a transcription factor transmitting signals induced by several key cytokines, has recently been identified as a genetic risk factor for rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Sjögren's disease (SD), thus indicating that multiple autoimmune diseases may share common biochemical pathways that lead to immune deregulation. Here we demonstrate for the first time, in a genetically homogeneous population, the association of the STAT4 rs7574865 G/T polymorphism, which has been shown to be associated with these autoimmune diseases, with susceptibility to type 1 diabetes (T1D). The susceptibility is associated with a significant increase of the frequency of the T allele (p = 0.0012, two-tailed chi(2), OR = 1.94, 95% CI = 1.29-2.91) in this single-nucleotide polymorphism (SNP). We also present an indication for association with Wegener's granulomatosis. These findings suggest that this variant form of STAT4 may have a putative key role in the development of a variety of autoimmune diseases, probably because of signaling defects that it causes in the IL-12 pathway.
18694362 Investigational C-C chemokine receptor 2 antagonists for the treatment of autoimmune disea 2008 Sep BACKGROUND: C-C chemokine receptor 2 (CCR2) antagonists belong to a group of chemokine blockers, which represent a new strategy for inflammatory diseases treatment by interfering with the complex system of chemokines and their receptors. A number of CCR2 antagonists are being developed for treatment of autoimmune diseases by different pharmaceutical and biotechnological companies. OBJECTIVE: In this article the dark and the bright side of therapeutic CCR2 antagonism is discussed, with a view to its potential efficacy in various autoimmune diseases, in which clinical trials are already in progress, such as multiple sclerosis and rheumatoid arthritis. We describe different modes of possible interactions with CCR2-chemokine CC motif ligand 2 (CCL2) axis, usefulness of experimental animal models, continuing clinical trials and future perspectives of CCR2 antagonists. METHODS: Until now only a few peer-reviewed articles providing data on the progress of preclinical and clinical trials with CCR2 antagonists have been published; therefore, we also present data based on preliminary reports, obtained from a number of press releases, conference communications and from the PharmaProjects database. RESULTS/CONCLUSION: Although there is growing evidence for a great therapeutic potential of CCR2 blockade in autoimmune diseases, especially well documented in experimental animal models, so far clinical trials with CCR2 antagonists in humans have been moderately encouraging or even disappointing, indicating a need to further elucidate the complex system of chemokine interactions.
18591340 Re-activation of bovine tuberculosis in a patient treated with infliximab. 2008 Jul Treatment with tumour necrosis factor-alpha inhibitors increases the risk of tuberculosis (TB). Screening for latent TB infection (LTBI) and prophylactic treatment has become mandatory. A 79-yr-old female with a history of severe erosive sero-positive rheumatoid arthritis was screened for LTBI before initiation of treatment with infliximab. The tuberculin skin test (TST) was negative, chest radiography was normal and she had no known risk factors for TB. After 4 months of treatment with infliximab, the patient developed ascites caused by Mycobacterium bovis. The TST was repeatedly negative. QuantiFERON-TB (QFT) testing performed during screening and immunosuppressive treatment was indeterminate, whereas the QFT test performed at the time of ascites puncture was positive. The patient history revealed previous work at a dairy, with probable exposure to unpasteurised milk from M. bovis-infected cattle. Re-activation of bovine tuberculosis is a risk in people with recent or previous exposure to unpasteurised dairy products. The QuantiFERON-TB test has the potential to detect Mycobacterium bovis infection. Indeterminate test results reflect either anergy, due to poor immunity, or technical problems and should be cautiously interpreted and as a minimum be repeated. Studies are ongoing to determine the role of QuantiFERON-TB testing in the screening for latent tuberculosis infection.