Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0033687 (proteinuria)
24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article summarizes the authors' experience and data from the literature regarding acadione, a medication like D-penicillamine with a thiol radical, in the treatment of rheumatoid arthritis. Two control studies versus placebo and two control trial versus D-penicillamine prove the effectiveness of the treatment and demonstrate a similar activity between 1 g of acadione and 600 mg of D-penicillamine. The side-effects of acadione are similar of those of D-penicillamine, essentially rash, toxic dermatitis, agueusia, proteinuria, which disappear upon discontinuation of the treatment. The fact that the patient exhibited a side effect with D-penicillamine, increases, the risk with acadione, but this is not systematic, which is the main advantage of this product.
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PMID:[Acadione, a new long-term treatment of rheumatoid polyarthritis]. 339 45

For over 50 years, gold therapy has played an important role in the treatment of rheumatoid arthritis. Since 1932, many clinicians and investigators have confirmed the beneficial effects of the water-soluble gold salts, aurothioglucose and gold sodium thiomalate. Gold therapy is indicated for patients with active disease who are not responsive to conservative therapy. To minimize patient risks, contraindications must be considered, and careful clinical and laboratory monitoring must be performed under close supervision by the physician during therapy. Side effects may include vasomotor reactions, dermatitis, stomatitis, leukopenia, proteinuria, nephrosis, and thrombocytopenia. During therapy, one of six patients may have an adverse reaction requiring suspension or termination of therapy. Of the five tolerating gold, one will not benefit, three may have marked improvement, and one may have a remission. The usual recommended dosage schedule is intramuscular injection of 25 to 50 mg of gold salt at weekly intervals until a total of 1,000 mg has been achieved. At this level, gold injections may be spaced biweekly, triweekly, and then monthly for an indefinite period.
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PMID:Parenteral gold in the treatment of rheumatoid arthritis. 622 81

A 6% incidence of nephrotic syndrome was noted in a colony of 400 Syrian hamsters (Mesocricetus auratus) over a period of 2 years. Clinical findings consisted of severe ascites and anasarca, anorexia, cachexia, and papular dermatitis. Serum and urine chemical analysis revealed proteinuria and hypoalbuminemia in all animals tested; hypoproteinemia and high concentrations of serum cholesterol, triglycerides, and creatinine were detected in some of the affected hamsters. Demodex aurati was detected in skin scrapings from 4 of 8 hamsters. Necropsy findings included subcutaneous edema, ascites, and hydrothorax, as well as atrophic kidneys and testes. Extensive deposits of type AA amyloid were detected histologically in kidney, liver, spleen, and adrenal gland; smaller deposits were found in thyroid gland and intestine. Other histologic findings included periodontitis and hyalinization of the small arteries of the testes.
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PMID:Nephrotic syndrome associated with renal amyloidosis in a colony of Syrian hamsters. 651 83

MRL-lpr/lpr mice spontaneously develop a severe autoimmune syndrome, characterized by massive generalized lymphadenopathy, arthritis, arteritis, dermatitis and immune complex-mediated glomerulonephritis. Bone marrow transplantation (BMT) from MHC-matched systemic lupus erythematosus (SLE)-resistant donors to susceptible recipients has proved effective in correcting autoimmune manifestations in autoimmune-prone mice. We investigated the effect of syngeneic BMT from MRL/lpr (donor) to immunocompromised MRL/lpr (recipient), after purging the bone marrow inoculum with MoAbs against mature T cells (anti-Thy 1.2). All the untreated mice developed lymphadenopathy and by the age of 36 weeks five of the eight were dead; in contrast, all the mice which underwent syngeneic BMT following acute immunosuppression with total body irradiation (900 cGy) (TBI) remained disease-free. In an additional experiment, it was found that conditioning with cyclophosphamide (CY) before BMT was more effective than TBI in inhibiting delayed-onset autoimmune manifestations (mean survival 350 days in the CY group and 305 days in the TBI group, versus 197 days in untreated controls). Under both immunosuppressive regimens T cell-depleted bone marrow grafts produced far better results than did unmanipulated BMT. Following syngeneic BMT the incidence of proteinuria and the level of serum anti-DNA (dd) antibodies were significantly reduced, compared with that of the age-matched untreated controls. CY was more effective than TBI in reducing the anti-DNA titres. Likewise, T depletion of bone marrow inocula before BMT induced a more drastic drop in autoantibodies, following both CY and TBI conditioning protocols. After syngeneic BMT (either CY or TBI) no signs of lymphadenopathy were observed even at an advanced age. Upon histopathological examination, the BMT-treated mice displayed normal glomeruli with occasional minimal signs of glomerulonephritis. Syngeneic T cell-depleted BMT following acute cytoreduction of anti-self immune lymphocytes may represent a new therapeutic approach for drug-resistant autoimmune diseases.
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PMID:Immunomodulation of autoimmunity in MRL/lpr mice with syngeneic bone marrow transplantation (SBMT). 769 9

