The Tangs Derma-Zema range comprises five formulas for eczema, atopic dermatitis, urticaria and related conditions. They are selected by pattern, not fixed to a diagnosis.

In Chinese medicine, eczema that keeps returning is usually related to weak digestive function allowing dampness to accumulate, together with a poorly defended body surface that wind repeatedly penetrates. Over time this depletes yin and blood, and the skin becomes dry, thickened and more intensely itchy.

This also explains a common puzzle: why the body can hold dampness while the skin itself is dry. In Chinese medicine the spleen distributes fluids around the body. When that function falters, fluid accumulates internally yet fails to reach the skin — so dampness and dryness can occur together.

This range therefore does not rely on strong bitter-cold herbs. It works instead by strengthening digestion and clearing dampness, consolidating the body surface, and nourishing yin and blood, helping the body restore its own regulation. Acute redness, weeping and erosion are addressed with the topical preparations.

Your physician considers whether your lesions are weeping or dry, when the itch worsens (for example whether it is worse at night), whether you perspire easily or feel averse to wind, and your digestion and bowel pattern, and selects the formula on that basis. These are prescription formulas and require consultation and pattern diagnosis by a physician.

Conditions Commonly Managed 

Atopic dermatitis, Eczema, Urticaria (hives), neurodermatitis (Lichen Simplex Chronicus), Seborrheic dermatitis, chronic prurigo (prurigo simplex), hypersensitive/allergic skin disease

Contraindications

Do Not Take Tangs Derma-Zema If You:

• are pregnant
• are taking warfarin or any other anticoagulant or antiplatelet medication — this formula contains Radix Salviae Miltiorrhizae (Danshen), which may increase bleeding risk
• have a known allergy to any ingredient listed below
• have significant liver or kidney impairment, unless cleared by your doctor

Do Not Take Together With:

Corticosteroids and other immunosuppressants, both conventional and herbal (including UVB and PUVA phototherapy). Full list: Corticosteroids or immunosuppressive drugs. (Herbal and Conventional)

Commonly overlooked items on that list include fish oil, flaxseed oil, evening primrose oil, turmeric, resveratrol, chia seeds, cordyceps, Centella asiatica and cassia seed. Please tell us everything you are taking, including supplements and health foods.

Have a known allergy to any ingredient listed below.

Stop and Seek Medical Attention If:

Widespread painful blistering with fever or feeling unwell (possible eczema herpeticum); rapidly spreading redness over most of the body; signs of skin infection such as increasing warmth, swelling, or pus; unusual bruising or bleeding; difficulty breathing or facial swelling.

Estimated Recovery Period
治愈时间

• For patients who have previously undergone treatment with immunosuppressants, the frequency and severity of relapses during the treatment process, as well as the length of time required for complete recovery, are positively correlated with the type, dosage, intensity, and duration of both topical and systemic immunosuppressive agents previously used. For example, the more frequently and for a longer duration that topical corticosteroids are used, the larger the area of skin they are applied to, and the more potent they are, the longer the required recovery time, and the more frequent and severe the relapses will be. Additionally, skin affected by more frequent and prolonged use of topical corticosteroids will also recover more slowly. Furthermore, the skin at the site of the rash may become darker after it fades, and continued treatment is necessary until the skin returns to its original white color and smooth texture to achieve complete recovery.
• These are individual observations recorded during clinic follow-up, not controlled outcome data, and they do not predict the course of any other patient. Eczema is currently regarded in modern medicine as a chronic relapsing condition for which no cure is established. We make no claim that Tangs Derma-Zema cures eczema or prevents relapse.

Prognosis of the Immunosuppressants Withdraw Syndrome:
波浪式反复 (免疫抑制剂反弹症)

Tangs Derma is not given alongside corticosteroids or other immunosuppressants. Where a patient is already receiving such treatment, any change must be planned and supervised by the doctor who prescribed it. Systemic corticosteroids in particular must never be stopped abruptly: abrupt withdrawal can cause adrenal insufficiency, and can trigger a severe generalised flare (erythroderma). We will not begin herbal therapy until a withdrawal plan has been agreed with the prescribing doctor. Patients with a history of immunosuppressant use will likely start to experience the so-called Wavelike Flare-up Cycle (above figure). This is known as the Immunosuppressant Withdrawal Syndrome. Symptoms of eczema which had previously been suppressed by immunotherapy will start to resurface with vigor after the immune system is no longer being curtailed. Over time, as Tangs Derma-Zema gradually takes effect in correcting the immune system’s function, the flareups will subside in frequency and intensity in a wavelike pattern (above figure). The time to reach the endpoint where the wave draws to a null will depend on the dosage and potency of the immunosuppressants that the user had formerly consumed.

