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ID PMID Title PublicationDate abstract
10820281 Thiol-reactive metal compounds inhibit NF-kappa B activation by blocking I kappa B kinase. 2000 Jun 1 Gold compounds are used in the treatment of rheumatoid arthritis. NF-kappa B is a transcription factor implicated in the expression of many inflammatory genes. NF-kappa B is activated by signal-induced phosphorylation and subsequent degradation of inhibitory I kappa B (inhibitory protein that dissociates from NF-kappa B) proteins, and a multisubunit I kappa B kinase (IKK) has been identified previously. We tested the effect of various gold compounds on the activation of NF-kappa B and IKK in LPS-stimulated RAW 264.7 mouse macrophages. A lipophilic gold compound, auranofin, suppressed the LPS-induced increase of nuclear kappa B-binding activity, degradation of I kappa B proteins, and IKK activation. Auranofin also blocked IKK activation induced by TNF and PMA/ionomycin, suggesting that the target of auranofin action is common among these diverse signal pathways. In vitro IKK activity was suppressed by addition of hydrophilic gold compounds, such as aurothiomalate, aurothioglucose, and AuCl3. Other thiol-reactive metal ions such as zinc and copper also inhibited IKK activity in vitro, and induction of IKK in LPS-stimulated macrophages. In vitro IKK activity required the presence of reducing agent and was blocked by addition of thiol group-reactive agents. Two catalytic subunits of IKK complex, IKK alpha and IKK beta, were both inhibited by these thiol-modifying agents, suggesting the presence of a cysteine sulfhydryl group in these subunits, which is critical for enzyme activity. The antiinflammatory activity of gold compounds in the treatment of rheumatoid arthritis may depend on modification of this thiol group by gold.
9336656 High frequency of neoplasia in patients with autoantibodies to centromere protein CENP-F. 1997 Oct OBJECTIVE: To study the clinical features of patients with autoantibodies to centromere protein CENP-F and the frequency of CENP-F autoantibodies in patients with various diseases. DESIGN: Retrospective clinical and serologic study. METHODS: Thirty-six patients with anti-CENP-F were identified by a characteristic pattern of indirect immunofluorescence (IIF) on HEp-2 cells. Fifty patients with melanoma, 50 with breast cancer, 10 with lung cancer, 354 with systemic sclerosis, 120 with systemic lupus erythematosus and 50 with rheumatoid arthritis were also studied. Recombinant proteins were produced from 5 CENP-F cDNA clones representing amino acids 2192-3317 (p-F1), 5561-7126 (p-F2), 5892-6883 (p-F3), 7538-10,116 (p-F4) and 9242-10,096 (p-F5). The presence of CENP-F antigen was studied in a breast carcinoma cell line, cryosections of breast carcinoma, normal breast tissue and tonsils. RESULTS: Twenty-two of 36 patients with CENP-F antibodies had neoplasms; breast (9/22) and lung (5/22) cancer were the most common diagnoses. Thirty-three sera were available for further study; when tested for reactivity to the recombinant peptides, the sera of 21 of 21 patients with neoplasms and 5 of 12 patients with other diseases bound the C-terminal p-F4 peptide. When the terminal third of the p-F4 peptide (p-F5) was studied, a significant difference in pattern of reactivity was not detected. By comparison, the frequency of reactivity with peptides representing other domains of CENP-F was less than that with p-F4 (p-F2 > p-F3 > p-F1). CENP-F autoantibodies were not found in any of the control sera from patients with systemic lupus erythematosus, rheumatoid arthritis or systemic sclerosis or in unselected sera from various malignancies. CENP-F antigens were identified in breast carcinoma tissue but were rarely observed in normal tissues. CONCLUSIONS: A high proportion of individuals with CENP-F antibodies have neoplasia, and there is a bias among their sera for reactivity with determinants in the carboxy terminal domain of CENP-F. CENP-F antigens appear to be highly expressed in malignant tissues.
