Biomedical subjects
Publications and source records attributed to W Graninger.
Candida endocarditis is an unusual but severe complication caused by Candida albicans or other fungal species. We describe a case of prosthetic valve endocarditis due to Candida tropicalis, complicated by multiple pseudoaneurysms.
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Clinical characteristics of patients with falciparum malaria, as well as sensitivity of Plasmodium falciparum to chloroquine and mefloquine, were investigated in 2 distinct strata within the same geographical area of the Amazon Basin. One stratum was the population living along the road, the other that living along the river, both near Rio Branco, capital of Acre State, Brazil. The clinical features did not differ between the 2 strata. Full in vitro sensitivity of P. falciparum to mefloquine was observed in both areas. However, significant differences in chloroquine sensitivity were observed between the 2 strata. EC50 values for chloroquine were 0.8484 mumol/litre for parasite isolates from the road stratum (E) and 0.4638 mumol/litre for parasite isolates from the river stratum (R). EC90 values were 2.8095 and 1.2549 mumol/litre in strata 'E' and 'R', respectively. Continuous drug pressure over years in area 'E' and relatively low drug pressure in area 'R' were presumably responsible for these differences.
Plasma levels of nitrogen oxide (NO), neopterin and C-reactive protein (CRP) were compared in 3 groups of Gabonese patients with Plasmodium falciparum malaria before and after therapy: adults with uncomplicated malaria, children with uncomplicated malaria, and children with severe malaria. Plasma levels of all 3 molecules were significantly higher in severe malaria than in uncomplicated malaria. High levels of neopterin and CRP during the acute phase of malaria significantly correlated with slow parasitological and clinical cure after therapy. In contrast, high NO plasma levels during the acute phase of malaria predicted accelerated cure. These findings provide further evidence for the protective role of NO in malaria. However, as NO levels were highest in severe disease, overproduction may be harmful for the patients.
BACKGROUND: Lipopolysaccharide (LPS) is a major trigger of sepsis-induced disseminated intravascular coagulation (DIC) via the tissue factor (TF)/factor VIIa-dependent pathway of coagulation. Experimental endotoxemia has been used repeatedly to explore this complex pathophysiology, but little is known about the effects of clinically used anticoagulants in this setting. Therefore, we compared with placebo the effects of unfractionated heparin (UFH) and low-molecular-weight heparin (LMWH) on LPS-induced coagulation. METHODS AND RESULTS: In a randomized, double-blind, placebo-controlled trial, 30 healthy male volunteers received LPS 2 ng/kg IV followed by a bolus-primed continuous infusion of UFH, LMWH, or placebo. In the placebo group, activation of coagulation caused marked increases in plasma levels of prothrombin fragment F(1+2) (P<0.01) and polymerized soluble fibrin, termed thrombus precursor protein (TpP; P<0.01); TF-positive monocytes doubled in response to LPS, whereas levels of activated factor VII slightly decreased and levels of TF pathway inhibitor remained unchanged. UFH and LMWH markedly decreased activation of coagulation caused by LPS, as F(1+2) and TpP levels only slightly increased; TF expression on monocytes was also markedly reduced by UFH. TF pathway inhibitor values increased after either heparin infusion (P<0.01). Concomitantly, factor VIIa levels dropped by >50% at 50 minutes after initiation of either heparin infusion (P<0.01). CONCLUSIONS: This experimental model proved the anticoagulatory potency of UFH and LMWH in the initial phase of experimental LPS-induced coagulation. Successful inhibition of thrombin generation also translates into blunted activation of coagulation factors upstream and downstream of thrombin.
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The amoebae's cytotoxicity test and the amoebae's lysis test were used to show possible interactions between rheumatoid factor (RF) and Entamoeba histolytica. Amoebae's cytotoxic activity (ACA) was inhibited by affinity chromatography purified antiamoebae rabbit IgG (RIgG). Enhanced inhibition could be demonstrated with RIgG plus RF. But the same marked inhibition of ACA could be seen when replacing RF by heat inactivated normal human serum as a control. About 50% amoebae's lysis occurred when amoebae were brought together with native normal human serum (NNHS) as a source of complement. Amoebae's lysis increased to 60% when incubated with NHS plus human antiamoebae antibodies. No further augmentation could be obtained by the addition of RF. Using RIgG instead of human antibodies the lysis rate did not increase. Incubation of amoebae, NNHS, RIgG and RF even reduced amoebae's lysis. RF neither has an effect on ACA nor on complement mediated AL in vitro.