Diagram of the Recovery Processs
治疗过程图解

Dosage

3000mg to be taken two times daily

Precaution

• During the course of Tangs Derma-Zema therapy, abstain from all immunosuppressants and oral contraceptive pills. Abstain from alcohol consumption and avoid late nights. Avoid hot baths, and do not aggravate the skin by scratching or peeling the eczema lesions. A more relaxed lifestyle is recommended.
• 皮质类固醇等免疫抑制剂药物 (包括UVB和PUVA) 和植物类免疫抑制剂药物 (甘草,白鲜皮,蝉蜕,大黄,金银花,雷公藤等),口服避孕药,饮酒,熬夜,刺激癣疹(搔抓搓),精神情绪不稳定,热水洗浴.
• Have a known allergy to any ingredient listed below／对下列任一成分已知过敏

Ingredients

Tangs Derma-zema (Derma-1), each 360mg extract equivalent to 2344mg raw herbs:
Radix Saposhnikoviae [1-4] 313mg
Radix Paeoniae Alba [5-13] 480mg
Radix Astragali [14-16] 588mg
Ramulus Cinnamomi [17-22] 300mg
Semen Coicis [23-29] 600mg
Radix Codonopsis [30-35] 63mg

Tangs Derma-2, each 360mg extract equivalent to 800mg raw herbs:
Radix Ophiopogonis [36-40] 100mg
Radix Salviae Miltiorrhizae [41-45] 100mg
Radix Scrophulariae [46-52] 270mg
Rhizoma Atractylodis Macrocephalae [53-59] 330mg

Tangs Derma-3, each 360mg extract equivalent to 1150mg raw herbs:
Radix Salviae Miltiorrhizae [41-45] 200mg
Radix Scrophulariae [46-52] 270mg
Rhizoma Atractylodis Macrocephalae [53-59] 230mg
Radix Asparagi [60-62] 100mg
Fructus Lycii [63-66] 350mg

Tangs Derma-4, each 360mg extract equivalent to 2310mg raw herbs:
Radix Salviae Miltiorrhizae [41-45] 200mg
Radix Scrophulariae [46-52] 270mg
Rhizoma Atractylodis Macrocephalae [53-59] 330mg
Fructus Lycii [63-66] 350mg
Folium Mori [67,68] 580mg
Flos Chrysanthemi [69-72] 580mg

Tangs Derma-5, each 360mg extract equivalent to 940mg raw herbs:
Radix Saposhnikoviae [1-4] 500mg
Radix Astragali [14-16] 150mg
Rhizoma Atractylodis Macrocephalae [53-59] 150mg
Rhizoma Zingiberis [73-82] 100mg
Fructus Jujubae [83-86] 40mg

Clinical Evidence

Radix Saposhnikoviae [1-4]: suppresses Th1 differentiation and function — reduced IFN-γ production and T-bet expression, decreased Th1/Th2 cytokine ratio — in murine allergic contact dermatitis, mediated in part by downregulation of dendritic cell maturation and costimulatory molecule expression [1]. Structural characterisation and further immunomodulatory data appear in [2-4].

Radix Paeoniae Alba [5-13]: suppresses Th2 cell-mediated responses — reduced serum IgE, decreased IL-4/IFN-γ ratios, reversal of Th2 skewing — and inhibits mast cell activation [5,6]. Paeoniflorin and total glucosides of paeony act on NF-κB, MAPK, PI3K/Akt and JAK/STAT signalling [7-9], and in rheumatoid arthritis, experimental autoimmune encephalomyelitis and atopic dermatitis models reduce disease severity and promote immune tolerance by shifting Th1/Th2 activity [10,11]. Paeoniflorin in hyaluronic acid hydrogel microspheres or as carbon dots in chitosan hydrogel shifts macrophage polarisation from M1 to M2 [12,13].

Radix Astragali [14-16]: flavonoids suppress Th1 and Th17 differentiation and cytokine production (IFN-γ, IL-17) while promoting Treg differentiation, via JAK/STAT and NF-κB signalling [14,15]. Other work reports the opposite direction — increased IL-4 and reduced IFN-γ indicating Th2 polarisation, together with increased CD8 expression supporting cytotoxic T cell activation [16].