Therapeutic effects of combined treatment with a Chinese medicine prescription, Ren-shen-yang-rong-tang (Japanese name: Ninjin-youei-to, NYT) and suboptimal doses of prednisolone (PSL) on pathological findings of autoimmune-prone MRL/lpr mice were examined. Six-week-old MRL/lpr mice were treated orally with 1000 mg/kg of NYT, 0.5 or 2 mg/kg of PSL, 1000 mg/kg of NYT plus 0.5 or 2 mg/kg of PSL (combined treatment) or solvent only (control) six times per week. The rates of signs and symptoms of autoimmune disease (lymphadenopathy, proteinuria, dermatitis, loss of hair) were suppressed significantly in groups given PSL (2 mg/kg) alone, NYT alone and combined treatment with PSL (2 mg/kg) plus NYT (1000 mg/kg) compared with control, respectively, whereas treatment with PSL (0.5 mg/kg) alone did not inhibit their occurrence. ConA response and IL-2 production were also improved significantly in lymphocytes of mice given the combined treatment. Interestingly, treatment with NYT alone enhanced further the augmented IFN-gamma production in MRL/lpr mice but the combined treatment suppressed such an augmented production. The combined treatment dramatically reduced the level of anti-DNA antibodies in serum of MRL/lpr mice. By contrast, NYT alone treatment had no effect on autoantibodies production. These results suggest that combined treatment with NYT plus a suboptimal dose of PSL could be effective for systemic lupus erythematosus without severe side-effects.
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PMID:Combined treatment of autoimmune MRL/MP-lpr/lpr mice with a herbal medicine, Ren-shen-yang-rong-tang (Japanese name: Ninjin-youei-to) plus suboptimal dosage of prednisolone. 784 56

CD40-CD40 ligand (L) interactions play a pivotal role in immune-mediated inflammatory responses via the activation of antigen-presenting cells (APCs). To investigate the effects of continuous activation of resident tissue APCs, in this case the Langerhans cells (LCs) of the skin, CD40L expression was targeted to the basal keratinocytes of the epidermis of mice using the keratin-14 promoter. Approximately 80% of the transgenic (Tg) mice spontaneously developed dermatitis on the ears, face, tail, and/or paws. Compared with littermates, Tgs had a >90% decrease in epidermal LCs yet increased numbers within the dermis suggestive of enhanced emigration of CD40-activated LCs. Tgs also displayed massive regional lymphadenopathy with increased numbers of dendritic cells and B cells. Moreover, a decrease in IgM and an increase in IgG1/IgG2a/IgG2b/IgE serum concentrations was detectable. Screening for autoantibodies revealed the presence of antinuclear antibodies and anti-dsDNA antibodies implicative of systemic autoimmunity. Accordingly, renal Ig deposits, proteinuria, and lung fibrosis were observed. Adoptive transfer of T cells from Tgs to nonTg recipients evoked the development of skin lesions similar to those found in the Tgs. Dermatitis also developed in B cell-deficient CD40L Tg mice. These findings suggest that in situ activation of LCs by CD40L in the skin not only leads to chronic inflammatory dermatitis but also to systemic mixed-connective-tissue-like autoimmune disorders, possibly by breaking immune tolerance against the skin.
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PMID:Overexpression of CD40 ligand in murine epidermis results in chronic skin inflammation and systemic autoimmunity. 1153 30

This paper documents the salient clinical and pathological features of porcine dermatitis and nephropathy syndrome (PDNS) in 96 pigs submitted from 55 units in the UK from 1993 to 1998. This series of cases pre-dated the emergence of post-weaning multisystemic wasting syndrome (PMWS) in the UK. The morbidity during outbreaks was 1% or less. Affected pigs ranged from 14 to 70 kg in weight and most died after a short clinical illness. Fifty-five pigs had multifocal or coalescing erythematous skin lesions, some progressing to dermal necrosis. Biochemistry showed raised serum urea, creatinine and gamma globulin levels accompanied by proteinuria. All cases showed bilateral renal enlargement with petechiae throughout the cortices. Microscopically these renal lesions ranged in chronology from acute necrotizing glomerulitis and vasculitis with multiple hyaline casts in renal tubules to chronic glomerular sclerosis with interstitial inflammation and fibrosis. Haemorrhagic dermatitis when present was associated with necrotizing vasculitis in the dermal vessels. Vasculitis was sometimes detected in other tissues including subcutis, lymph nodes, spleen, liver, joint synovial membrane, gastric and intestinal submucosa or serosa and meninges but its frequency and distribution varied considerably in individual pigs. Immunostaining showed deposits of IgG and IgM in damaged glomeruli, renal casts and skin lesions. The aetiology and pathogenesis of the condition remain unknown but the histopathological and immunological findings suggest a systemic immune-complex disorder resulting in vasculitis with particular predilection for kidney and skin.
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PMID:Porcine dermatitis and nephropathy syndrome. clinical and pathological features of cases in the United Kingdom (1993-1998). 1245 Jan 93