15989628 Phospholipase A2 inhibitors in development. 1997 Mar To date, three isoforms of phospholipase A2 (PLA2) have been identified. Of these, the two Ca2+-dependent isoforms, secretory (sPLA2) and cytosolic phospholipase A2 (cPLA2), are targets for new anti-inflammatory drugs. The catalytic mechanisms and functions of the third isoform, Ca2+-independent cytosolic phospholipase A2 (iPLA2), are unknown at present. sPLA2 and cPLA2 are both implicated in the release of arachidonic acid and prophlogistic lipid mediators. However, recent findings provide evidence that cPLA2 is the dominant isoform in various kinds of inflammation, such as T-cell-mediated experimental arthritis. A triple function of PLA2-derived lipid mediators has been suggested: causing immediate inflammatory signs, involvement in secondary processes, e.g., superoxide free radical (O2) generation, apoptosis, or tumour necrosis factor-alpha (TNF-alpha)-cytotoxicity, and controlling the expression and activation of pivotal proteins implicated in inflammation and cell development, e.g., cytokines, adhesion proteins, proteinases, NF-kappaB, fos/jun/AP-1, c-Myc, or p21ras. In the past, research predominantly focused on the development of sPLA2 inhibitors; however, present techniques enable discrimination of cPLA2, sPLA2, and iPLA2, and specific inhibitors of each of the three isoforms are likely to appear soon. Over the last decade, between 40 and 50 sPLA2 inhibitors have been described; and the list is growing. However, of these, few have the potential for clinical success, and those that do are predominantly active site-directed inhibitors, e.g., BMS-181162, LY311727, ARL-67974, FPL67047, SB-203347, Ro-23-9358, YM-26734, and IS-741. At present, there are no likely clinical candidates emerging from the ranks of cPLA2 and iPLA2 inhibitors in development. Indications for which PLA2 inhibitors are being pursued include, sepsis, acute pancreatitis, inflammatory skin and bowel diseases, asthma, and rheumatoid arthritis. The three main obstacles to the successful development of PLA2 inhibitors include, insufficient oral bioavailability, low affinity for the enzyme corresponding to low in vivo efficacy and insufficient selectivity.
11862320 Vasoactive intestinal peptide in the immune system: potential therapeutic role in inflamma 2002 Jan Vasoactive intestinal peptide (VIP), a neuropeptide that is produced by lymphoid as well as neural cells, exerts a wide spectrum of immunological functions, controlling the homeostasis of the immune system through different receptors expressed in various immunocompetent cells. In the last decade, VIP has been clearly identified as a potent anti-inflammatory factor, which acts by regulating the production of both anti- and pro-inflammatory mediators. In this sense, VIP has been described to prevent death by septic shock, an acute inflammatory disease with a high mortality. In addition, VIP regulates the expression of co-stimulatory molecules, this being an action that may be related to modulating the shift toward Th1 and Th2 differentiation. We have recently reported that VIP prevents the deleterious effects of an experimental model of rheumatoid arthritis, by downregulating both inflammatory and autoimmune components of the disease. Therefore, VIP has been proposed as a promising candidate alternative treatment for acute and chronic inflammatory and autoimmune diseases such as septic shock, arthritis, multiple sclerosis, Crohn disease, or autoimmune diabetes.
10325665 The detection of DNA from a range of bacterial species in the joints of patients with a va 1999 Mar OBJECTIVE: Bacteria have been implicated in the pathogenesis of many types of inflammatory arthritides. The aim of this study was to identify any bacterial DNA in synovial fluid (SF) from patients with a range of inflammatory arthritides. METHODS: A highly sensitive, broad-range, nested polymerase chain reaction (PCR) protocol targeting the bacterial 16S rRNA gene was designed and applied to SF from 65 patients with a range of rheumatic diseases. RESULTS: Bacterial DNA was detected in 26 SF samples, including eight from patients with rheumatoid arthritis and five with juvenile arthritides. PCR products were identified by sequencing and searching of bacterial genomic databases; 'best fits' included Haemophilus influenzae, Bordetella and Yersinia. CONCLUSIONS: These finding suggest an association between bacterial infection and inflammatory arthritides in some patients. Further research is required to determine the role of these organisms in the pathogenesis and whether such patients might respond to prolonged antibiotic therapy.
