Psoriasis - Science topic
A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis.
Questions related to Psoriasis
Exfoliative dermatitis is a flare, a common severe for form many dermatosis like psoriasis, atopic dermatitis, pityriasis rubra pilaris etc. Cytokine load might be a major cause of that downgrading state of diseases. So, there might be any relation of cytokine surge with ED.
In psoriasis candle grease sign is a confirmatory sign, in this sign we are suppose to scratch the patches of psoriasis with a sharp edge like scale or knife and if scales are collected on that and they are having greasy nature then this sign will be positive. But in my patients scales are there but they are of dry nature scales are not greasy so should I consider this as candle grease sign positive or negative? Please guide?
Hi! I am doing a researvh on psoriasis and would like to induce psoriasis-like keratinocytes using HaCat cell. Does anyone have a reference protocol I can use? I will use this psoriasis model for preliminary anti-psoriasis drug screening. Thank you.
lease suggest which kind of biochemical test to be performed after animal study in case of psoriasis?
New scary large valid studies recently showed an increased prevalence of
diabetes mellitus during the pandemic - I am convinced we will see an increase of
Hidrosadenitis Suppurativa, Psoriasis and Atopic Dermatitis ?
In marts 2021 I wrote
Corona COVID-19 obesity and increase in autoimmune diseases
Obesity appears to be a major environmental factor contributing to the onset and progression of autoimmune diseases. In Demark we have registered a significant increase
In BMI especially in studies among schoolchildren
COVID-19 binds to ACE2-receptor and initiate a cascade of cytokine-activation inkluding IL1-beta, IL-12, TNF-alpha and especially an increase of IL-6 and might initiate a so-called cytokine storm.
Can prospective studies with patients with and without Corona COVID-19 theoretical show and increase in the incidence of autoimmune diseases in the Corona group , including our patients with dermatological conditions such as Hidrosadenitis Suppurativa, Psoriasis and Atopic Dermatitis ?
Are such studies of relevance ?
Carsten Sauer Mikkelsen
Specialist in dermato-venereology
Skin problems affect all ages from the
neonates to the elderly of both sexes, they always face
physical, emotional & social embarrassment in the
social life. Large community prevalence studies have
demonstrated that between 20-30% of the population
have various skin problems which require attention.
Anyone have research done on how a cell responds differently if you inhibit the ligand (ie inhibit IL17 cytokine) versus inhibitor the receptor (ie. inhibit IL17RA).
If we inhibit a ligand, it cannot bind to the receptor to do it's function. If we inhibit the receptor the ligand cannot bind to do its function. Both may result in the same inhibition but in different mechanisms. I am looking into how these two mechanism can cause different results in disease (psoriasis).
If we inhibit the ligand, a cell can release more ligand. Likewise, if we inhibit the receptor, a cell can upregulate receptor expression to get more?
Psoriasis has different types like plaque, flexural, guttate, pustular and nail psoriasis etc. having different signs like silvery scales, patches, red spots or pus filled etc, so why they are different? mean there are different triggers for each types which causes it and shows different signs? and if like this, so what are the difference in triggers that cause each types of psoriasis?
a patient with eruptive psoriasis need to start biologic treatment but have an increased liver enzymes X3 of the normal value, what treatment would you suggest ? I am looking for new Articles providing the latest therapy.
Till date over 1600 cases of psoriasis, including 1. Papular psoriasis, 2. Guttate psoriasis, 3. Pustular psoriasis, 4. Nail psoriasis, 5. scalp psoriasis, 6. Plaque psoriasis, 7. Inverse psoriasis, 8. Erythrodermic psoriasis, 9 Psoriatic arthritis, 10. Linear psoriasis and 11. Palmop-plantar psoriasis, were treated with Wrightia tinctoria extract. Taking aetiological factors in mind, the patients were advised to follow healthy life style and taking healthy diet and drinks.. The patients were advised to avoid animal protein, including eggs, meat, beef, chicken, fish and flesh of animal origin. Psoriasis flared up in patients who took animal protein during treatment.
I'm trying to make my own evidence based practice question for my research paper. Any suggestion for my question please?
Psoriasis is completely cured with extracts from Wrightia tinctoria. The patient is advised to meet the needs of the body via air, water, food, yoga or exercise, excretion through breathing, sweat, urine, stool, rest and sleep in time, and positive emotions.
