Successful treatment of disseminated strongyloidiasis.

OBJECTIVE: To report the successful treatment of Strongyloides stercoralis hyperinfection, which is usually lethal but in this case was diagnosed in its early stages. CLINICAL FEATURES: A 44-year-old woman, who had spent much of her life in Fiji and India, was treated with a high dose of prednisolone for rheumatoid arthritis complicated by gold lung. The onset of abdominal symptoms, an exacerbation of respiratory symptoms, and a persistent high eosinophil count and serum IgE level, led to the detection of numerous Strongyloides larvae in her faeces and sputum. INTERVENTION AND OUTCOME: She was treated with thiabendazole for five days, then mebendazole for one month, and the dose of prednisolone was reduced. Clinical symptoms and signs improved within days and after one week parasites could not be found in her faeces. After six months, enzyme-linked immunosorbent assay for Strongyloides infection gave a reading which was 40% of the initial level but still in the positive range. CONCLUSION: Steroid therapy in individuals with chronic, subclinical strongyloidiasis predisposes to the insidious development of hyperinfection syndrome, which has a high mortality rate. If detected early, this complication can be treated effectively. It can be prevented by actively seeking Strongyloides infection, by faecal microscopy and culture techniques and by serological tests, in high-risk individuals, such as immigrants from endemic areas.

Disposition of and clinical response to salicylates in patients with rheumatoid disease.

The disposition of salicylic acid (SA) and its metabolites and the clinical response to long-term aspirin treatment at varying doses were assessed in patients with rheumatoid disease. Steady-state kinetics of SA (total and unbound), salicyluric acid (SUA), gentisic acid (GA), and clinical status were estimated weekly in 10 patients with rheumatoid arthritis. Eight received a soluble aspirin form and two received an enteric-coated form. The starting dose of aspirin in each patient was 1.8 gm (soluble) or 1.95 gm (enteric-coated) daily. Weekly increments in dose were made until a satisfactory clinical outcome was achieved. The final aspirin dose range was 3.6 to 8.1 gm daily, which resulted in mean steady-state plasma SA concentrations (CpSA) from 56 to 375 mg/l. Since the mean total CpSA increased approximately proportionately over the dose range, there was little change in total SA clearance. By contrast, increasing aspirin dosage resulted in decreased clearance and disproportionate increases in unbound SA (CpuSA). The maximum velocity of conversion of SA to SUA (Vm) increased significantly, from 57.3 +/- 11.7 mg/hr at an aspirin dose of 1.8 gm/day to 71.4 +/- 19.4 mg/hr at the next highest dose (2.7 to 3.6 gm/day), with no further change with increasing dosage. Km ranged from 0.4 to 1.2 mg/l for CpuSA and from 5.5 to 17.2 for total CpSA. Renal clearance of SUA (ClSUA) ranged from 124 to 893 ml/min and correlated with creatinine clearance. ClGA ranged from 23 to 164 ml/min, and ClSA ranged from 0.1 to 17.1 ml/min; neither correlated with creatinine clearance.(ABSTRACT TRUNCATED AT 250 WORDS)

In vivo and in vitro studies on the binding of salicylate to human plasma proteins: evidence for one type of binding site.

In vivo and in vitro binding of salicylate to plasma proteins was studied by ultrafiltration at room temperature. The nonlinearity of the Scatchard and Klotz plots were explained by the presence of lipid-soluble substances in plasma. Delipidation of plasma resulted in changes of the binding characteristics of plasma in that more moles of salicylate could be bound per mole of protein. This changed the appearances of the Scatchard and Klotz plots so that a much larger range of salicylate concentration could be accommodated by the linear portion of the graphs. The equilibrium constant for the in vitro salicylate binding was identical for the delipidated and untreated plasma. However, the in vivo binding constant for salicylate in plasma was higher than the in vitro binding constant.