Guttate Psoriasis - anyone else have this along w/ other conditions?


Senior Member
Was wondering if there were others that have the same or close to the same set of conditions as me. And if so, maybe start a discussion...

Guttate Psoriasis isn't something I've seen mentioned here much. But I got this not long ago, and have Hashimoto's, hypothyroidism, and EBV.


Senior Member
I had one area of what I suspected was regular psoriasis on my ankle, which was there for years, and nothing seemed to help in any permanent way.

Then several years ago I tried a unique antioxidant called tempol, and within 10 days my psoriasis not only fully cleared up, but never returned. By coincidence, I recently posted a thread about this tempol treatment on a psoriasis forum.

Tempol mimics the effect of the body's natural antioxidant superoxide dismutase (SOD), and one study found that in psoriasis, SOD activity is low — see here.

I may now try tempol again to see what effect it has on my red spots, which could well also be psoriasis. Might also try tempol topically on the red spots, rather than just orally. The spots did not clear up when I tried tempol a few years ago, but maybe it requires a higher dose or topical treatment.
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Senior Member
@Hip You might find these studies interesting:

HERVs & psoriasis

High Prevalence of an IgG Response Against Murine Leukemia Virus (MLV) in Patients With Psoriasis (2003)
Increasing evidence suggests that human endogenous retroviruses (HERV) could participate in the pathogenesis of autoimmune diseases such as multiple sclerosis and lupus erythematosus. To assess a possible association of murine leukemia virus (MLV)-like group of HERVs with psoriasis we searched for antibodies against MLV proteins in the sera of patients. We showed that anti-MLV antibodies (total) were detected in both psoriatic and control sera. However, they were detected with a higher frequency in psoriasis when compared with controls (91 vs. 53%, respectively, P=0.001). In addition, the IgG response was dramatically increased in psoriasis (86 vs. 8%, respectively, P<0.0001). This immunoreactivity was observed against the products of both the gag and env genes, and the most antigenic proteins were the gp65-70. Moreover, we observed that anti-p30 MLV antibodies reacted with an epidermal protein with a molecular weight of 50 kDa in protein extracts from both normal and psoriatic skin cultures. These observations suggest that HERVs of the MLV-like group could contribute to the immunopathogenesis of psoriasis.
Differential expression of a human endogenous retrovirus E transmembrane envelope glycoprotein in normal, psoriatic and atopic dermatitis human skin (2004)
Background Psoriasis is a common inflammatory skin disease characterized by uncontrolled proliferation of keratinocytes and recruitment of T lymphocytes into the skin. The possible role of human endogenous retroviruses (HERVs) in the induction of psoriasis has been suggested, based upon the previous observations of retrovirus‐like particles in psoriasis from skin lesional plaques, urine and stimulated lymphocytes.

Objectives To investigate the expression of HERV‐E transmembrane envelope glycoprotein (HERV‐E env) in normal, psoriatic and atopic human skin, and to examine the influence of ultraviolet (UV) B irradiation on HERV‐E env expression in normal human epidermal keratinocytes.

Methods The analysis was performed on both skin biopsies and organotypic skin cultures using immunofluorescence and Western immunoblotting. UVB irradiation (312 nm) of cultured normal human keratinocytes was performed using a dose of 30 mJ cm−2.

Results Positive staining was observed in most of the psoriatic and atopic skin samples, whereas only 15% of the normal skin samples were faintly positive. In addition, the pattern of expression of HERV‐E env differed markedly in psoriasis vs. atopy. By Western blotting analysis, two main proteins of 54 and 57 kDa were detected in extracts of normal skin, normal keratinocyte cultures and reconstructed epidermis from psoriatic and normal punch biopsies. An increased level of expression of these proteins was noted in extracts from psoriatic vs. normal reconstructed epidermis. The overexpression of the 57‐kDa protein in normal human cultured keratinocytes was dramatically reduced by UVB irradiation.

Conclusions These data suggest for the first time that HERV‐E env is expressed in normal and pathological human skin. Further studies are now required to elucidate the role of such viral proteins in the pathogenesis of psoriasis.
A new endogenous retroviral sequence is expressed in skin of patients with psoriasis (2005)
Background The origin of psoriasis, a chronic inflammatory skin disease involving keratinocyte proliferation, immune disturbances and complex inheritance, remains unknown. Human endogenous retroviruses (HERVs) are part of the normal human genome and their participation in the pathogenesis of various human diseases with complex genetic traits has been proposed. A possible role of HERVs in the induction of psoriasis was suggested many years ago. However, to date no study has searched for HERV expression in psoriasis.

Objectives To determine firstly, which HERV families are expressed in the psoriatic lesion and secondly, whether specific variants can be detected.