Present literature is flooded with psoriasis terming it an autoimmune disease and a genetic disorder. Almost all patients visiting us opined that doctors, they visited, said that psoriasis can not be cured. Our experience with psoriasis treatment with Wrightia tinctoria is contrary to that. So far we treated over 1000 cases, which include 1. Erythrodermic psoriasis, 2. Pustular psoriasis, 3 Guttate psoriasis, 4. Scalp psoriasis, 5. Inverse pssoriasis, 6. Palmoplantar psoriasis, 7. Congenital psoriasis, 8. Infantile psoriasis, 9. Plaque psoriasis, 10. Papular psoriasis, 11 Psoriatic arthritis and 12. Nail psoriasis; and Bullous phempigoid and other diseases. The feed back from the patients suggest that psoriasis is cured. The psoriatic lesions disappeared in 3 months time followed by 3 months to normalize skin. The patients stopped herbal, but followed healthy diet and life style. The patients were advised to take healthy diet and drink, regular exercise, regular excretion, positive emotions, timely eating and early sleeping.
Many environmental risk factors are incriminated to cause psoriasis. We want to record our experience in treating psoriasis. In a span of 10 years we studied over 2350 cases of psoriasis. Cure of psoriasis obtained in most cases. Relapse of psoriasis observed in the patients having following environmental factors:
Stress, including that caused due to psoriasis
Juice containing preservatives
Cool drinks containing chemicals including preservatives.
Health foods containing chemicals including preservatives
Inadequate sleep and rest in night time workers
Animal protein, including prawn, chicken, mutton and beef
Immune system and Inflammation impact on the Gut-Brain axis !
The Gut/Immune/Nervous (GIN) communication
New insights into how immune system and inflammation play a role in Parkinson's Disease
New research indicates that the earliest stages of Parkinson's disease (PD) may occur in the gut with a likely relation to inflammatory bowel disease (IBD).
Parkinsonism is not just a brain disorder, but a group of diseases that may have their onset in the GIT. It is strongly suggested that individuals with an increased tendency for peripheral inflammation have a higher risk to acquire PD. Given the potentially critical role of gut pathology in the pathogenesis of PD, IBD may impact PD risk.
Peripheral immune system alterations may play a role in PD, which has the potential for new therapeutic strategies. Understanding and appreciating the importance of the so-called gut-brain axis, the connection between gut and the brain in PD, has grown rapidly in recent years.
The inflammatory processes have naturally led to discussion of an association between IBD and PD since the two share some basic characteristics. IBD is currently considered an inappropriate immune response to the microbiota in the intestines, characterized by chronic pro-inflammatory immune activity, a trait now also suggested to be a fundamental element of neurodegenerative disorders.
Highlighting the relevance of the immune system, large genome-wide association studies (GWAS) and pathway analyses identified 17 shared loci between PD and seven autoimmune diseases including celiac disease, rheumatoid arthritis (RA), type 1 diabetes, multiple sclerosis, psoriasis, ulcerative colitis and Crohn's disease.
Many epidemiological and genetic studies have found that there seems to be an increased risk of developing PD among people with IBD. The association between IBD and PD may simply be that IBD is just one type of intestinal inflammation, so it is not IBD specifically that increases the PD risk but perhaps intestinal or peripheral inflammation in a broader sense.
Inflammation of the gut is only one of many symptoms on the list of changes in the gut and is associated with neural structures in PD patients. Thus, IBD might be just one of many sources of intestinal inflammation.
While IBD patients are more likely to get PD, the risk is still very small. Yet, for a given IBD patient, the probability of not getting the diagnosis is 95%-97%.
Future pharmacological therapies aiming at slowing or stopping PD progression should not only target patients well into the course of the disease, but also be administered to patients in the very early phases of the disease or at risk for developing PD.
Clinicians should be aware of early Parkinsonian symptoms in IBD patients but also in patients with chronic inflammatory disorders.
A focus on the potential role of the immune system and of systemic inflammation these neurological diseases is encouraged.
A clear knowledge of the mechanisms implicated in Gut/Immune/Nervous communication could help improve the prognostic and therapeutic tools leading to better quality of life for patients, reducing the exacerbation of PD symptoms, and delaying the progression of the disease.