9567207 Update on clinical trials in the rheumatic diseases. 1998 Mar Therapeutic trials in rheumatoid arthritis (RA), osteoarthritis, seronegative spondyloarthopathies, back pain, systemic lupus erythematosus, and systemic sclerosis are reviewed. For RA, minocycline has been proven effective in some subsets of RA, whereas tumor necrosis factor receptor IgG fusion protein appears quite effective for treating the symptoms of RA in a more resistant group. The latter trial illustrates the importance of tumor necrosis factor in RA. Also, the triple combination of hydroxychloroquine, sulfasalazine, and methotrexate is very effective even in resistant RA. In osteoarthritis, the effects of nonsteroidal anti-inflammatory drugs, intra-articular steroids, and biologics are reviewed, with generally nondifferentiable nonsteroidal anti-inflammatory drug effects and some short-term intra-articular effects of new biologics. Sulfasalazine is moderately effective for ankylosing spondylitis and psoriatic arthritis, although the large placebo response in the latter makes it more difficult to show responses. Trials in the treatment of back pain are beginning to be published, with a large cohort study over 1 year favoring surgery for early relief of pain in both sciatica and lumbar stenosis, but not showing a clear advantage in functional outcome at 1 year. Finally, early reports show the ability of dihydroepiandrosterone to decrease steroid use in systemic lupus erythematosus, whereas Relaxin appears to be effective in decreasing skin involvement in systemic sclerosis. These trials demonstrate in numerous ways the need to consider the elements of good trial design when testing therapeutic modalities in the rheumatic diseases. These key elements include 1) careful patient definition and selection; 2) removal of bias (requiring blinding, randomization, prospective studies, and often, placebo); 3) use of well-defined outcomes; and 4) careful analytic techniques.
9540786 [Problems associated with the use and monitoring of cyclosporin. Experience at a Clinical 1997 Dec BACKGROUND: A study on cyclosporine A (CyA) monitoring in the January 1992-December 1995 period is reported. The aim of this work was to give epidemiological data on the use of CyA, to verify the progressive increase of CyA determinations and to evaluate the use in other diseases as well as to compare the different technics of CyA assay in blood samples, to stress the timing of blood samples and to underline the CyA monitoring importance. METHODS: The CyA dosage was evaluated by fluorescence polarization immunoassay (FPIA) and high-performance liquid chromatography (HPLC). RESULTS: The study showed that 70% of CyA determinations come from patients undergone to renal, bone marrow and liver transplantations; the remaining 30% was associated to other diseases (psoriasis, uveitis, diabetes, rheumatoid arthritis). CONCLUSIONS: The results obtained showed a progressive and constant increase of CyA determinations. Moreover, the use of drug was increased in autoimmune diseases. It is stressed that CyA monitoring in blood samples is essential to optimize the therapeutic efficacy of drug and minimizing its toxicity.
9150112 Stem cell transplantation for severe autoimmune disorders, with special reference to rheum 1997 May Animal models of autoimmune disease have been successfully used to explore peripheral stem cell transfusion and bone marrow transplantation. Allogeneic marrow transplants have been shown to suppress lupus-like disease and experimental allergic encephalomyelitis. Autologous transplantation has also been successful in adjuvant arthritis. Operationally, these may be considered as graft versus autoimmunity effects. In humans, adoptive autoimmunity, in which the donor becomes apparent in the recipient, has been documented for myasthenia gravis and insulin dependent diabetes mellitus. Of 9 allogeneic bone marrow transplants for rheumatoid arthritis, 4 patients have done well for many years while one relapsed after 2 years. In 2 cases, autologous marrow transplant has been used specifically to treat autoimmune disease: one patient with CREST had only a transient response and one patient with myasthenia gravis had remission. While allogeneic bone marrow transplant is the most rational procedure, its use in nonmalignant disorders must be very carefully considered secondary to its toxicity and potential morbidity. The use of peripheral blood CD34+ cells with T cell depletion, may promise complete or partial longterm remission but results of this therapy need to be compared with other immunosuppressive combinations.
9107563 Molecular mimicry: can epitope mimicry induce autoimmune disease? 1997 Apr Mimicry of host antigens by infectious agents may induce cross-reactive autoimmune responses to epitopes within host proteins which, in susceptible individuals, may tip the balance of immunological response versus tolerance toward response and subsequently lead to autoimmune disease. Epitope mimicry may indeed be involved in the pathogenesis of several diseases such as post-viral myocarditis or Chagas disease, but for many other diseases in which it has been implicated, such as insulin-dependent diabetes mellitis or rheumatoid arthritis, convincing evidence is still lacking. Even if an epitope mimic can support a cross-reactive T or B cell response in vitro, its ability to induce an autoimmune disease in vivo will depend upon the appropriate presentation of the mimicked host antigen in the target tissue and, in the case of T cell mimics, the ability of the mimicking epitope to induce a proliferative rather than anergizing response upon engagement of the MHC-peptide complex with the T cell receptor. B cell presentation of mimicking foreign antigen to T cells is a possible mechanism for instigating an autoimmune response to self antigens that in turn can lead to autoimmune disease under particular conditions of antigen presentation, secondary signalling and effector cell repertoire. In this review evidence in support of epitope mimicry is examined in the light of the necessary immunological considerations of the theory.
