A case of chronic actinic dermatitis that responded completely to treatment with oral colostrum‐macrophage‐activating factor (colostrum‐MAF)

A 41-year-old Japanese male patient with a half-year history of pruritic severe erythema on his face, neck, trunk and upper extremities, specifically on his sun-exposed areas, was diagnosed with chronic actinic dermatitis (CAD) at the Department of Dermatology at Yamaguchi University Hospital and was referred to the Saisei-Mirai Clinic in Kobe, Japan in September, 2015. He was hypersensitive to UVA at a dose of 1.7 J/cm2 (tested with a TOREX/FL20S-BL/DMR, Toshiba emitting light ranging from 315~410 nm, peaking at 360 nm; normal minimal erythema dose = > 10-15 J/cm2 ), but had a normal response to UVB (minimal erythema dose: 114 mJ/cm2 , tested with a Philips TL20W/12RS emitting light from 270 ~ 360 nm, peaking at 310 nm; normal minimal erythema dose= 60-100 mJ/cm2 ). This article is protected by copyright. All rights reserved.

A case of chronic actinic dermatitis that responded completely to treatment with oral colostrum-macrophage-activating factor (colostrum-MAF) A 41-year-old Japanese male patient with a half-year history of pruritic severe erythema on his face, neck, trunk, and upper extremities, specifically on his sun-exposed areas, was diagnosed with chronic actinic  Chronic actinic dermatitis is a rather rare photosensitive disease commonly affecting elderly men 4 and often is difficult to differentially diagnose from photoaggravated dermatitis, although CAD can arise in young people with pre-existing dermatoses, such as allergic contact dermatitis, atopic dermatitis, and HIV infection. 5 An alternative diagnosis in this patient was severe photoaggravated dermatitis, especially as the patient's sensitivity was to UVA rather than UVB.
The exact pathological mechanism of CAD still remains to be clarified. It had been regarded as a contact dermatitis-like reaction, 6 but Ko et al 7 recently proposed that CAD may be caused by a Th1/ Th2 dysbalance, based on the positive relationship between clinical severity and total IgE level and eosinophilia in the peripheral blood of patients with CAD.
For the correct diagnosis of CAD, photosensitivity tests using an artificial light source from UVB to visible light are essential, and patch tests using European Standards Allergen Series plus sunscreens, corticosteroids cosmetic series, and photo-patch tests are also recommended. 6,7 In this case, a patch test was not performed, since the patient did not agree to that test.
For clinical management, the avoidance of active wavebands is basically the most important. To manage acute eczematous dermatitis, topical use of corticosteroid-or calmodulin inhibitor-containing ointments is commonly recommended, but these topical treatments are not so effective in most patients with CAD. The present 41-year-old male patient was photosensitive to UVA and was refractory to topical treatment with the strongest class corticosteroids for more than 3 months and to oral intake of small amounts of predonisolone (5 mg/d) for approximately 2 months.
Severe exudative erythema with scratch marks on his face responded quite well to oral uptake of two capsules of bovine colostrum-MAF. The exact amount of colostrum-MAF contained in each F I G U R E 2 A, Suppressive effect of colostrum-MAF against TNF-α production induced by LPS and IFN-γ. Mouse peritoneal macrophages were cultured in 24-well plates at a density of 5 × 10 5 cells/well in serum-free RPMI 1640 for 18 h. The cultured cells were washed two times with serum-free RPMI and were then treated with LPS (1 μg) + IFN-γ (10 ng) with or without colostrum (100 ng) or colostrum-MAF (100 ng) for 24 h. The supernatants were then collected and assayed with an ELISA kit for Mouse TNF-α (ELISAReady-SEF-Go). The combination of LPS (1 μg) and IFN-γ (10 ng) significantly induced TNF-α production by mouse peritoneal macrophages. In contrast, the addition of colostrum (100 ng) or colostrum-MAF (100 ng) to LPS + IFN-γ significantly decreased the production of TNF-α, just like curcumin (20 μM) that was used as a positive control. Data are expressed as means and standard deviations from three independent experiments. The statistical significance was determined by Student's t test. *P < 0.05 B. Effect of colostrum-MAF on the polarization of M2 macrophages. Mouse peritoneal macrophages were treated with IL-4 (30 ng) + IL-13 (30 ng), colostrum (10 ng), or colostrum-MAF (10 ng) for 24 h. After fixation with methanol for 10 min, the cells were dried and incubated overnight with 1 mL 1% BSA at 4°C. After washing with PBS, immunocytochemical staining was performed for macrophage mannose receptor (CD206) on permeabilized cells to visualize cell surfaces. Treatment with IL-4 and IL-13 (each 20 ng) was used as a positive control to induce M2 macrophages. Colostrum-MAF (100 ng) significantly induced M2 macrophages but in contrast, colostrum alone (100 ng) did not induce M2 macrophages. All experiments were performed in triplicate, and data are reported relative to the fluorescence intensity of the control. Each error bar represents the standard deviation. *P < 0.05 [Colour figure can be viewed at wileyonlinelibrary.com] In the present study, we found that colostrum-MAF increased the number of and activated M2 macrophages, but not M1 macrophages, and significantly suppressed LPS-induced inflammatory cytokines activation in an in vitro study of mouse intra-peritoneal macrophages.