Safety and efficacy of kunzea oil-containing formulations for the management of psoriasis: a randomized, controlled trial.

WHAT IS KNOWN AND OBJECTIVE: Anecdotally, topical kunzea oil has been used to treat various skin conditions, including psoriasis and eczema, with good results. This study compared the clinical efficacy of kunzea oil (20%)-containing formulations in mild to moderate psoriasis. METHODS: A randomized, comparative, double-blind, 8-week study was undertaken. Thirty patients (age range: 25-74 years and mean ± SD: 52·8 ± 13·6 years) with mild to moderate psoriasis (affecting at least 10% of one or more body regions: arms, head, legs and trunk) randomly received ointment and/or scalp lotion containing 20% kunzea oil (test group) or control medications not containing kunzea oil (control group). Formulations in both treatment arms also contained 5% liquor carbonis detergens (LCD) and 3% salicylic acid. The clinical responses to the test and control formulations were evaluated using the Psoriasis Area and Severity Index (PASI). RESULTS AND DISCUSSION: After 8 weeks of treatment, both test and control groups demonstrated a significant (P < 0·05) improvement in PASI scores. Subjects in the test group had a decrease in mean±SD PASI score from 12·7 ± 7·9 to 6·7 ± 7·2, whereas the control group showed a decrease in PASI score from 8·1 ± 4·6 to 3·5 ± 4·7. Comparative efficacy analysis between the test and control groups did not reveal any significant difference (P > 0·05). WHAT IS NEW AND CONCLUSIONS: The inclusion of kunzea oil made no difference to the efficacy of topical formulations containing LCD and salicylic acid for the treatment of psoriasis.

Toenail onychomycosis: an important global disease burden.

Onychomycosis is a fungal infection of the nail plate or nail bed. It does not usually cure itself and it can trigger more infectious lesions in other parts of the body. The reported prevalence of onychomycosis is increasing in Western countries, presumably due to lifestyle changes and the ageing of the population. Approximately 10% of the general population, 20% of the population aged>60 years, up to 50% of people aged>70 years and up to one-third of diabetic individuals have onychomycosis. Care should be taken for the accurate diagnosis and timely treatment of toenail onychomycosis to prevent complications. Current treatment options have relatively limited therapeutic success, particularly long-term. Oral medications are associated with high recurrence rates and treatment failure, and are not suitable for many cases due to potential adverse effects. Topical medications are recommended only for mild to moderate cases. The cost of therapies may also be prohibitive in some cases. In the light of these issues, more research is warranted for the investigation and development of more effective and economical options for the treatment and prophylaxis of toenail onychomycosis. In patient populations such as diabetic individuals, where onychomycosis can provoke lower extremity complications, professional podiatry care of toenails and feet should be encouraged.

Hyperbaric oxygen therapy increases free radical levels in the blood of humans.

It has been postulated that exposure to high concentrations of oxygen results in increased oxygen radical production which may account for the toxic effects of excessive exposure to oxygen. Examination of blood from persons undergoing hyperbaric oxygen (HBO) exposure, by low temperature electron spin resonance (ESR) spectroscopy, demonstrated a marked increase in the magnitude of a signal with properties consistent with a free radical (g = 2.006). The signal diminished to baseline levels within 10 minutes of cessation of HBO exposure. Further in vitro studies of blood revealed an ESR signal generated in red blood cells by oxygen, and dependent on oxyhaemoglobin, which had characteristics indistinguishable from those of the ESR signal of ascorbate radical and the signal in blood from persons undergoing HBO exposure. It is postulated that HBO exposure increases ascorbate radical levels in blood, which is likely to reflect increased ascorbate turnover in human red blood cells.

Delayed recovery from NG-nitro-L-arginine in the conscious sheep.

1. In the chronic, awake, instrumented sheep model NG-nitro-L-arginine (NOLA) an inhibitor of nitric oxide synthesis, injected at a dose of 40 mg/kg, produced a significant increase in systolic blood pressure (from 110 +/- 6 to 145 +/- 8 mmHg after 5 min) which persisted for at least 1 h but returned to baseline after 24 h. 2. When NOLA was repeated 1 and 4 days after the first injection, the blood pressure response was significantly attenuated, and at 1 day was no greater than the response to an equivalent volume of saline. The blood pressure response returned to the initial response with an 8 day interval between injections. 3. There was no significant blood pressure response to 100 mL of saline before the NOLA injection; however, 1 and 4 days after NOLA there was a significant rise in blood pressure.

Indomethacin inhibits the chemical carcinogen benzo(a)pyrene but not dimethylbenz(a)anthracene from altering Langerhans cell distribution and morphology.

Treatment of murine skin with the polyaromatic hydrocarbon carcinogens benzo(a)pyrene (BP) or dimethylbenz(a)anthracene (DMBA) for 3 weeks resulted in an increase and a decrease in epidermal Langerhans cell (LC) numbers, respectively, compared with solvent-treated skin. Implantation of subcutaneous indomethacin pellets prior to carcinogen treatment prevented the changes in LC numbers and morphology in BP, but not DMBA-treated skin. Indomethacin treatment was also found to reduce elevated prostaglandin E2 (PGE)2 levels in the skin of BP-treated mice, whereas PGE2 levels were not significantly raised in DMBA-treated mice. There thus appears to be a link between altered prostaglandin levels and LC numbers in murine skin treated with BP, but not DMBA. In the latter, LC numbers were reduced by mechanisms not reversed by indomethacin. It is concluded that increased prostaglandin levels may contribute to the impairment of cutaneous immunity previously observed in BP-treated mice by altering LC density and morphology within the epidermis.