11196524 The arthritis of inflammatory childhood myositis syndromes. 2001 Jan OBJECTIVE: Arthritis has been an associated finding in juvenile dermatomyositis (JDM), but its prevalence, course, and response to therapy has not been well described. We investigated the frequency, course, and clinical and radiographic features in a large cohort of patients with JDM. METHODS: The charts of 94 patients with idiopathic myositis (1984-99) were reviewed: 80 JDM, 3 juvenile polymyositis (JPM), 5 amyopathic JDM, and 6 overlap myositis syndromes. Compiled data included demographics, clinical features, a detailed description of the arthritis, investigations (radiographs, autoantibodies), course, and response to therapy. All radiographs were independently reviewed by a single radiologist. RESULTS: Sixty-one percent (95% CI 50-72%) of patients with JDM had arthritis. The arthritis was reported a median 4.5 mo (range -73.6 to 76.6 mo) after the JDM onset. When compared to patients with no arthritis, the occurrence of arthritis was not significantly related to sex, race, positive antinuclear antibody or rheumatoid factor, calcinosis, nodules, vasculitis, or Raynaud's phenomenon. The initial involvement was pauciarticular in 67% and polyarticular in 33%. In the pauci group, asymptomatic knee effusions were the predominant finding (n = 19, 58%), and in 18 patients may have been the result of steroid therapy. Two patients evolved from a pauci onset to a polyarticular course. All responded to therapy (corticosteroids; 47 were taking other medications) with remission of the arthritis within a median of 2.0 mo (range 0.1-64.5 mo). However, the arthritis recurred in 39% as the corticosteroids were tapered. Four patients with JDM eventually required corticosteroid wrist injections, with resolution of the arthritis. The arthritis was nonerosive in all cases. No patient with JPM had arthritis. Three of 5 patients with amyopathic JDM and 4 of 6 with overlap myositis syndrome had a nonerosive polyarthritis. CONCLUSION: Nonerosive arthritis involving the knees, wrists, elbows, and fingers is a frequent manifestation of JDM and other idiopathic childhood myositis. The arthritis is seen early in the course of JDM and often responds to treatment. However, the arthritis may recur with tapering of corticosteroids despite remission of the JDM. In a significant proportion of JDM cases, arthritis is the major sequela and may warrant further medical therapy or intraarticular corticosteroid injections.
11731212 Tuberculous arthritis mimic arthritis of the Sjögren's syndrome: findings from sonography 2001 Dec A patient with a history of Sjögren's syndrome developed chronic arthritis of left ankle. It was diagnosed as arthritis of the Sjögren's syndrome initially. However, joint pain persisted despite corticosteroid therapy. Sonography disclosed a multiloculated cystic lesion with peripheral hyperechoic enhancement around left ankle and extended to Achilles tendon and subcutaneous region. Computed tomography (CT) confirmed the findings. Magnetic resonance imaging (MRI) revealed increased signal intensity of the lesion after gadonillium enhancement on T1-weighted images. These abnormalities showed inhomogenous high signal intensities on T2-weighted images. Tuberculous arthritis was diagnosed by positive synovial tuberculous culture. Sonography is a valuable tool that offers significant advantages for the initial evaluation of arthritis of the Sjögren's syndrome and help early suspicious of tuberculous arthritis, because of its cost-effectiveness, superior differentiation between the cyst and solid lesions, convenience for guiding biopsy and drainage.
11719687 Salivary glands and lesions: evaluation of apparent diffusion coefficients with split-echo 2001 Dec The authors investigated the feasibility of performing diffusion-weighted (DW) magnetic resonance (MR) imaging with split acquisition of fast spin-echo signals (hereafter, split echo) for the assessment of salivary glands and salivary lesions. Eighteen patients without salivary disease and 10 patients with Sjögren syndrome, chronic parotitis, or focal salivary masses underwent split-echo and echo-planar DW MR imaging. DW MR images and apparent diffusion coefficient maps of the salivary gland had higher quality with split-echo rather than with echo-planar DW MR imaging.
