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Biomedical subjects

D M Chang

Publications and source records attributed to D M Chang.

At least 37 records · Page 2Linked to original sources
PubMed1999

Mechanism of immunosuppression of the antirheumatic herb TWHf in human T cells.

OBJECTIVE: To investigate the immunosuppressive mechanism of Tripterygium wilfordii Hook-F (TWHf) in human T cells. TWHf, a traditional Chinese medicinal herb for rheumatoid arthritis, has been shown to inhibit the function of immune effector cells such as neutrophils, macrophages, and B lymphocytes. METHODS: T cell survival was evaluated with trypan blue exclusion assay, morphologic changes with Wright's stain, the induction of endonuclease activity with DNA fragmentation assay, and the subdiploid DNA content with flow cytometry. T cell activation was measured with interleukin 2 (IL-2) ELISA and the expression of several surface molecules with flow cytometry. RESULTS: At high dosages, TWHf caused inhibition of T cell proliferation and this mechanism was mediated through the induction of apoptosis. TWHf, in noncytotoxic dosages, was as potent as cyclosporin A and more potent than prednisolone and cyclophosphamide in inhibiting IL-2 production from activated T cells. TWHf also inhibited both phorbol 12-myristate 13-acetate induced IL-2Ralpha expression and ionomycin induced CD40 ligand expression. TWHf did not reverse downregulated expression of CD3 and CD4 by phorbol ester stimulation. CONCLUSION: This is the first evidence that the immunosuppressive mechanism of TWHf in T cells was mediated through both downregulation of T cell receptor signaling pathway and induction of cellular apoptosis, which is defective in autoimmune diseases.

Antirheumatic Agents↗
PubMed1998

The clinical features and prognosis of male lupus in Taiwan.

Our objective was to describe the clinical manifestations, laboratory data, and prognosis in male Chinese lupus patients in Taiwan. Seventy-two male lupus patients, diagnosed and followed in Tri-Service General Hospital between 1983 and 1996, were studied and their clinical data analyzed, retrospectively. The mean age at diagnosis was 34+/-16 y (mean+/-s.d., range: 13-82 y). The peak incidence of age at diagnosis was between 13 and 40 years. The three most frequent clinical manifestations were renal disease, 75%; malar rash, 61%; and arthritis, 53%. The three most frequent abnormal laboratory findings were anti-nuclear antibodies (ANA), 97%; hypocomplementemia, 76%; and anti-ds DNA, 57%. The 1-, 5-, and 10-year survival rates were 85%, 76%, and 75%, respectively. In summary, a higher frequency of renal disease, malar rash and photosensitivity, but a lower frequency of arthritis and lymphadenopathy were demonstrated in our 72 ethnic Chinese male Taiwanese lupus patients compared to previous reports of Caucasians. The prognosis seems to be similar to that of both Chinese and Caucasian males but seems to be poor when compared to either Chinese or Caucasian female lupus patients.

Adolescent↗
PubMed1998

Protective agents used as additives in University of Wisconsin solution to promote protection against ischaemia-reperfusion injury in rat lung.

1. An intervention to reduce ischaemia-reperfusion lung injury will be an important advance in transplant medicine. Although the mechanisms associated with producing ischaemia-reperfusion endothelial injury have not been completely elucidated, many of the injury mediators have been studied in detail. While no single pharmacological therapy is likely to be totally effective in eliminating this complex injury, we have developed a mixture of agents that are known to block pathways involved in producing ischaemia-reperfusion-associated lung vascular injury.2. The present study modified University of Wisconsin solution (UW) by adding one of the protective agents prostaglandin E1 (PGE1), dexamethasone (Dex) or dibutyryl cAMP (Bt2-cAMP), or a combination of these, to the perfusate of rat lungs exposed to 4 h of cold ischaemia followed by 1 h of reperfusion. Nine modified UW solutions were studied: (1) UW+Dex, (2) UW+PGE1, (3) UW+Bt2-cAMP, (4) UW+Dexx3, (5) UW+PGE1x3, (6) UW+Bt2-cAMPx3, (7) UW+Dex+PGE1, (8) UW+Dex+Bt2-cAMP, (9) UW+PGE1+Bt2-cAMP. These solutions were utilized in individual experiments to assess haemodynamic changes, lung weight gain, the capillary filtration coefficient (Kfc) and pathology in all lungs.3. The results indicate that lung weight gain and Kfc values were significantly lower than with UW alone in groups 1, 2 and 3, which contained only one additional protective agent. In groups 4, 5 and 6, which contain three times the concentration of each protective agent, both Kfc and lung weight gain were similar to those measured in groups 1, 2 and 3, i.e. lungs were protected but the protection was not dose dependent. In groups 7, 8 and 9, which contained two protective agents, lung weight gain and Kfc were greatly reduced compared with UW alone. Histopathological studies showed similar decreases in the injury profiles of lungs.4. Although UW contains several antioxidant protective agents such as allopurinol and glutathione, it did not provide effective protection in our ischaemia-reperfusion lung injury model. UW modified with an additive of PGE1, Dex or Bt2-cAMP attenuated ischaemia-reperfusion injury. Furthermore, UW containing two of these protective agents augmented the protection. Among the modified solutions, it appears that UW+PGE1+Bt2-cAMP protects the lungs to a greater extent than all other solutions used in our study. We suggest that preservation solutions containing PGE1-Bt2-cAMP will provide additional protective effects to organs stored for transplantation.

