Notalgia paresthesica successfully treated with narrow‐band UVB: report of five cases

Background Notalgia paresthesica is a disorder of unknown origin characterized by pruritus localized to the patients’ back. Local pain, burning or paresthesias have also been described. No definite treatments have been found for this disorder and most of those reported to date are anecdotal. Topical capsaicin is the option most widely used among dermatologists. Transcutaneous electrical nerve stimulation, gabapentin, oxcarbazepine and botulinum toxin have recently shown promising effects. UVB has been used for decades to treat different pruritic skin diseases, but its benefits in the management of NP have not been stated to date. Objectives To test the effects of UVB in notalgia paresthesica. Methods We used a course of UVB narrow band to treat five patients with notalgia paresthesica. The treatment was administered following a phototype protocol in a UV 7002 cabinet. Results We provide the results of a course of UVB narrow‐band phototherapy in five patients. Phototherapy contributed substantially to improve pruritus in all of them. Conclusion Given the benefits achieved, we stress the interest of UVB narrow‐band as a safe and well tolerated alternative treatment for notalgia paresthetica.     

Phototherapy and photochemotherapy

The treatment of skin diseases with ultraviolet radiation represents an important therapeutic modality in clinical dermatology, and the number of skin diseases that improve under the phototherapeutic modalities of today is still growing. While clinical phototherapy was originally based on empirical observations, our present understanding of the underlying mechanisms has improved substantially due to important progress in photobiological science. The better understanding of this scientific basis of treatment allows to both choose the correct phototherapeutic modality and determine the most effective treatment regimen. The aim of this article is to discuss the appropriate indications for phototherapy as well as its safe and effective employment, providing practical help in daily clinical phototherapeutic practice.     

Variables in full‐body ultraviolet B treatment of skin diseases

Ultraviolet B (UVB) treatment is most often performed according to a fixed schedule, not necessarily considering important variables such as UV intensity, type of UVB source and skin pigmentation. These variables can rather easily be taken into consideration by the right choice of dosing unit. The advantage of going from dosing in time to Joule to standard erythema dose or to minimal erythema dose is considered. The size of most variables may be diminished considerably. Following these guidelines, it is possible to increase the efficacy of UVB phototherapy without increasing the risk of unintentional burning.     

他扎罗汀和窄谱中波紫外线联合对角质形成细胞他扎罗汀诱导基因3 mRNA的影响

目的:研究他扎罗汀和窄谱中波紫外线(NB-UVB)对培养的正常人角质形成细胞增殖和他扎罗汀诱导基因3(TIG3)mRNA表达的影响.方法:用0.1～1.0μmol/L他扎罗汀和/或50～100 mJ/cm2 NB-UVB处理正常人角质形成细胞24 h后,用MTT法和实时荧光定量RT-PCR法分别检测细胞增殖和TIG3 mRNA水平的改变.结果:0.1～1.0μmol/L他扎罗汀处理角质形成细胞后,可抑制细胞的增殖和上调TIG3 mRNA的水平,且较高剂量(1 μmol/L)的他扎罗汀的作用强于较低剂量(0.1 μmol/L)的他扎罗汀;NB-UVB单独作用时,未能明显抑制角质形成细胞的增殖和上调TIG3 mRNA的水平;二者联合作用时,对角质形成细胞的增殖抑制作用和TIG3 mRNA的诱导作用更强,且强于二者单独作用.结论:他扎罗汀单独处理可抑制角质形成细胞(KC)的增殖和上调TIG3 mRNA水平,但NB-UVB单独照射无此作用;二者联合作用时可协同抑制角质形成细胞的增殖和上调TIG3 mRNA的水平.     

Expression of nitric oxide synthases in keratinocytes after UVB irradiation

The importance of nitric oxide (NO) in mediating vasodilation, neurotransmission, and immune and inflammatory responses has been demonstrated. Human keratinocyte express inducible nitric oxide synthase (iNOS) and the neuronal constitutive isoform of NOS (ncNOS). We established an in vitro model in keratinocytes to investigate changes in NO, iNOS and ncNOS expression after UVB exposure. We demonstrated a large induction of NO after UVB exposure and that the source of NO produced in UVB-exposed keratinocytes was increased expression of iNOS and ncNOS. The increased NO production with increased expression of iNOS and ncNOS may contribute to the pathological and physiological features of UVB-induced erythema and skin inflammation.     