Methods HERV expression was analysed at the mRNA level after degenerated reverse transcription–polymerase chain reaction (RT–PCR) of retroviral pol sequences followed by sequencing. Screening for a specific variant was performed by RT–PCR on lesional and nonlesional psoriatic skin and compared with normal and atopic dermatitis skin.

Results We report the expression of three HERV families in psoriatic lesions, namely HERV‐W, K and E. We then partially characterized a new endogenous retroviral variant, which was related to the ERV‐9/HERV‐W family. This sequence contains at least two open reading frames that could encode for a gag protein and a retroviral protease. The expression of this sequence was detected in 29 of 43 lesional psoriasis skin samples and rarely in normal (two of 21) or atopic dermatitis (three of 14) skin samples.

Conclusions In psoriatic lesions, HERV sequences of the W, K and E families are expressed and a new variant of the ERV‐9/HERV‐W family has been characterized. The possible role of HERV‐related sequences in the pathogenesis of psoriasis is under investigation.
Reverse Transcriptase Activity in Human Normal and Psoriatic Skin Samples (2007)
Background: About half of the human genome is composed of ancient transposable elements that became integrated in the genome throughout the course of evolution by DNA transposition or by retrotransposition. Most of these elements have degenerated. However, a few of them have conserved their coding capacities and could still have a role in physiological and pathological processes. OBJECTIVES To investigate whether reverse transcriptase (RT) of human endogenous retroelements can be expressed at the protein level and can also be functional, and to associate RT expression and activity to a pathological situation, namely psoriasis.

Methods: Expression of RT proteins was investigated by immunohistochemistry on normal (n = 11), psoriatic (n = 19) and atopic (n = 12) skin sections and by Western blot on normal skin protein extracts. RT activity was measured by a colorimetric method in protein extracts from normal (n = 17) and lesional psoriatic (n = 35) skin. Two assays were performed in each extract: one was optimized for Moloney murine leukaemia virus or mammalian C-type retroviruses, and the other for mouse mammary tumour virus or D-type retroviruses.

Results: RT proteins were detected in the uppermost layer of the epidermis and in a few dermal cells of normal skin. The main protein had a molecular weight of 57 kDa. An increased number of RT-positive cells was stained in the psoriatic lesion both within the epidermis and within the dermal compartment. In addition, a massive staining was noted in Munro's abscesses. Finally, RT activities were 2-3 times higher in psoriatic protein extracts than in normal skin protein extracts.

Conclusions: Active endogenous retroelements can produce functional RT proteins. In normal skin, we observed RT expression in all samples tested whereas RT activity was barely detectable. In psoriatic samples, the number of RT-positive cells was increased, as was the RT activity. This latter characteristic allowed us to determine a subset of psoriatic samples with an increased Mg(2+) RT activity. These results suggest that a basal level of endogenous retroelement activity exists in normal skin and that keratinocyte hyperproliferation and/or inflammation observed in psoriasis promote this activity. The role of endogenous retroelements in skin physiology and pathology deserves attention.


Plasmacytoid Dendritic Cells in the Duodenum of Individuals Diagnosed with Myalgic Encephalomyelitis Are Uniquely Immunoreactive to Antibodies to Human Endogenous Retroviral Proteins (2013)
Myalgic encephalomyelitis (ME) is a debilitating illness of unknown etiology characterized by neurocognitive dysfunction, inflammation, immune abnormalities and gastrointestinal distress. An increasing body of evidence suggests that disruptions in the gut may contribute to the induction of neuroinflammation. Therefore, reports of human endogenous retroviral (HERV) expression in association with neuroinflammatory diseases prompted us to investigate the gut of individuals with ME for the presence of HERV proteins. In eight out of 12 individuals with ME, immunoreactivity to HERV proteins was observed in duodenal biopsies. In contrast, no immunoreactivity was detected in any of the eight controls. Immunoreactivity to HERV Gag and Env proteins was uniquely co-localized in hematopoietic cells expressing the C-type lectin receptor CLEC4C (CD303/BDCA2), the co-stimulatory marker CD86 and the class II major histocompatibility complex HLA-DR, consistent with plasmacytoid dendritic cells (pDCs). Although the significance of HERVs present in the pDCs of individuals with ME has yet to be determined, these data raise the possibility of an involvment of pDCs and HERVs in ME pathology. To our knowledge, this report describes the first direct association between pDCs and HERVs in human disease.

Chlamydophila Psittaci & Psoriasis

Detection of DNA of Chlamydophila Psittaci in Subjects With Psoriasis: A Casual or a Causal Link? (2012)
Background: Recent evidence indicates that subclinical infection by Chlamydophila psittaci occurs in a significant percentage of patients with chronic inflammatory polyarthritis, including psoriatic arthritis.

