Hair transplantation for therapy-resistant alopecia areata of the eyebrows: is it the right choice?

Alopecia areata is a common skin disorder of presumed autoimmune etiology and it usually shows an unpredictable course. Treatment of alopecia areata is challenging. There is very little information on the use of surgical therapies for the treatment of alopecia areata in the medical published work. A 24-year-old male patient was referred to a private hair transplantation clinic owned by one of the authors for the treatment of therapy-resistant alopecia areata affecting both eyebrows. He had quickly lost all body hair 4 years prior beginning from the scalp. He received psoralen and ultraviolet A (PUVA) therapy for alopecia universalis and all body hair re-grew except his eyebrows. Alopecia areata was stable for the 18 months following the last medical treatment he received. Because there was no response to various medical therapeutic agents, we decided to transplant occipital hairs to the eyebrow area. After the patient understood and accepted all risks, occipital hairs were transplanted to the eyebrows by using the follicular unit extraction technique. Postoperatively, the patient did not receive any topical or systemic therapies for alopecia areata. Although 40% hair re-growth was detected in his eyebrows at 1 year postoperation, this rate was 80% by 2 years postoperation. However, there was resistance to re-growth in the medial eyebrow regions. New eyebrows grew as occipital hairs and required trimming. His satisfaction from the surgical procedure was 90% at the end of the 24th postoperative month. Surgical treatment of diseases like alopecia areata is still controversial. Our case report offers an additional contribution to the published work on the surgical methods used in the treatment of stable alopecia areata.

Saving the zone of stasis in burns with activated protein C: an experimental study in rats.

Salvage of the zone of stasis is a major subject of focus in burn research. Use of various antithrombotic, anti-inflammatory and antioxidant drugs have been studied experimentally, with reports of favourable results; however, none became popular in clinical practice. Activated protein C (APC) is a well-known physiologic anticoagulant. Recent studies revealed that APC contributes not only to systemic anticoagulant activities but also to anti-inflammatory activities by inhibiting leucocyte activation associated with TNF production. The likely favourable effects of APC on salvage of the zone of stasis were investigated on a well-described experimental rat burn model representing the zone of stasis according to the 'burn comb model'. Twenty Sprague-Dawley rats were used and randomly separated into experimental and control groups. Two hours after inducing injury, 100 microg kg(-1) APC (Sigma, Boehringer Ingelheim, Germany) was administered to the experimental group through the caudal vein while 0.9% saline was injected through the same route in the control group. Laser Doppler flowmetry measurements and autoradiography were used for evaluation of perfusion and viability in the zone of stasis. At day 3, the differences between the results obtained from the treatment and the control groups were found to be statistically significant (p<0.05). Our experimental study revealed that APC improved tissue perfusion and decreased the area of skin necrosis in the zone of stasis in rats. The dual effect of APC, each of which has been shown to be favourable in saving the zone of stasis, may make this agent effective with a single effect in treatment of burn injury.

Thalidomide decreases the plasma levels of IL-1 and TNF following burn injury: is it a new drug for modulation of systemic inflammatory response.

TNF and IL-1, which are produced from phagocytic cells, can produce a significant systemic inflammatory response independently by inducing systemic leukocyte and endothelial cell activation. These cytokines play a pivotal role in development of systemic inflammatory response after severe burn. Thalidomide has been shown to decrease the secretion of TNF from phagocytic cells, therefore suppression of TNF and IL-1 production from activated phagocytic cells might be a successful treatment modality for prevention of systemic inflammatory response following severe burn. To address this issue, we aimed to show whether thalidomide treatment decreased or suppressed plasma levels of TNF and IL-1 following burn in rats. Following the injury, 36 rats were randomly separated into two experimental groups at the third and seventh days. Rats in the experimental group had oral thalidomide (10mg/kg day) treatment for three and seven consecutive days whereas animals in control groups had no treatment. Thalidomide treatment decreased TNF and IL-1 significantly in both experimental groups at both the points (P<0.05). Although in this study we just showed inhibitory effect of thalidomide on plasma the level of TNF and IL-1, we speculate that thalidomide may have modulatory effect on the systemic inflammatory response after burn by decreasing plasma levels of TNF and IL-1.