Photo(chemo) therapy for vitiligo

Vitiligo has always been difficult to treat. Several modes of treatment are available, but the therapeutic effect varies greatly, and rarely does one achieve complete repigmentation. One of the most efficient treatment methods is photo(chemo) therapy. Already in ancient Egypt, vitiligo lesions were treated with extracts of the Ammi maius plant followed by exposure to the sun. This principle is at the basis of the photochemotherapy or PUVA therapy, whereby UVA irradiations are given 2 h after administration of 8-methoxypsoralen, a photosensitizer. Another efficient treatment form is UVB phototherapy, particularly narrow-band UVB. This not only gives good therapeutic results but also has the advantage of eliminating the need for a photosensitizer. All these treatments must be applied for many months to be efficient. They can also be combined with various surgical skin-grafting techniques. A newer approach is targeted UVB phototherapy, whereby xenon-chloride lasers or monochromatic excimer light is used.     

Direct effects on proliferation,antigen expression and melanin synthesis of cultured normal human melanocytes in response to UVB and UVA light

BACKGROUND/PURPOSE: Ultraviolet (UV) radiation; induces a variety of responses in the skin, including tanning and inflammation, and may also act as a carcinogen. As epidermal melanocytes are seen as the major targets of UV light, the present study was conducted to evaluate the direct effects of UVA and UVB irradiation on melanocytes in vitro. METHODS: Normal human epidermal melanocytes (NHM) were exposed on 3 consecutive days to UVA (0.072-7.2 J/cm2) and UVB (7.2-48 mJ/cm2), respectively, and changes of morphology, cell number, melanin synthesis and antigen expression (APAAP technique) were determined 5 days after the first exposure. RESULTS: UVA radiation caused only minimal effects on NHM by slightly inducing expression of the activation marker HMB-45 and decreasing expression of the proliferation marker Ki-67. No changes of morphology, cell number or melanin synthesis were detectable with any of the applied doses. On the other hand, UVB radiation significantly induced dendrite formation and decreased the number of NHM in a dose-dependent manner (74% of the controls at 7.2 mJ/cm2, 64% at 14.4 mJ/cm2 and 28% at 36 mJ/cm2). Significant induction of the activation marker HMB-45 was found in parallel to decreased expression of the differentiation marker K.1.2.58. UVB doses >or=9.6 mJ/cm2 also resulted in significant downregulation of the proliferation marker Ki-67, confirming the data of the cell counts, and melanin content was increased in NHM (20% over the controls, P<0.01) after applying 7.2 mJ/cm2 UVB. CONCLUSION: Our results may suggest that the effect of UVB radiation in skin is due to direct activation of melanocytes, whereas skin tanning caused by UVA is mediated rather in an indirect way.     

UVB照射配合中药治疗白癜风疗效观察

目的：观察UVB疗法配合中药治疗白癜风的临床疗效。方法：UVB照射每周3次，照射前2h外用“白殿净”，同时根据气血不足，淤血阻滞、肌肤气血失和致皮肤白斑，治宜补气养血、活血通络配合光敏性中药治疗半年，评定结果。结果：治疗组与对照组有效率比较差异有显著性（P〈0．05）。结论：采用UVB照射配合中药治疗白癜风其疗效优于单纯口服中药组。     

Effects of inhibition of urokinase-type plasminogen activator (u-PA) by amiloride in the cornea and tear fluid of eyes irradiated with UVB

The purpose of the present study was to test our hypothesis that amiloride, a specific u-PA inhibitor, effectively decreases u-PA activity in cornea as well as in tear fluid and favourably affects corneal healing. Therefore, comparative histochemical and biochemical studies of u-PA and the effects of amiloride were performed on rabbit corneas and tear fluid using the sensitive fluorogenic substrate Z-Gly-Gly-Arg-7-amino-4-trifluoromethylcoumarin. Rabbit eyes were repeatedly irradiated with UVB for 9 days and during the irradiation topically treated with amiloride (1 mg/ml saline) or placebo (saline) (dropwise, 5 times daily). Results show that in placebo-treated eyes, UVB evoked the appearance of u-PA activity in cornea and tear fluid in early stages of irradiation, and u-PA levels increased during irradiation. Corneal epithelium was gradually lost and remnants of the epithelium as well as keratocytes in the upper part of corneal stroma showed high u-PA activity. Finally, corneas lost their epithelium completely. In corneal stroma, numerous u-PA-containing inflammatory cells were present. Corneas were vascularized. When amiloride was dropped on the eye surface on the first day of irradiation and subsequently daily until the end of the experiment, u-PA activity in both cornea and tear fluid was strongly inhibited. Corneas were covered with a continuous epithelium until the end of the experiment. The number of inflammatory cells was significantly decreased. Corneal vascularization was reduced by 50%. In conclusion, early application of amiloride inhibited u-PA activity in UVB-irradiated corneas as well as in tear fluid and diminished the development of corneal pathology.