Administration of anti-tumor necrosis factor (anti-TNF) agents is beneficial in a variety of chronic inflammatory conditions, including psoriasis. We describe 5 patients in whom psoriasiform skin lesions developed 6-9 months after the initiation of anti-TNF therapy for longstanding, seropositive rheumatoid arthritis (etanercept or adalimumab), typical ankylosing spondylitis (infliximab), and Adamantiades-Behçet's disease (infliximab). In all 5 patients, the underlying disease had responded well to anti-TNF therapy. Four patients developed a striking pustular eruption on the palms and/or soles accompanied by plaque-type psoriasis at other skin sites, while 1 patient developed thick erythematous scaly plaques localized to the scalp. In 3 patients there was nail involvement with onycholysis, yellow discoloration, and subungual keratosis. Histologic findings from skin biopsies were consistent with psoriasis. None of these patients had a personal or family history of psoriasis. In all patients, skin lesions subsided either with topical treatment alone, or after discontinuation of the responsible anti-TNF agent. The interpretation of this paradoxical side effect of anti-TNF therapy remains unclear but may relate to altered immunity induced by the inhibition of TNF activity in predisposed individuals.

Objective-To report clinical experience from patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) who were receiving recommended doses of hydroxychloroquine for more than six years, and were monitored for evidence of hydroxychloroquine related retinopathy every six months. Methods-A prospective (and continuing) evaluation was made of the potential retinal toxicity ofhydroxychloroquine in a cohort of 360 Greek patients followed for RA and SLE, 58 Sjogren's syndrome, together with their antithrombotic and lipid decreasing action and lack of life threatening toxicity are likely to lead to a continuing increase in the number of patients treated with these drugs.'1 The recently proposed mechanism of immunological action of antimalarial agents, namely interference with normal antigen presentation by increasing the intracytoplasmic pH,4 provides an exciting basis for the usefulness of these agents. However, because of the well known ocular toxicity of antimalarial agents, some rheumatologists underutilise them, while fear of sustaining damage to their eyes deters many patients from taking them. According to the information leaflet that currently accompanies hydroxychloroquine medication, the practitioner prescribing the drug should expect to receive an assessment report from the patient's ophthalmologist every three months.The present study was begun in 1985 and is a continuing longitudinal evaluation of the potential retinal toxicity ofhydroxychloroquine in Greek patients suffering from RA and SLE (S Papazoglou et al: preliminary findings presented at the XVIIth International League of Associations for Rheumatism Congress of Rheumatology, Rio, Brazil, 1989). From a total of 360 patients included in the study up to May 1995, the clinical experience from a subgroup of 58 patients receiving the drug in recommended doses for more than six years is described here. Patients and methods STUDY POPULATIONThis prospective study included consecutive patients with RA or SLE, followed at the Departments of Clinical Therapeutics and Internal Medicine of the Athens University Medical School and the Rheumatology Department of the General Hospital, Athens, Greece, who were being treated with hydroxychloroquine. Abnormality of visual function or retinal appearance at baseline were the only exclusion criteria. Of 360 patients that have been studied to date, the subgroup who have received long term treatrment comprised 58

The metabolic effects of honey - alone or combined with other foods - were investigated in type II diabetics using 2 protocols: A) 33 g honey and 50 g bread (same amounts of carbohydrate) were given on alternate days to 12 patients. Blood levels of glucose, insulin and triglycerides were determined in venous samples before and every 30 min after meal ingestion (for a total of 3h). Areas under glucose curves were equal, although honey - compared to bread - resulted in higher blood sugar concentrations at 30 min (p less than 0.01) and lower at 90 min (p less than 0.05). B) Another 19 type II diabetics consumed on separate days 3 different meals: H (30 g honey), HA (30 g honey, 100 g almonds), HB (30 g honey, 125 g cheese, 10 g bread, 10 g butter). HA and HB contained the same amount of fat, but were different in fiber. No significant differences in the areas under glucose curves were observed. However, meal H produced earlier hyperglycemia than HA and HB (30 min: p less than 0.01). Insulin levels were higher after HB compared to H (p less than 0.05). Meals HA and HB were followed by higher triglyceride levels than H (p less than 0.05). It is concluded that: 1) honey and bread produce similar degrees of hyperglycemia in type II diabetics. 2) Fat-rich foods added to honey do not alter the total hyperglycemic effect but result in higher triglyceride and insulin serum concentrations.

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In an open randomized study the safety, efficacy and kinetics of a twice-daily amikacin (7.5 mg/kg bd) regimen (group A) was compared with a once-daily dosage (15 mg/kg) schedule (group B). Thirty patients were enrolled in each group. They were suffering from urinary tract infections (37), respiratory tract infections (17), soft-tissue infections (3), exacerbation of chronic prostatitis (1), acute cholangitis (1) and abdominal abscess (1). Aggravating factors were present in 77% and 60% of the groups respectively. The pathogens isolated included strains of various Enterobacteriaceae (53) and Pseudomonas aeruginosa (10) In 76.7 vs 97% (P less than 0.05) the clinical result was satisfactory with pathogen eradication in 80 vs 86.7%. However, there were proportionately more patients in the 7.5 mg/kg bd regimen with respiratory tract infection (40 vs 13%) and fewer patients with urinary tract infections (40 vs 80%). Mild and transient nephrotoxicity and ototoxicity was observed in five and three patients respectively. More patients in group B had amikacin trough concentrations less than or equal to 5 mg/l and peak levels greater than 40 mg/l (P less than 0.001) as well as serum bactericidal titres greater than or equal to 1:16 (P less than 0.05) without significant serum amikacin accumulation over time. It is concluded that amikacin administered once daily is well tolerated and provides better serum bactericidal activity than the twice-daily regimen.