Adenosine↗
PubMed1997

Interleukin-1 receptor antagonist modulates the progression of a spontaneously occurring IgA nephropathy in mice.

Cytokines, such as interleukin-1 (IL-1), may play a key role in the pathogenesis of IgA nephropathy (IgAN). This study was conducted to evaluate the effects of IL-1 receptor antagonist (IL-1ra) in the treatment of a spontaneously occurring experimental IgAN in established phase. ddY mice (12/group) were injected twice daily with 3 mg/kg of IL-1ra, intraperitoneally, for 8 consecutive weeks. The placebo mice were injected with saline only. As normal controls, ddY mice, which were not treated with IL-1ra or saline, were killed at 6 weeks of age. Results showed a significant reduction of proteinuria in the IL-1ra-treated mice, compared with saline-treated mice (urinary albumin/creatinine, 0.24 +/- 0.04 v 0.39 +/- 0.03, P < 0.001). A significant improvement of renal 51Cr-EDTA (ethylenediaminetetra-acetic acid) clearance was observed in the IL-1ra-treated mice (t1/2, 12 +/- 2.7 minutes, compared with saline-treated mice 25 +/- 2.0 minutes, P < 0.001). Similarly, serum levels of creatinine (1.0 +/- 0.4 v 2.4 +/- 0.3 mg/dL, P < 0.001) and urea nitrogen (46 +/- 6 v 58 +/- 2 mg/dL, P < 0.01) were significantly lower in IL-1ra-treated mice than in saline-treated mice. In renal tissue studies, the IL-1ra-treated mice exhibited significantly decreased mesangial cell proliferation, compared with saline-treated mice (P < 0.001), as shown by light and electron microscopy. In addition, the IL-1ra-treated mice showed significantly lower glomerular expression of collagen type IV, fibronectin, laminin, and IL-6 (P < 0.001) than saline-treated mice, although they still showed higher glomerular expression of collagen type IV (P < 0.01), fibronectin (P < 0.01), laminin (P < 0.001), IL-1 (P < 0.001), and IL-6 (P < 0.01) than did normal control mice. Meanwhile, glomerular C3 deposition was significantly lower in IL-1ra-treated mice than in saline-treated mice (P < 0.001). These findings indicate that IL-1ra partially prevented the progression of spontaneously occurring IgAN in this experimental model. Data from these experiments also confirm the pathogenic effects of IL-1 in the established phase of IgAN in ddY mice.

Animals↗
PubMed1997

Familial amyloidosis in one Chinese family: clinical, immunological, and molecular genetic analysis.

Three members of a Taiwanese kindred developed severe, systemic, early onset (< age 25 years), biopsy-proven amyloidosis. Clinical features included upper and lower extremity sensorimotor neuropathy, abdominal pain, vomiting, corneal ulcerations, cardiomyopathy, and syncope. Immunohistochemical analysis indicated that the deposits consisted of transthyretin. Molecular genetic studies revealed a heterozygous codon 55 point mutation, resulting in a proline for leucine-substitution, a mutation previously associated with aggressive familial amyloidosis in a US kindred of Dutch and German descent. The clinical courses and echocardiographic findings are typical for many types of amyloidosis; the pathologic data and genetic studies were necessary to establish a precise diagnosis.