10883527 [Renal scleroderma crisis. Role of scleroderma vasculopathy in the induction of cutaneous 2000 Jan Although fibrosis and vasculopathy coexist in most patients with progressive systemic sclerosis, it is not clear if these events are the result of an unique etiologic factor or if one is consequence of the other. We report two cases of progressive systemic sclerosis that evolved to a renal scleroderma crisis. A 36 years old female presented with a Sjögren syndrome and painful subcutaneous nodules whose biopsy showed perivascular lymphocytic infiltration, perivascular thickening and normal skin. The ESR was 100 mm/h. She developed an hypertensive crisis and progressive renal failure, followed by a rapidly evolving progressive systemic sclerosis. The patient died in the course of this crisis. A 32 years old female with a progressive systemic sclerosis refractory to D-penicillamine treatment, receiving cyclosporin, presented a renal scleroderma crisis, that was successfully treated, with complete recovery of renal function. We highlight the different evolution of these cases, probably due to an early diagnosis and a better experience in the management of this condition.
10403284 Octreotide treatment of chronic intestinal pseudoobstruction secondary to connective tissu 1999 Jul Chronic intestinal pseudoobstruction (CIPO) is a rare syndrome that may occur in association with connective tissue diseases (CTD). Effective management is a major challenge. We report 3 cases in which subcutaneous octreotide was efficacious in the treatment of digestive symptoms in CIPO. In 2 of the 3 cases, previous treatment with domperidone, cisapride, or erythromycin had been unsuccessful. All 3 patients underwent a regimen of oral antibiotics along with octreotide to stimulate small bowel motility. The effects of octreotide were evident within 48 hours after the first injection in all patients. In 2, the efficacy seemed to decrease after 1 week and 6 months respectively, but increasing the dosage led to another remission. CIPO in CTD is a severe condition that can evolve regardless of the underlying disease activity. Octreotide appears to be efficacious in improving both clinical symptoms and manometric patterns. When its therapeutic effect diminishes, increasing the dosage can be useful.
9427040 Sex-specific patterns of spleen recolonization in semiallogeneic "Sjögren-mice". 1997 Sep "Sjögren-mice" were produced by the transfer of two entire spleen equivalents of cells from parental strain mice to non-irradiated, adult F1 hybrids. The recipients developed an autoimmune exocrinopathy resembling primary Sjögren's syndrome. Since donor and host mice are haploidentical, no new antigens are introduced into the recipients. Donor cells may react against recipient antigens, eliciting a graft versus host (GVH) reaction. The origin of spleen cells was investigated by flow cytometry, using antibodies against murine MHC antigens. The results showed different colonization patterns: spleens of female recipients, grafted with cells from female donors, were almost completely colonized by donor type cells, whereas spleens of male recipients, grafted with either male or female cells, showed partial or complete colonization by donor type cells. The results suggest that the sex of both donor and host influences cellular reactions in lymphohaemopoietic chimeras.
11200724 Localised nodular pulmonary amyloidosis in a patient with sicca syndrome. 2000 Sep A 52 year old Chinese woman with a 25 year history of sicca syndrome (primary Sjogrens syndrome) was investigated for 3 episodes of haemoptysis. Clinical examination was unremarkable except for the presence of dry eyes and xerostomia. Computed tomography of the chest revealed a lobulated mass in the posterior basal segment of the left lower lobe. Histopathological examination of this resected nodule confirmed the diagnosis of nodular amyloidosis. The normal radiolabelled serum amyloid P component scintigraphy and the absence of monoclonal plasma cell dyscrasia in the bone marrow strongly support the diagnosis of localised nodular pulmonary AL amyloidosis in this patient. Nodular pulmonary amyloidosis can be associated with sicca syndrome and often simulates bronchogenic carcinoma, bronchiectasis or pulmonary tuberculosis.
11070934 [Autoimmune hemolytic anemia associated with adult-onset Still's disease]. 2000 Sep A 37-year-old woman was admitted to our hospital in March 1995 because of high fever and cervical lymph node swelling. She had received prednisolone (PSL) therapy for autoimmune hemolytic anemia (AIHA). Laboratory examinations revealed increased serum levels of liver enzymes and C-reactive protein. Levels of rheumatoid factor and anti-nuclear antibody were within normal limits. On the basis of these criteria, she was diagnosed as having adult-onset Still's disease (AOSD). Although her fever ameliorated and physical symptoms disappeared immediately after a moderate dose of PSL, hemolysis recurred when attempts were made to reduce or withdraw the steroid. The patient is now receiving low-dose PSL therapy and is free of AIHA and AOSD.