Ramulus Cinnamomi [17-22]: the evidence is anti-inflammatory in direction. Ramulus Cinnamomi essential oil, in which (E)-cinnamaldehyde is roughly 65% of content, inhibits N-acylethanolamine acid amidase, preventing degradation of PEA and OEA and reducing nitric oxide and TNF-α in LPS-stimulated macrophages [17]. In collagen-induced arthritis, Cinnamomi Ramulus extract reduced paw volume, arthritis index and TNF-α, IL-17A, IL-6 and IL-1β, implicating the TNF and IL-17 pathways and NF-κB p65 [18]. An ethanol extract blocks Src/Syk-mediated NF-κB activation [19], and cinnamaldehyde suppresses macrophage cytokine output only in the presence of activated T cells, by eliminating reactive oxygen species [20].

Semen Coicis [23-29]: the effect depends on which fraction is studied. A (1→6)-α-glucan and a branched fructoglucan inhibit LPS-induced inflammation in RAW264.7 macrophages and reduce acute inflammatory swelling in vivo [23], and structure-dependent immunomodulatory, antioxidant and microbiota-regulatory activities of Coix polysaccharides are reviewed in [24-26]. The phenolic constituent coixol suppresses the HSP70/TLR4/NF-κB pathway in hepatic macrophages, reducing HMGB1, TNF-α and iNOS [27], and in colitis modulates macrophage polarisation, elevates Axin1 to promote β-catenin degradation, and expands colonic ILC3 driving IL-22-dependent mucosal healing — an effect abolished by IL-22 neutralisation [28]. Coix seed oil, a lipid extract distinct from the whole raw seed used here, inhibits Th17 differentiation by reducing the leptin–PPARγ interaction [29].

Radix Codonopsis [30-35]: polysaccharides maintain homeostasis of CD4+ and CD8+ T cells, Th1, Th2, Treg and Th17 populations in murine immunosuppression models, stabilising the CD4/CD8 ratio and modulating TNF-α, IL-1β and IL-10 [30-32]. Polyacetylenol glycosides inhibit nitric oxide production and decrease TNF-α and IL-6 in vitro [34,35]. In imiquimod-induced psoriasis in mice, Codonopsis polysaccharide delivered as a microneedle patch with antioxidant polyphenol nanoparticles attenuated inflammation through inhibition of the IL-23/IL-17 axis [33].

Radix Ophiopogonis [36-40]: ameliorates eczema-like lesions in murine models by suppressing skin thickening, mast cell activation and pro-inflammatory cytokine expression; ophiopogonin D inhibits p38 and ERK activation and reduces NF-κB nuclear translocation in inflamed human keratinocytes [36,38]. Aqueous extract and its constituents show anti-inflammatory activity [37], and polysaccharide preparations enhance splenocyte proliferation and modulate cytokine production [39,40].

Radix Salviae Miltiorrhizae [41-45]: tanshinones I and IIA suppress Th1 differentiation by inhibiting STAT3/STAT5 phosphorylation, reducing IFN-γ production [41,42]. Salvianolic acid A and tanshinone IIA decrease Th2 cytokines (IL-4, IL-13) in allergic models [43]. Polysaccharides promote Treg differentiation and enhance CD8+ T cell cytotoxicity; those findings come from tumour-bearing mice and cancer patients [44,45].

Radix Scrophulariae [46-52]: the polysaccharide and iridoid fractions act in opposite directions. Four polysaccharide fractions (SRPs40–100) enhance macrophage pinocytic activity and NO and TNF-α production, raise IL-1β, IL-6, TNF-α and PTGS2 mRNA and TLR2 expression, and increase phosphorylation of p38, ERK, JNK, p65 and IκB; anti-TLR2 antibody abolishes the response, confirming TLR2-driven MAPK and NF-κB activation — an immunostimulatory action [46]. Conversely, crude polysaccharide extract of S. ningpoensis reduced IL-6 and TNF-α dose-dependently in LPS-stimulated mice [47], and the iridoid scropolioside B — isolated from a related Scrophularia species rather than from S. ningpoensis itself — blocked TNF, IL-1β and IL-32 expression through NF-κB inhibition (IC₅₀ 1.02 μmol/L) and lowered NLRP3 inflammasome expression, outperforming the structurally related catalpol, which lacked NF-κB inhibitory activity [48]. Iridoid and phenylpropanoid glycosides act synergistically on immune biomarkers [49]; broader phytochemistry and pharmacology are reviewed in [50-52].

