Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Piroxicam (Feldene) and isoxicam (Vectren) form a part of a new family of non-steroid anti-inflammatory drugs (NSAID) highly used in France: the oxicams. The cutaneous accidents of all kinds are frequent, estimated from 1 to 3 p. 100 of the patients with piroxicam (16, 20). In addition to the maculo-papular eruptions, there has been reported: lichenoid eruption (21), erythroderma (7), purpuric vasculitis (1, 10, 21), pemphigus (12, 14), bullous dermatosis difficult to classify (15), erythema multiforme and Stevens-Johnson's syndrome (3, 6, 7, 9, 13, 21, 23) and at last many photosensitization accidents (3, 8, 11, 19, 20, 21). We report 11 observations of Lyell's syndrome (8 cases) or Stevens-Johnson's syndrome (3 cases) occurred during treatments by isoxicam or piroxicam. Eight women and 3 men aged from 35 to 80 years begin a Lyell's syndrome or a Stevens-Johnson's syndrome after 9 to 45 days (at an average of 16 days) of a treatment by isoxicam (6 cases) or piroxicam (5 cases). Five patients attacked by a Lyell's syndrome are intubated and ventilated and 2 patients die of a septic shock at the ninth and the thirteenth day of evolution: the duration of hospitalization is from 11 days to 3 and a half months for the Lyell's syndromes survivors and from 7 to 19 days in the cases of Stevens-Johnson's syndrome: 7 surviving patients have ocular sequelae with in 2 cases a complete or partial blindness. A slight hepatic cytolysis is observed 5 times and a neutropenia mainly as a lymphopenia 4 times. In 2 observations, the CMV serology is positive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lyell's syndrome and ectodermosis pluriorificialis during treatment with oxicams: 11 cases]. 409 6

Case records of 26 patients with Lyell Syndrome were reviewed for studying haematologic abnormalities. Eosinophilia, neutropenia, thrombopenia were uncommon. Circulating immature granulocytic cells were frequently encountered during the second week of evolution, mostly when leucocytosis was present. Anemia was frequent, the lowest haemoglobin titer beeing reached by the 15th day. Reticulocytosis was initially low and reached a peak during the second week. At that time biological markers of inflammatory syndrome were getting worse. So the originating anemia seems primarily of medullary origin and independent of inflammatory syndrome. Lymphopenia was constant and sometimes marked, with no circulating lymphocytes in two cases. The lowest numbers of lymphocytes were observed during the first week. These haematological abnormalities may have some pathogenic significance.
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PMID:[Hematologic anomalies in Lyell's syndrome. Study of 26 cases]. 688 53

BACKGROUND AND DESIGN--The pathophysiology of toxic epidermal necrolysis (TEN) remains largely unknown. Toxic epidermal necrolysis is considered a hypersensitivity reaction to drugs, but direct evidence of an immunologic mechanism is still lacking. Lymphopenia and a decrease in the numbers of circulating CD3- and CD4-positive lymphocytes have been reported in acute phase, but, to our knowledge, no study of cellular immune functions of patients with TEN has been reported so far. Herein, we investigated several T-cell functions in a series of 11 patients with TEN. Peripheral blood mononuclear cells (PBMC) obtained in the acute phase were tested together with PBMC obtained after the patient's recovery and compared with those of age- and sex-matched healthy control subjects. RESULTS--Phytohemagglutinin-induced proliferations and lymphocyte responses in allogeneic mixed lymphocyte reactions were not impaired in the acute phase compared with those after recovery in the same patients and with those in control subjects. In contrast, natural killer cytotoxicity and allogeneic cytotoxic responses were significantly decreased in early TEN. The most striking feature was the significantly impaired ability of acute-phase lymphoid cells to activate allogeneic T cells. Patient PBMC in acute-phase TEN did not inhibit the proliferation induced by patient PBMC after recovery, suggesting that their defect was not related to the presence of radioresistant suppressor cells. The phenotypic expression of HLA-DR, -DQ, and -DP antigens on circulating peripheral blood lymphocytes was then assessed by immunoalkaline phosphatase staining and flow cytometry. Results showed decreased percentages of HLA-DR-positive mononuclear cells and a decreased density of HLA-DR antigens, mainly on monocytes, in acute-phase TEN. CONCLUSIONS--These results demonstrate that peripheral blood lymphocytes of patients with TEN have an impaired ability to activate allogeneic T cells. This defective antigen presentation is not secondary to the presence of suppressor lymphocytes, but it is probably related to a decreased expression of HLA-DR antigens on circulating mononuclear cells in acute-phase TEN.
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PMID:Impaired antigen presentation in toxic epidermal necrolysis. 850 74

This case report describes a patient with arthritis of the large joints, bilateral sacroiliitis, and positive anti-SSA and anti-dsDNA antibody, who received sulfasalazine and shortly thereafter became critically ill. He developed toxic epidermal necrolysis, hemolytic anemia, lymphopenia, markedly elevated ferritin, and muscle wasting. A diagnosis of systemic lupus erythematosus was made, and mycophenolate mofetil and systemic glucocorticoids brought this severe disease under control. Toxic epidermal necrolysis-like lesions and hemophagocytic syndrome have been reported as manifestations of systemic lupus erythematosus. This patient possibly had spondyloarthritis or an undifferentiated connective tissue disease at presentation, and we suggest, based on the timing of events, that sulfasalazine may have acted as a trigger of the severe disease manifestations.
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PMID:Toxic Epidermal Necrolysis-Like Lesions and Systemic Lupus Erythematosus Possibly Triggered by Sulfasalazine. 2747 75