Adult↗
PubMed1997

PGE1, dexamethasone, U-74389G, or Bt2-cAMP as an additive to promote protection by UW solution in I/R injury.

A method to reduce ischemia-reperfusion (I/R) injury can be an important criterion to improve the preservation solution. Although University of Wisconsin solution (UW) works as a lung preservation solution, its attenuation effect on I/R injury has not been investigated. We attempted to determine whether, by adding various protective agents, modified UW solutions will enhance the I/R attenuation by UW. We examined the I/R injury in an isolated rat lung model. Various solutions, e.g., physiological salt solution (PSS), UW, and modified UW solutions containing various protective agents such as prostaglandin E1, dexamethasone, U-74389G, or dibutyryl adenosine 3',5'-cyclic monophosphate were perfused individually to evaluate the I/R injury. Isolated rat lung experiments, with ischemia for 45 min, then reperfusion for 60 min, were conducted in a closed circulating system. Hemodynamic changes, lung weight gain (LWG), capillary filtration coefficient (Kfc), protein content of lavage fluid, concentration of cytokines, and lung histopathology were analyzed. Results showed that the acute I/R lung injury with immediate permeability pulmonary edema was associated with an increase in tumor necrosis factor-alpha (TNF-alpha) production. A significant correlation existed between TNF-alpha and Kfc (r = 0.8, P < 0.0001) and TNF-alpha and LWG (r = 0. 9, P < 0.0001), indicating that TNF-alpha is an important cytokine modulating early I/R injury. Significantly lower levels of Kfc, LWG, TNF-alpha, and protein concentration of lung lavage (P < 0.05) were found in the UW-perfused group than in the control group perfused with PSS. Modified UW promoted the protective effect of UW to further decrease Kfc, LWG, and TNF-alpha (P < 0.05). Histopathological observations also substantiated this evidence. In the UW+U-74389G group, bronchial alveolar lavage fluid contained lowest protein concentration. We conclude that the UW solution attenuates I/R injury of rat lung and that the modified UW solutions further enhance the effect of UW in reducing I/R injury. Among modified solutions, UW+U-74389G is the best. Further investigation of the improved effects of the modified UW solutions would be beneficial in lung transplantation.

Adenosine↗
PubMed1997

Interleukin-1 in ischemia-reperfusion acute lung injury.

Interleukin-1 (IL-1) is a proinflammatory cytokine produced by blood-borne and resident inflammatory lung tissue involved in the thrombotic occlusion of the pulmonary microcirculation and the increase of the vascular permeability following a wide variety of injuries and sepsis. The locally accentuated, organ-related activation of this cytokine seems to be responsible for the development of acute lung injury. The present study was conducted to determine if IL-1beta was produced in an ischemia-reperfusion (I/R) rat model subjected to lung injury. We measured sequential perfusate levels of IL-1beta by ELISA and we measured IL-1 gene expression in the rat lung tissue by a reverse-transcriptase polymerase chain reaction method. Little IL-1beta gene expression was observed in normal rat lung tissue. Perfusate IL-1beta slightly increased 2 h after induced ischemia and 3 h after reperfusion. IL-1beta gene expression rapidly increased as early as 30 min after ischemia and continued to increase for up to 120 min. IL-1beta gene expression was dramatically upregulated during reperfusion after cessation of ischemia, reached a peak at 1 h, and then gradually decreased (2 to 3 h) to near baseline levels. During ischemia, the increased IL-1 gene expression was not significantly different between the ventral and dorsal sites of the lung. However, IL-1 gene expression markedly increased on the dorsal part (the dependent site for a rat in a supine position) after reperfusion. From these results, it appears that IL-1 may have an important role in I/R lung injury.

Acute Disease↗
PubMed1997

The effects of traditional antirheumatic herbal medicines on immune response cells.