Rhizoma Atractylodis Macrocephalae [53-59]: the polysaccharide and lipophilic fractions act in opposite directions. Total polysaccharides promote macrophage NO, ROS, cytokine and chemokine production and enhance phagocytic activity, with NF-κB and STATs identified as the key regulators of TNF-α and IL-6 and NF-κB nuclear translocation as an early event [53,54]; in lymphocytes they raise IFN-γ, IL-1α, IL-21, CCL4, CXCL9 and CXCL10 and increase CD4+/CD8+ subpopulations, binding directly to the TCR on T cells and membrane immunoglobulin on B cells [55]. Immunostimulatory activity depends on rhamnogalacturonan-I side-chain structure and molecular weight [56], and a defined xyloglucomannan normalises CD4+/CD8+ and Treg ratios in cyclophosphamide-induced immunosuppression [57]. Conversely, atractylenolide III inhibits IκBα and p65 phosphorylation, blocking NF-κB transcriptional activity and reducing TNF-α and IL-6 [58], and atractylenolide I suppresses M1 macrophage polarisation, reducing CD86, IL-12p40, TNF-α, IL-6 and iNOS via MAPK and IRF signalling [59].

Radix Asparagi [60-62]: in murine models of acute and chronic cutaneous inflammation, extract inhibited TNF-α and IL-1β, suppressed neutrophil myeloperoxidase activity and improved histopathological markers of dermatitis [60]. Photoprotective activity against UVB and increased antityrosinase activity with suppressed melanin synthesis were shown for fermented preparations processed with Aspergillus [61,62]; those findings have not been shown to apply to the unfermented extract used in this formula.

Fructus Lycii [63-66]: flavonoids including quercetin inhibit TNF-α, MCP-1 and IL-1β production and downregulate ICAM-1 and VCAM-1 in LPS-stimulated endothelial cells [64]; Lycium barbarum polysaccharides show broad immune-modulating and antioxidant activity [63,66].

Folium Mori [67,68]: the available evidence concerns immune enhancement. Two purified polysaccharide fractions, MLP-1 (9.31×10⁴ Da) and MLP-2 (2.22×10⁶ Da), stimulate proliferation of mouse splenic lymphocytes in vitro, MLP-2 the more active; in chickens immunised with Newcastle disease vaccine, oral MLP-2 raised serum antibody titres and increased IL-2, IFN-γ and secretory IgA in tracheal and jejunal lavage fluid [67].

Flos Chrysanthemi [69-72]: has demonstrated antiallergic effects by inhibiting antigen-induced degranulation and scratching behaviour in mice [71]. Its flavonoids, phenolic acids and polysaccharides suppress IL-1β, IL-6 and IL-8, inhibit oxidative stress and modulate macrophage and mast cell activity in vitro and in animal models [69,70].

Rhizoma Zingiberis [73-82]: (dried ginger) — the two studies performed on dried ginger as such point in opposite directions. Dried ginger extract restores Th1/Th2 balance in immunocompromised mice, normalising IFN-γ and Th2 cytokine responses [73]; a neutral glucan isolated from Zingiberis Rhizoma is pro-inflammatory, upregulating IL-6, IL-1β, TNF-α and reactive oxygen species in RAW264.7 cells via TLR4/IKKβ/NF-κB [74]. The remaining evidence is compound-level: ginger phenylpropanoids suppress IL-1β, PGE₂ and thromboxane B₂ in human whole blood and monocytes by inhibiting iPLA2 and cPLA2 [75]; 6-gingerol and 6-shogaol inhibit human monocyte-derived dendritic cell responses to TLR ligands via NF-κB, MAPK and mTOR, 6-shogaol being the more potent and additionally engaging AMPK and NRF2 [76]; gingerols reach measurable plasma concentrations after oral intake [77]; and IKKβ inhibition with M1-to-M2 repolarisation is summarised in [78-80], with further TLR4-dependent effects in monocytes in [81,82]. .

Fructus Jujubae [83-86]: polysaccharides enhance lymphocyte proliferation, increase splenic and thymic indices and modulate cytokine production, with upregulation of Th1-, Th2-, Th17- and Treg-associated cytokines and a shift in CD4+/CD8+ ratios [83-85]. Standardized jujube extract suppresses LPS-stimulated NF-κB activity and pro-inflammatory cytokine expression in murine macrophages [86].

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