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In this open pilot study, the potential therapeutic efficacy of Cyclosporin A (CsA) in systemic sclerosis (scleroderma) was investigated. Eight patients with severe scleroderma (skin manifestation and at least three organ manifestations such as pulmonary, intestinal, cardiac, renal, and severe hypertension) were included in the study. CsA administration was started at a dose of 5 mg per kg body weight per day and then, to obtain whole blood levels of 300-500 ng/ml, adjusted to a mean dosage of 4.3 mg/kg/day. Therapeutic effects were evaluated by monitoring the measures of cutaneous, pulmonary, cardiac, gastrointestinal, and renal involvement as well as laboratory parameters. After 6 to 12 months of CsA-administration, cutaneous abnormalities improved in seven, arterial oxygen tension slightly increased in four, pulmonary hypertension decreased in five, and smooth muscle esophageal contraction amplitudes improved in three patients. However, the disease progressed in one patient. No serious side effects were observed, and occurring renal side effects were mild. Taken together, these observations indicate that CsA administration may be effective mainly in the skin involvement, but also in some organ manifestations of scleroderma. The results of this pilot investigation therefore indicate that a controlled study of the efficacy of CsA in scleroderma is needed and ought to be performed.
In this study, technical, clinical and genetic aspects of anti-Ro/SSA, anti-Sm, and anti-RNP are discussed; different techniques may reveal differences in autoantibody frequencies and associations. Finally, the importance of anti-RA33, a new autoantibody characteristic of rheumatoid arthritis, is evidenced.
Five methods for the detection of antibodies against ds-DNA and nucleoprotein were compared with respect to their usefulness for the diagnosis and monitoring of SLE: filter radio-immunoassay (filter RIA), enzyme immunoassay (EIA N) and Crithidia lucilia assay (CL-IF) for detecting anti-ds-DNA antibodies as well as enzyme-immunoassay (EIA NP) and a latex test (LE test NP) for detecting anti-NP antibodies. In testing 32 SLE patients we obtained the following sensitivities: filter RIA 78%, EIA N 87%, CL-IF 47%, EIA NP 73% and LE test NP 25%. Among 95 patients having ANA greater than or equal to 1:100 in their sera, but who had no clinical signs of SLE, anti-ds-DNA antibodies were detectable in 12% (filter RIA), 16% (EIA N) and 4% (CL-IF) as well as anti-NP antibodies in 35% (EIA NP) and 4% (LE test NP). Only filter RIA and EIA N were of significant value in differentiating active from inactive SLE.
In 20 patients with rheumatoid arthritis the plasma fibronectin concentrations were measured and correlated with the levels of C-reactive protein, alpha 1-antitrypsin, alpha 2-macroglobulin, fibrinogen, C3, C4 complement fractions and alpha 2-antiplasmin in serum respectively plasma. Patients with rheumatoid arthritis showed plasma fibronectin concentrations within reference levels. However, the concentrations of C-reactive protein, alpha 1-antitrypsin, alpha 2-antiplasmin, fibrinogen and C3-complement fraction were significantly higher in comparison to the healthy controls. The results indicate that fibronectin does not belong to the group of "acute phase proteins". Measurement of plasma fibronectin give no additional information about the activity of rheumatoid arthritis.
OBJECTIVE: To determine the value of the circulating intercellular adhesion molecule (cICAM-1) as a marker for the inflammatory and fibrotic processes in systemic sclerosis (SSc). METHODS: We determined serum levels of cICAM-1 and of the soluble interleukin-2 receptor (sIL-2R) by an enzyme-linked immunosorbent assay in 33 patients with SSc. These values were compared to the concentrations of acute phase reactants and to the extent of skin involvement in diffuse and limited scleroderma. RESULTS: cICAM-1 was elevated in patients with diffuse SSc (498 +/- 134 ng/ml) as compared with 82 healthy controls (312 +/- 71 ng/ml) (mean +/- SD, p < 0.0001). The elevation of cICAM-1 did not correlate with the duration of disease, the pattern of organ manifestations or the type of treatment. While the concentrations of acute phase proteins were not elevated in SSc, a significant correlation between increased serum sIL-2R and cICAM-1 was observed. CONCLUSION: Increased levels of cICAM-1 indicate an activation of immune processes in SSc. The clinical value of the cICAM-1 determination in SSc can only be judged in longitudinal studies.
OBJECTIVE: To evaluate sucrose permeability as a non-invasive test for the monitoring of upper gastrointestinal mucosal damage (uGMD) in patients treated with NSAIDs. METHODS: 40 patients with non-inflammatory joint pain were enrolled in a prospective study. Before and after 14 days of ibuprofen treatment (3 x 400 mg/day), the rates of urinary sucrose excretion after an oral sucrose load were assessed. Individuals with increased sucrose permeability underwent endoscopy. RESULTS: 8 patients (20%) showed abnormal sucrose permeability before taking any NSAID. In 5/20 patients (25%) who completed 2 weeks of ibuprofen medication, sucrose excretion increased above the normal level. Endoscopic examination and biopsy revealed mild uGMD, but no ulceration in 8/11 (72%) patients with increased permeability to this marker. CONCLUSION: Sucrose permeability testing is a sensitive procedure for research protocols on NSAID-induced gastropathy. Since this test also seems to detect slight and clinically insignificant mucosal damage, however, its use in clinical decision-making regarding gastroprotective medication is limited.
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