Objective: To assess the prevalence of Chlamydiae infection in a large cohort of well-characterized patients with psoriasis.

Methods: The presence of a subclinical C. psittaci infection was investigated in 64 patients with psoriasis, including 12 patients with psoriatic arthritis. Two hundred and twenty-five healthy controls were also investigated. The presence of infection was assessed in peripheral blood mononuclear cells using several polymerase chain reaction protocols, targeting different regions of the bacterial genome. The DNA of other species (Chlamydophila pneumoniae and Chlamydia trachomatis) was also investigated.

Results: Chlamydophila psittaci infection was observed in a significantly higher percentage of patients with psoriasis (11/64, 17%) compared with healthy controls (1/225, 0.4%) (odds ratio 46.49, 95% confidence interval 5.87-368.03; P < 0.0001). No differences in age, sex or disease duration were noticed between positive and negative patients, but the majority of the positive patients were on immunomodulatory treatments.

Conclusion: Chlamydophila psittaci may be an infectious trigger possibly involved in the pathogenesis of psoriasis.
I got infected with 2 HERV retrovirus. I unexpected found them by mNGS Metagenomic Sequencing. If the quantities of RNA virus enough in your blood then could be detected by mNGS.

There are many Chinese patients also got unknown viruses infections and request government to research and treatment but nothing found at 2011. Diagnostic methods is not advanced at that moment. Now government has no any assist to them.





Senior Member
@Hip You might find these studies interesting:

Autoimmune diseases of various sorts have been linked to HERVs. Psoriasis is an autoimmune condition, so not surprising to find HERV activity.

It is interesting that antiretroviral drugs are known to improve the autoimmune condition of multiple sclerosis. It's been theorized this may be because antiretrovirals are targeting the HERVs found in ME/CFS.


Senior Member
Then several years ago I tried a unique antioxidant called tempol, and within 10 days my psoriasis not only fully cleared up, but never returned. By coincidence, I recently posted a thread about this tempol treatment on a psoriasis forum.
What are the risks with tempol?


Senior Member
What are the risks with tempol?

Like many substances sold for research purposes only, it's safety profile is not tested.

This materials safety sheet says:
4-Hydroxy-TEMPO has a moderate acute toxicity by oral and a low toxicity by dermal exposure. The substance causes severe eye damage. 4-Hydroxy- TEMPO is not irritating to the skin, not sensitizing and not mutagenic / clastogenic.

But it does not indicate the dose level at which toxicity starts. If you read the materials safety sheet for cooking salt, you'd find similar warnings. The safety sheet says it is not mutagenic.

At high concentrations of 2 mM it can start to cause some retinal toxicity, according to this paper. But by my calculation you would need at least 14 grams taken orally to get that blood concentration.

I took around 30 mg of tempol daily as an oral dose when I used it, but I expect for psoriasis purposes, it might work just as well or better when used topically at that dose range.

In fact since I learnt from @sometexan84's post that my red spots (that I describe in this thread) are likely guttate psoriasis, for the last 7 days I have been placing around 30 mg of tempol dissolved in a few drops of water on these spots daily, with pretty encouraging results so far.

With daily tempol, my spots look like they are slowly healing, but it's too early to tell. If tempol does cure them like it did with my regular psoriasis, then I'll post all the details here and on my other thread.


Senior Member
Topical tempol seems to have worked quite well in getting rid of my guttate psoriasis red spots.

Here is a picture of the guttate psoriasis red spots on my chest before applying tempol:

(1) Guttate Psoriasis Red Spots Before Tempol Treatment
Guttate psoriasis red spots on skin before treatment.jpg

Then I applied around 30 mg of tempol powder dissolved in a few drops of water to these spots on a daily basis for around 2 weeks, and this is the result:

(2) Guttate Psoriasis Red Spots After Tempol Treatment
Spots after daily topical tempol treatment for 2 weeks.jpg

As you can see in picture (2), lots of spots which had previously been red in picture (1) have now faded to a light brown color, looking like they have turned into skin moles (see the faded spots in the brown circles). And you can see many spots which were quite red before are less red after the tempol treatment. SO it looks like topical tempol is a good treatment for guttate psoriasis.

Within a week of applying tempol, I noticed the red spots had started healing, and I continued topically applying tempol daily for a total time of around 2 weeks (I stopped because I ran out of tempol).

Then I waited a further few weeks (without applying any more tempol) before taking the picture (2) above, to see whether the healing might be permanent, or whether the red spots would return after cessation of tempol treatment. So far it is looking like the healing is permanent.

I am going to buy some more tempol powder (from here), and will continue applying it topically on my guttate psoriasis red spots, in the hope of completely curing this guttate psoriasis.