OBJECTIVE: Clinically, some traditional Chinese herbal medicines have been thought to be effective in treating rheumatic diseases such as rheumatoid arthritis and systemic lupus erythematosus. To examine the mechanism by which such herbal remedies might be effective, we investigated the ability of Tripterygium wilfordii Hook-f (TWHf) and tetrandrine (TTD) to affect human immune responsiveness in vitro. METHODS: We measured the ability of these agents to affect cytokine secretion from monocytes or T cells, prostaglandin E2 (PGE2) secretion from monocytes, IgG production from B cells, and the phagocytosis of bacteria by neutrophils. RESULTS: These studies revealed that both TWHf and TTD significantly inhibited interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), IL-6, and IL-8 secretion from monocytes, IgG secretion from B cells, and phagocytosis of bacteria by neutrophils; however, only TWHf inhibited IL-2 and IL-4 production from lymphocytes, and PGE2 secretion from monocytes. CONCLUSION: TWHf and TTD exert a powerful suppressive effect on human immune responses. This action might account for their therapeutic effectiveness in rheumatic diseases, and might support broader and more rigorous clinical trials.

Alkaloids↗
PubMed1996

Acceleration of skin graft healing by growth factors.

A special local burn wound treatment, using a healing promotion factor, attempted to achieve earlier wound closure. Clinically it is not difficult to harvest autologous human platelet-derived wound healing factor (HPDWHF) from burn patients. Another study has proved that porcine pituitary extract (PPE) could be one of the supplements for growing human keratinocytes in vitro (Wang HJ, Chen TM, Tung YM et al. Burns 1995). Initially, using the ELISA immunoassay, we detected titres of platelet-derived growth factor heterodimer AB (PDGF-AB) and epidermal growth factor (EGF) in HPDWHF and PPE. After elevating a 6 X 9 cm2 flap on the backs of Sprague-Dawley (SD) rats 1 ml of heterologous HPDWHF and PPE were sprayed topically on the wound and followed by grafting six pieces of 1 cm2 autologous full-thickness skin. The flap wound was then closed with a piece of large-pore Biobrane interposed between the skin graft wound and the flap. On postgraft day 7, the wound was reopened to measure the area of the full-thickness skin graft (FTSG) using micrographic paper; the results are reported as the percentage of graft expansion beyond the original size. In the cytokine study, we found that the concentrations of PDGF-AB dimer in HPDWHF and PPE were 5222 +/- 102 and 375 +/- 12 pg/ml (both values are reported after a 1:10 dilution) (n = 3), whereas the EGF concentration was 245 +/- 9 pg/ml, and undetectable in undiluted PPE (n = 3), thereby proving that the PDGF-AB and EGF fibres in the HPDWHF were significantly higher than in the PPE Both the HPDWHF (n = 6, with each animal grafted with six skin graft samples) and PPE (n = 7) demonstrated significant accelerations of FTSG growth, with 14.41 +/- 1.08 per cent and 13.16 +/- 3.25 per cent increases in the FTSG size when compared to the sham control group 1.39 +/- 3.26 per cent (n = 5) (P < 0.05). Comparisons between the treatment groups showed no evidence to indicate that the HPDWHF is superior to the PPE in accelerating FTSG growth (P > 0.05). This supports the hypothesis that PDGF appears to transduce its signal through wound macrophages and may trigger the induction of positive autocrine feedback loops and synthesis of endogenous wound PDGF and other growth factors, thereby enhancing the cascade of tissue repair (Pierce GF, Mustoe TA, Altrock B et al. 1991; J Cell Biochem 1991; 45: 319-326), and the effect that PDGF-AB on wound healing is not dose dependent (Mustoe TA, Cutler NR, Allman RM et al. Arch Surg 1994; 129: 213-219). In future studies we expect to show that autologous HPDWHF and heterologous PPE will promote skin graft wound healing in burn patients since they contain a high concentration of PDGF-AB.

Adult↗
PubMed1996

Cytokine production during hemodialysis: effects of dialytic membrane and complement activation.

Interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) are closely associated with acute and chronic inflammatory processes in hemodialytic patients. However, the mechanisms concerning cytokine production by monocytes during hemodialysis are still conflicting. With the use of the more specific monoclonal antibody ELISA method, contamination detection and crossover protocol of complement-activating and noncomplement-activating hollow fibers, we were able to confirm augmented II-1 beta production by zymosan-stimulated monocytes with complement-activating hollow fiber as compared to noncomplement-activating hollow fiber before (1,411.9 +/- 865.7 +/- 149.9 pg/ ml/2 x 10(6) monocytes, p < 0.01). at the 15th minute (530.6 +/- 89.1 vs. 247.3 +/- 45.2 pg/ml/2 x 10(6) monocytes, p < 0.01) and at the end of dialysis (1,201.8 +/- 135.1 vs. 707.4 +/- 109.3 pg/ml/2 x 10(6) monocytes, p < 0.01). Similar results were observed with TNF-alpha production. IL-1 beta as well as TNF-alpha production decreased significantly at the 15th min of dialysis, thereafter they increased and approached the baseline levels towards the end of hemodialysis with both hollow fibers. Plasma C3a at the 15th minute correlated positively with postdialysis IL-1 beta and TNF-alpha production, while plasma C3a did not change in patients dialyzed with noncomplement-activating hollow fiber. Complement activation with complement-activating hollow fiber as well as monocyte-membrane interaction with complement-activating and noncomplement-activating hollow fiber might be involved in the pathogenesis of cytokine production during hemodialysis. Uremic toxin removal as well as stimulation of cytokine production inhibitor might contribute to the decreased cytokine production at the 15th minute of hemodialysis and monocyte-membrane interaction with or without complement activation resulted in augmented cytokine production toward the end of hemodialysis with both hollow fibers. We thus concluded that hollow fiber of bioincompatibility triggered much more cytokine production throughout the dialysis procedure.

Cellulose↗
PubMed1996

The production and characterization of a modified recombinant interleukin-1 receptor antagonist.

The increasingly complex cytokine network involves both positive and negative regulatory pathways. Natural inhibitors of cytokines are of great importance both as analytical tools and as potential therapeutic agents. Interleukin-1 (IL-1) inhibitory bioactivity including a specific receptor antagonist of IL-I (IL-1ra) has been described both in cultured cell supernatants and in human body fluids. In the current studies, the cDNA of IL-1ra from human monocytes was obtained by the techniques of mRNA isolation and reverse transcription/polymerase chain reaction (RT/PCR). The IL-1ra cDNA/pET-15b was transfected into DE3 cells and the recombinant protein expressed. The purified protein was demonstrated as a single band with molecular mass of 20 KD by SDS-PAGE; it had strong IL-1 inhibitory activity. This IL-1 inhibitor competed with IL-1 for their receptor as assessed by flow cytometer. The existence of this naturally occurring specific cytokine receptor antagonist may lead to a different perspective of the cytokine network. The availability of this recombinant IL-1 receptor antagonist allows us to test its role on the cytokine network, and on possible disease modification.

Base Sequence↗
PubMed1996

Heterogeneous clinical characteristics of identical twins concordant for systemic lupus erythematosus: a report of one pair of twins.

Lupus is a mysterious disease without definite etiology and pathogenesis. The heterogeneous clinical manifestation of systemic lupus erythematosus (SLE) increases the delay and difficulty of diagnosis and the complexity of pathogenesis. Even in twins with identical genome and similar environmental milieu, the incidence of concordance for SLE is not high. Identical twins, concordant for SLE with discordance to disease onset and expression, are reported. Besides genetics, multiple factors are responsible for the pathogenesis of SLE.

Adult↗
PubMed1996

Acute myocarditis as an initial manifestation of systemic lupus erythematosus: a case report.

A rare case of systemic lupus erythematosus with initial manifestation of myocarditis is reported here, found in a 24-year-old female who presented first with an episode of exertional dyspnea, later developing life-threatening arrhythmia, and left ventricular dysfunction. There were no classical clinical manifestations of SLE such as arthragia or malar rashes as initial symptoms. Subsequently, the only clue was traced with positive ANA screening test. Central nervous system manifestations were found and proteinuria was detected. We ordered intravenous "pulses" of methylprednisolone, followed by maintenance of daily glucocorticoid because the criteria of SLE seemed applicable. The patient responded well and rapidly. This initial manifestation for SLE is so rare and unusual that it has not previously been described.

Acute Disease↗
PubMed1995

Cellular signals for the induction of human interleukin-1 receptor antagonist.