10627427 Impaired microvascular response to cholinergic stimuli in primary Sjögren's syndrome. 2000 Jan OBJECTIVE: Signs of a parasympathetic dysfunction have been revealed in primary Sjögren's syndrome (SS). Its role in the pathogenesis and the clinical picture of the disease is not clear. To investigate the responsiveness of SS patients to a cholinergic agonist, a model was used involving examination of the cutaneous microcirculation. The microvascular response to the administration of carbachol was measured, a muscarinic cholinergic agonist. METHODS: Twenty two SS patients and 12 controls were examined. Carbachol and 0.9% saline solution were administered intracutaneously into the forearm skin at two distinct places. Skin blood flow (SBF) in the injected areas was measured continuously before and for 10 minutes after the injections by means of a laser Doppler perfusion monitor. The increase in SBF in response to carbachol (dSBF), reflecting vasodilatation, was calculated by a formula including the baseline and the maximum SBF values after the injections of carbachol and saline solution. RESULTS: The vasodilatation was significantly lower in SS patients than in the controls (mean dSBF: 2.1 (range: 1.0-4.5) versus 3.3 (range: 1.7-7.6), p=0.02). With non-responder patients defined as those in whom a smaller response was observed than in any of the controls, 11 of the 22 SS patients proved to be non-responders to carbachol. Comparisons of demographic, clinical and laboratory characteristics and HLA class II genotypes between responder and non-responder SS patients did not show any significant differences. CONCLUSIONS: A diminished or absent response to carbachol indicates a cholinergic dysfunction in SS patients. A disturbance in the neurotransmission at a receptorial or postreceptorial level is hypothesised. Unresponsiveness to cholinergic stimuli may contribute to exocrine insufficiency.
9448593 Chronic sialadenitis in patients with nodal osteoarthritis. 1997 Dec Amongst the patients attending our combined oral medicine/rheumatology clinic, we have identified a subset presenting with xerostomia due to non-specific sialadenitis, who also suffer from generalized nodal osteoarthritis (NOA). We have called this combination SOX syndrome: sialadenitis, osteoarthritis and xerostomia. In this study, we have examined the characteristics of these patients clinically and histologically, and then determined the prevalence of SOX syndrome in patients with NOA compared to healthy age-matched controls. Patients were obtained from rheumatology clinics and a local old people's home. The series consisted of 35 patients with NOA and 18 age- and sex-matched controls without evidence of NOA or inflammatory rheumatic disease. There was no significant difference in age and sex between the two groups. None were on drugs known to induce xerostomia. The subjects were assessed for whole salivary, parotid saliva and lacrimal flow, autoantibodies, rheumatoid factor (RF) and erythrocyte sedimentation rate (ESR). The whole saliva flow (mean +/- 95% CI) was 0.32 +/- 0.07 ml/min for the NOA group and 0.54 +/- 0.17 ml/min for the control group. The difference is statistically significant (P < 0.05, two-tailed Student's t-test). No statistically significant difference was found in the parotid and lacrimal flow rates of NOA and controls. Nine of the 35 NOA patients had reduced whole salivary flow (normal range > 0.02 ml/min) compared with only one out of 18 in the control group (P > 0.05, chi 2 test). All NOA patients with xerostomia and reduced whole salivary flow were RF, anti-Ro and anti-La negative, and had a normal ESR. Thus, 25% of subjects with NOA had clinical and laboratory features of SOX syndrome, suggesting that this is a defined disease entity.
9413297 Intravenous immunoglobulin-induced lichenoid dermatitis: a unique adverse reaction. 1997 Dec Intravenous immunoglobulin (IVIG) therapy has been used to treat various diseases. Generalized allergic reactions (types I, II, and III) to IVIG are uncommon and are usually related to the rate of infusion. Cutaneous reactions have been anecdotally described. Herein we describe a 73-year-old man with Sjögren's syndrome who had development of a lichenoid cutaneous eruption after administration of IVIG therapy. CD3 immunostaining demonstrated the overwhelming presence of T lymphocytes within a lesional skin biopsy specimen, and thus we present an alternative cell-mediated immune mechanism (type IV) by which allergic reactions to IVIG may occur.