Asthma is orchestrated by cytokine products of activated T cells. Glucocorticoids are thought to ameliorate asthma at least partly through T cell inhibition. Consequently, other T cell immunomodulatory agents have been assessed for asthma therapy. Since these agents may have serious unwanted effects, attention has been focused on patients with severe asthma refractory to maximal topical, and additional systemic glucocorticoid therapy. Although gold salts show a modest but significant glucocorticoid-sparing effect in severe asthma, lung function is not improved and not all patients respond. The minimum duration of a valid trial of therapy is probably 6 months. Unwanted effects include dermatitis, hepatic dysfunction, proteinuria and interstitial pneumonitis. Meta-analysis of trials of methotrexate in oral glucocorticoid-dependent asthma have confirmed that concomitant weekly methotrexate for a minimum of 3 to 6 months enables significant (approximately 20%) overall reduction in oral glucocorticoid requirements, although only approximately 60% of patients show a significant response. There is little effect on lung function. Blood count and liver function must be monitored. Opportunistic infection is rare but potentially fatal. Cyclosporine, administered for at least 3 months, is effective in only a proportion of patients with oral glucocorticoid-dependent asthma, where it may improve disease severity and/or enable oral glucocorticoid dosage reductions. Regular monitoring of renal function, blood pressure and blood concentrations of cyclosporine is required. The evidence that intravenous immunoglobulin (Ig) is of any benefit in patients with glucocorticoid-dependent asthma is at present equivocal. The therapy is expensive and associated with a high incidence of unwanted effects (fever, aseptic meningitis, urticaria). The macrolides tacrolimus (FK506) and sirolimus (rapamycin) have end effects similar to those of cyclosporine. Brequinar sodium, mycophenolate mofetil and leflunomide are inhibitors of de novo synthesis of pyrimidines and purines, to which T cells are particularly sensitive. Such drugs may in theory be beneficial for therapy of patients with oral glucocorticoid-dependent asthma. Humanized anti-CD4, anti-IgE and anti-interleukin (IL)-5 monoclonal antibodies, and other cytokine inhibitors such as soluble IL-4 receptor have entered early trials. The worth of current immunomodulatory drugs is limited since: (i) not all patients respond, and response cannot be predicted a priori; (ii) the high incidence of unwanted effects makes it difficult to assess overall benefit/risk ratios; (iii) there is increased risk of opportunistic infection and (theoretically) neoplasia; (iv) there are many relative and absolute contraindications to therapy; and (v) there is lack of knowledge about the long-term effects, beneficial or otherwise, of therapy.
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PMID:Asthma refractory to glucocorticoids: the role of newer immunosuppressants. 1472 75

The purpose of this study was to develop a model for canine systemic lupus erythematosus. Systemic lupus erythematosus (SLE) is a systemic autoimmune syndrome defined by clinical and serological features, including arthritis, glomerulonephritis, dermatitis and autoantibodies. SLE was induced in eight normal dogs by immunization with heparan sulphate, the major glycosaminoglycan of the glomerular basement membrane. All the heparan sulphate-immunized dogs showed mild-to-moderate levels of proteinuria and skin disease. Cutaneous signs associated with SLE including alopecia, erythema, crusting, scaling and seborrhoea were observed. Immunohistological examination of the skin lesions revealed deposition of immunoglobulin M and complement in the dermal-epidermal junction. Three of eight dogs showed lameness. The antinuclear antibody tests were positive with the antibody titres higher than 1:128. Therefore, this experimental SLE model could be useful for studying immune-mediated skin disease and autoimmunity.
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PMID:Development of canine systemic lupus erythematosus model. 1553 23

Autoimmunity results from loss of mechanisms controlling self-reactivity. Autoimmune disorders play an increasingly important role and CD40-CD40 ligand (CD40L) interaction on immunocompentent cells is able to break established immunotolerance. To study the effects of the calcineurin-inhibitor FK506 on CD40L-induced systemic autoimmunity, CD40L transgenic (tg) mice, which spontaneously develop a mixed connective tissue-like disease, were treated with FK506 after onset of overt autoimmunity. Interestingly, FK506-treated CD40L tg mice showed significantly reduced autoimmune dermatitis scores and markedly decreased numbers of lesional infiltrating leukocytes. This finding was associated with diminished lymphadenopathy induced by FK506 treatment. Furthermore, FK506 suppressed the development of cytotoxic/autoreactive CD8(+) T cells as evidenced by the reduced expression of T cell activation markers in treated CD40L tg mice. Importantly, FK506 induced a significant reduction in autoantibody titers in the serum of CD40L tg animals. As CD40L tg mice develop nephritis leading to loss of renal function proteinuria was determined after FK506 injections. Notably, FK506 treatment re-established renal function as indicated by significantly reduced uric protein concentrations of treated CD40L tg mice. Together, these findings show the beneficial therapeutic effects of FK506 for the treatment of CD40L-induced autoimmunity. Additionally, these results demonstrate that FK506 is able to suppress ongoing severe autoimmune responses.
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PMID:FK506 controls CD40L-induced systemic autoimmunity in mice. 1670 68


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