Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty randomly selected asthmatic patients were studied. In each the sex, age, time of onset of symptomatology, symptomatologic score (from 0 to 3), blood eosinophilia, IgE by the PRIST method and Tart cells in blood (investigated by the same method as is used in the search of LE cells in collagen diseases) were considered. Tart cells were recognized as in Miale Haemotology (9) as monocytes and occasionally polymophonuclar leucocytes with one or two round inclusions in their protoplasm owing to the phagocytosis of leukocyte nuclei. In contrast with LE cells, these inclusions are not homogeneous contain chromatin and nuclear membrane material and often have a dark ring of hyperchromic material. We have found that these cells can not be evoked passively by application of patient serum to normal leukocytes. In no case of positive Tart cells was antinuclear serum factor found by immunofluorescence as seen in lupus erythematous disease. 33 per cent of the 50 asthmatic patients tested had Tart cells in their blood. They were very scarce, only one or two in four Wright stained smears. This fact is probably why these cells were not recognized before. The positive Tart cell group was on the average the same age as the negative group. On the other hand, in the positive Tart cell group the proportion of men with respect to women, the time span from the onset of asthmatic symptoms (p less than 0,05), the symptomatology score (p less than 0,005) and blood eosinophilia (p less than 0,005) were increased. In contrast IgE was decreased on the average (p less than 0,05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Finding of Tart cells in asthmatic patients. Relation to IgE and other parameters]. 620 75

Interferon alpha (INF-alpha)--In systemic diseases, most indications for INF-alpha result from its effect on haematological or hepatological manifestations. The spectacular effect of INF-alpha in chronic myeloid leukemia has led to its use for the treatment of hypereosinophilia syndrome and systemic mastocytosis. Over the last 6 years, we have treated 7 patients with the hypereosinophilia syndrome who were resistant to corticotherapy and had markers of myeloproliferation. Although both hydroxyurea and INF-alpha can be effective alone, their combination led to a decrease in the eosinophilia count to 1,000/ml, a decrease which was long-lasting in most cases. INF-alpha is also used in histiocytosis X alone or in combination with retinoids or with etoposide and has been found effective in several observations. In carcinoid syndromes whether treated priorly or not with a 5-fluoro-uracil-streptozoticin combination, INF-alpha leads to an objective response in two-thirds of the patients. Several multicentric protocols are currently assessing the efficacity of INF-alpha in mixed cryoglobulinaemias. In most observations these cryoglobulinaemias are seen in patients with markers of hepatitis C (mainly HCV) and the early results are encouraging. Temporary improvement has been reported in discoid or subacute lupus in 8 out of 10 cases. Haemangiomas of the infant, when life-threatening and corticoresistant, may be a good indication for INF-alpha. Thus 20 newborns or infants (including 4 with Kasabach-Merrit syndrome) have been treated with good results in 18. Interferon gamma (INF-gamma).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Interferons. Interferons alpha and gamma: indications in systemic diseases]. 817 44

Systemic lupus erythematosus, chronic cutaneous lupus erythematosus and subacute and acute cutaneous lupus erythematosus are associated with distinct cutaneous manifestations, and each disease has a particular clinical course and prognosis. Dermatomyositis, an immune-mediated disorder of unknown etiology that is often associated with a malignancy, consists of an inflammatory myopathy combined with characteristic cutaneous findings. Some patients with dermatomyositis also have clinical features that overlap with those of systemic lupus erythematosus or scleroderma. Manifestations of scleroderma range from cutaneous involvement alone to multisystem internal disease. Morphea, progressive systemic sclerosis, eosinophilic fascitis, eosinophilia myalgia syndrome and mixed connective tissue disease are all within the spectrum of scleroderma.
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PMID:Cutaneous manifestations of selected rheumatologic diseases. 862 90

A 19 year old female was admitted to our hospital with complaints of fever, dyspnea and chest pain. Chest x-ray film showed a massive right pleural effusion. She was diagnosed to have systemic lupus erythematosus (SLE) because of malar rash, serositis (pleuritis), positive antinuclear antibody and positive anti-DNA antibody. Then she was successfully treated with 50 mg/d prednisolone. This case was unusual and of interest in that she had eosinophilia in the peripheral blood and exudative pleural effusion and a marked elevation of serum IgE level despite no history of allergic diseases and no evidence of parasite infections.
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PMID:[A case of SLE with the onset of pleuritis showing eosinophilia and elevation of serum IgE]. 868 35

The cause of toxic oil syndrome (TOS) has not yet been definitively determined, but some genetic susceptibility factors (certain HLA antigens and female sex) have been identified in 236 patients. Similarities with genetic factors for scleroderma and hydralazine-induced lupus (i.e. in TOS female sex and HLA-A24, Pcorrected = 0.00001 and DR4, Pcorrected = 0.04, respectively) may provide a clue to the responsible xenobiotic and its pathogenesis, and may also help in understanding the basis of the related eosinophilia-myalgia syndrome associated with tryptophan ingestion. In this paper it is also established that a human class I antigen (HLA-A24) and, independently, an HLA class II haplotype (DR4-DQ8, Pcorrected = 0.04) and arginine 52 in the alpha-DQ chains (Pcorrected = 0.03) are associated with TOS susceptibility, similarly to insulin-dependent diabetes. This further supports the classification of TOS as an autoimmune disease. Also, the increased frequency of a particular set of low-frequency HLA class I antigens in chronic TOS patients (i.e. B27, B37, B38 and B49) and the probable decrease in the frequency of HLA-B homozygotes in surviving patients (Pcorrected = 0.008) may provide an objective model to explain the maintenance of the HLA polymorphism: less frequent HLA alleles may be more advantageous in the event of unexpected human contact with unusual xenobiotics (not only microbes); however, other mechanisms working together to preserve and generate HLA polymorphism may coexist.
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PMID:Frequencies of HLA-A24 and HLA-DR4-DQ8 are increased and that of HLA-B blank is decreased in chronic toxic oil syndrome. 880 34