The polypeptide cytokine interleukin-1 (IL-1) mediates a broad spectrum of inflammatory, metabolic, physiologic, hematopoietic, and immunologic properties. An inhibitor of IL-1 (IL-1ra) has been purified from monocytes, and its DNA has been cloned. Human immunoglobulin G stimulates monocytes to make IL-1ra, but the monocyte receptor(s) for this induction remains a mystery. Therefore, the cellular Fc receptors (Fc gamma R) for IgG that induce IL-1ra production were tested. The Fc gamma R were defined and quantitated by flow cytometer. Anti-Fc gamma RIII (CD16), anti-Fc gamma RII (CD32), and anti-Fc gamma RI (CD64) had no blocking effect on IL-1ra production from monocytes after IgG stimulation. Monocytes express Fc gamma RI and II and respond as anti-CD32 to secrete IL-1ra; neutrophils express Fc gamma RII and III and respond as anti-CD16 to secrete IL-1ra; macrophages express Fc gamma RI, II, and III and respond as both anti-CD16 and anti-CD32 to secrete IL-1ra. These studies strongly suggested that both Fc gamma receptor II and III play a key role in IL-1ra production.

Cell Adhesion↗
PubMed1995

Immunoregulatory effects of a synthetic monosaccharide.

Investigative attempts to identify novel therapy for inflammatory connective tissue diseases continue to evolve. Amiprilose hydrochloride (amiprilose HCl) is a synthetic carbohydrate shown to have anti-inflammatory effects in animal models of inflammatory arthritis and in a multicenter clinical trial. Interleukin-1 (IL-1) is an important mediator of immune regulation, inflammation and joint destruction in arthritis. In the present study, the effects of amiprilose HCl on IL-1 activity, production and receptor distribution were investigated. Drug effects on IL-2 production and receptor distribution on lymphocytes were also explored. Potential regulation of IL-1 activity was determined by monitoring the effects of amiprilose HCl on IL-1 stimulated proliferation of murine thymocytes and human synovial cells. Inhibitory effects on IL-1 beta and IL-2 production by stimulated human peripheral blood monocytes were measured by ELISA and lymphocyte IL-1 beta and IL-2 receptor distribution were analyzed by flow cytometry. The results from in vitro studies demonstrated that low concentrations of amiprilose HCl (1-100 micrograms/ml) stimulated thymocyte proliferation and enhanced the proliferative response of IL-1 stimulated human synovial fibroblasts. IL-1 beta production in cultures of human peripheral blood monocytes was significantly decreased after exposure of the cultures to varying doses of amiprilose HCl as determined by ELISA. Exposure of mitogen activated human peripheral blood lymphocytes to amiprilose HCl resulted in decreased IL-2 production at high concentrations of drug as compared to control. However, at doses of amiprilose HCl previously found to stimulate thymocyte proliferation (1-10 micrograms/ml), increased levels of culture supernatant IL-2 were observed. No amiprilose HCl mediated changes in lymphocyte IL-1 beta or IL-2 receptor expression were observed. The regulatory effects of amiprilose HCl on cytokines support the potential of this drug as a therapeutic agent for the treatment of inflammatory arthritis.

Adjuvants, Immunologic↗
PubMed1995

Acquired immunodeficiency syndrome with CNS toxoplasmosis: a case report.

Central nervous system (CNS) toxoplasmosis is an important infectious complication of acquired immunodeficiency syndrome (AIDS) which appears to result from reactivation of a previously acquired infection and requires prolonged treatment. A 31-year-old male presented in a drowsy mental state and with an unstable gait. Computerized tomographic (CT) scan and magnetic resonance imaging (MRI) showed multiple nodular lesions in the cerebrum and cerebellum; the seropositivity for the human immunodeficiency virus (HIV-1) and high serum IgG toxoplasma titers were also demonstrated. A presumptive diagnosis of CNS toxoplasmosis was based on neurological signs and neuroradiological findings. This was confirmed by improvement in both clinical and neuroradiological pictures during treatment with pyrimethamine and clindamycin. Four months later, however the patient died of intracranial hemorrhage and massive upper GI bleeding.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Coexisting IgA nephropathy and leukocytoclastic cutaneous vasculitis associated with ankylosing spondylitis: a case report.

A patient with ankylosing spondylitis and coexisting IgA nephropathy and leukocytoclastic cutaneous vasculitis is described. Renal biopsy demonstrated mesangial proliferative glomerulonephritis with prominent IgA, C3 and fibrin deposition in the glomeruli. Simultaneously, leukocytoclastic cutaneous vasculitis with prominent IgG, IgA and C3 deposition of dermal vessel wall was also observed in the skin biopsy specimen. Such associations have been previously reported in only four cases. This report once again indicates that antigenic mucosal stimulation may play an important role in the pathogenesis of ankylosing spondylitis.

Adult↗