Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022575 (keratoconjunctivitis sicca)
 772 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present 5 patients in whom thallium poisoning (1) mimicked systemic lupus erythematosus (SLE) with positive antinuclear antibodies; (2) caused a SLE-like illness with positive antinuclear antibodies and rheumatoid factor that was followed by a persistent chronic polyarthritis; (3) mimicked SLE with negative antinuclear antibodies and no residual disease; (4) caused arthralgia, Raynaud's phenomenon and palmar erythema with negative antinuclear antibodies followed by keratoconjunctivitis sicca; and (5) triggered the onset of SLE with diffuse proliferative glomerulonephritis. Although the notion exists that thallium poisoning may simulate seronegative SLE, these associations between connective tissue diseases and thallium poisoning have not been previously recorded.
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PMID:Connective tissue disease features after thallium poisoning. 278 3

The medical records of 158 dogs with visceral leishmaniasis confirmed cytologically and/or serologically were reviewed. Ages of affected dogs varied from nine months to 15 years, with a male-to-female ratio of 1.3. The most common clinical manifestations of the disease were variable cutaneous lesions such as exfoliative dermatitis and skin ulcerations, chronic renal failure, peripheral lymphadenopathy or lymph node hypoplasia, masticatory muscle atrophy (i.e., chronic myositis), ocular lesions (i.e., conjunctivitis, keratoconjunctivitis sicca, blepharitis, and uveitis), and poor body condition. Ascites, nephrotic syndrome, epistaxis, polyarthritis, and ulcerative stomatitis were seen only in a small number of cases. Clinical splenomegaly was not a common finding. The clinicopathological abnormalities were nonregenerative anemia, hyperproteinemia, glomerular proteinuria, and symptomatic or asymptomatic azotemia. In this study, an indirect immunofluorescence assay's diagnostic sensitivity was found to be higher than that of lymph node aspiration cytology.
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PMID:Clinical considerations on canine visceral leishmaniasis in Greece: a retrospective study of 158 cases (1989-1996). 1049 12

In dogs with symptomatic or asymptomatic leishmaniasis, Leishmania infantum appears to induce a mixed Th1/Th2 immune response that in the sick dog may eventually result in tissue damage via different pathomechanisms, notably granulomatous inflammation (eg, nodular dermatitis, osteomyelitis), immune complex deposition (eg, glomerulonephritis), and/or autoantibody production (eg, polymyositis). This is a compensatory but detrimental mechanism generated mainly because of the insufficient killing capacity of macrophages against the parasite in the susceptible dog. Clinical disease is typically exemplified as exfoliative and/or ulcerative dermatitis, with or without nasodigital hyperkeratosis and onychogryphosis, glomerulonephritis, atrophic myositis of masticatory muscles, anterior uveitis, keratoconjunctivitis sicca, epistaxis, and/or polyarthritis, appearing alone or in various combinations. The pathogenesis of these clinical conditions has recently been highlighted, to a greater or lesser extent. The usually subclinical conditions expressed as chronic colitis, chronic hepatitis, vasculitis, myocarditis, osteomyelitis, orchiepididymitis, and meningoencephalomyelitis, though uncommon, are of pathologic importance from a differential point of view. The leading cause of death among canine leishmaniasis patients is chronic proteinuric nephritis that may progress to end-stage kidney disease, nephrotic syndrome, and/or systemic hypertension. However, even the asymptomatic proteinuria, when profuse, may be a serious problem because it predisposes to arterial thromboembolism and eventually contributes to the deterioration of the body condition.
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PMID:Pathologic mechanisms underlying the clinical findings in canine leishmaniasis due to Leishmania infantum/chagasi. 2451 Sep 47