Authors report a case in which relapsing polychondritis had been diagnosed two years before myelodysplastic syndrome developed and terminated in eosinophilic leukemia. The observation that relapsing polychondritis may precede myelodysplasia is not in concordance with some of the previous reports regarding relapsing polychondritis as a paraneoplastic phenomenon of myelodysplastic syndrome. The terminally developed eosinophilic leukemia is not supposed to be a blastic phase of the underlying myelodysplasia, much rather a second malignant process. This opinion may be confirmed by the early presence of blast cells in the myelodysplastic process without eosinophilia. It seems interesting to note that both our patient and his daughter suffered from diseases of autoimmune origin: acquired vitiligo and subacute cutan lupus erythematodes, respectively.
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PMID:[Relapsing polychondritis associated with myelodysplasia and acute eosinophilic leukemia]. 917 85

We have characterized the activation of the HPA axis in the chronic inflammatory stress model of adjuvant-induced arthritis. Alteration in the hypothalamic control mechanism, where CRF is no longer the major corticotrophin-releasing factor, has been noted in a number of other immune-mediated disease models, including experimental allergic encephalomyelitis, eosinophilia myalgia syndrome, systemic lupus erythematosus, and leishmaniasis. These changes occur in both the mouse and the rat, suggesting this may be a common mechanism to chronic immune activation. We have good evidence to suggest that AVP takes over as the major stimulator of the axis. The arthritic rat is unable to mount a response to acute stressors, such as restraint or ip hypertonic saline. However, these animals are able to mount a response to an acute immune challenge. These data provide further evidence for a differential activation of the HPA by acute stress or acute immune stimulation. This presumably reflects an adaptive response to the development of chronic inflammation. We have demonstrated that central neurotransmitter systems are able to influence the severity of peripheral inflammation. In particular we have shown that depletion of serotonin at the time of the development of the inflammatory episode reduces the severity of the inflammation. These findings suggest the possibility of novel therapeutic strategies targeting neurotransmitter systems to alleviate inflammation.
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PMID:The hypothalamic-pituitary-adrenal axis in autoimmunity. 929 47

Minocycline is the most commonly used systemic antibiotic in the long-term treatment (weeks to months) of severe acne vulgaris. Currently much attention is being paid in the Dutch and international literature to the safety of minocycline, after several reports on serious adverse events. The clinical efficacy of minocycline in the treatment of acne vulgaris is better than that of tetracycline and equal to that of doxycycline. The serious adverse events of minocycline therapy described consist of hyperpigmentation of various tissues, autoimmune disorders (systemic lupus erythematosus, autoimmune hepatitis) and serious hypersensitivity reactions (hypersensitivity syndrome reaction, pneumonitis and eosinophilia, and serum sickness-like syndrome). In relation to the number of prescriptions, the number of serious adverse events of minocycline described is small. However, it is very important that prescribing doctors should be aware of the possibility of these adverse events occurring during long-term minocycline therapy and able to recognize the characteristic symptoms at an early stage.
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PMID:[Side effects of minocycline in the treatment of acne vulgaris]. 955 Jul 42

We describe a patient with quiet systemic lupus erythematosus who developed a hypereosinophilic syndrome. The patient presented with gastrointestinal eosinophilia which caused diarrhoea, malabsorption and anaemia due to deficiencies of vitamins. The hypereosiniphilic syndrome completely resolved after treatment with prednisone.
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PMID:Hypereosinophilic syndrome presenting with diarrhoea and anaemia in a patient with systemic lupus erythematosus. 955 31

Autoantibodies to CRP were reported previously in patients suffering from toxic oil syndrome. This syndrome resembles autoimmune diseases such as systemic lupus erythematosus (SLE) or systemic scleroderma. We therefore examined the prevalence of antibodies to CRP and other acute-phase proteins in autoimmune diseases, including SLE, subacute cutaneous lupus erythematosus (SCLE), systemic scleroderma (SSc), and primary biliary cirrhosis (PBC), as well as in bone marrow transplantation-induced chronic graft-versus-host disease and eosinophilia-myalgia syndrome. IgG antibodies to CRP were found in 78% of SLE and in 30% of SCLE patients, while 16% of patients with PBC were positive. In up to 45% of patients with SSc predominantly IgG antibodies to ceruloplasmin were detectable. Lack of systemic involvement as in discoid lupus erythematosus and localized scleroderma (morphea) correlated with low or absent antibody formation. However, no correlation was found between anti-acute-phase protein antibodies with liver disease or other organ involvement. Adsorption studies revealed that non-native epitopes on the CRP molecule, termed modified CRP, are the main target of antibodies. Chronic inflammatory tissue injury in systemic autoimmune disease might increase the presentation of cryptic epitopes of CRP to the threshold required for T cell activation.
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PMID:Autoantibodies to C-reactive protein (CRP) and other acute-phase proteins in systemic autoimmune diseases. 973 58


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