Parkinson's disease is a slowly progressive disorder that affects movement, muscle control and balance. It is the second most common age-related neurodegenerative disorder affecting about 3% of the population by the age of 65 and up to 5% of individuals over 85 years of age. During the 20th century, PD was thought to be primarily a brain disorder, however, research has shown that it may actually begin in the enteric nervous system, the part of the autonomic nervous system that controls the gastrointestinal organs.
Source: Brudek, T. et al. (2019) Inflammatory Bowel Diseases and Parkinson’s Disease. Journal of Parkinson's Disease. doi.org/10.3233/JPD-191729
I invented a cream with some chemicals dissolved in vaseline, which may help to alleviate eczema. I tested on my hands and feet and I am quite well now. At this stage, I need to test on some volunteers for clinical trials. If anyone is interested please contact me.
I would like to run a study in Psoriatic animal model; however I am looking for the best animal model (recapitulate most features of the human disease) for Psoriasis. Furthermore, I am looking for an efficient method to induce Psoriasis in animal model. On the other hand, due to my research budget I would like to use reasonable animal model as well.
Thank you in advance.
Biologics have made a revolutionary change in the course of immune-mediated diseases especially psoriasis. It's still very young to judge the long-term effects of this type of therapy, but from your understanding to the human immune system and its non-ending tricks, what can be the consequences?
Actually I'm working in psoriasis disease I have patient report as well kindly share your mail I will send you. Please help me and suggest me best plant for psoriasis
Female, 35 years, para one, normotensive, non-obese with h/o skin lesions (2 in number) since 4 months over the right flexed arm, inner aspect, asymptomatic at present. Started with itching and mild pain.
Discoid lupus erythematosus?
Any other disorders you might suggest?
I am a rheumatologist seing patients with all kinds of arthritis.
These days, psoriatic arthritis is extremely common. It can be typical peripheral arthritis with digitis or axial spondylitis or both. At times, it is limited to tendinitis and really hard to diagnose.
Can HLA typing help the diagnosis of psoriatic arthritis?
It is my understanding that any marker of psoriasis, like HLA-C06, will help the diagnosis of uncharacterized arthritis, by at least, pointing to the underlying psoriasis background.
However, some studies suggest that developing psoriatic ARTHRITIS requires extra genes, different from HLA-C06 which predisposes to skin psoriasis. These studies are based on the comparison of HLA genes between patients with isolated skin psoriasis (usually, patients from Dermatology Clinics) and patients with psoriatic arthritis (usually from Rheumatology Clinics). Does this comparison make sense?
Are we talking about different diseases or different stages of one unique disease???
I am searching for a clinical trial or studies which shows medicinal effect of Ganoderma lucidum on treatment of Psoriasis.
Chronic autoimmune skin disease. This condition occurs when the immune system sends out wrong signals .These signals increase the speed of the skin's growth cycle, that is, excessive increase in skin cells from the amount of shedding them.so I want to know that can we prevent this wrong signals by using things like electrodes.?
Many researches stated the semi-therapeutic effect of regimen in mice model of Imiquimod induced psoriasis like skin disease. That is IMQ and the drug are applied for almost similar time period (6-7 days). I wish to know whether there are researcher who are performing this experiments with therapeutic approach. I mean first induction of psoriasis-like condition (eg. applying of IMQ for 6 days) and then (after completion of IMQ application) administration of the drug. I will be happy to get the suggestions from the researchers doing this sorts of experiment or published papers !!
Thanks in advance !
I am trying to get a large and reliable source of Imiquimod cream for research (without prescription), but all the companies I've been in touch with provide it only to vendors or distributors.
Interleukin 17 (IL-17) is a class of closely related molecules known to be increased in the human body by exposure to Fluoride by ingestion from water and food, or metabolism of Fluorocarbon anaesthetics and propellants. IL-17 causes Autoimmune Diseases including Psoriasis, Rheumatoid Arthritis, Asthma, Lupus, Multiple Sclerosis, Inflammatory Bowel Disease, Transplant rejection, and destruction of Liver and Heart Cells. IL-17 is also implicated in Skin Cancer.
Other Interleukins are known to be elevated by Fluoride, leading to attacks on other critical cellular and organ systems. Australia's National Health and Medical Research Council actively suppresses this Interleukin science while promoting Water Fluoridation using industrial waste. Can the science community influence this behaviour?
I need to evaluate the antipsoriatic activity of medicinal plants formulation on albino rat models (psoriasis induced by ultra violet beta rays). Suggest me the lab to do the research.
While treating psoriasis patients with Wrightia tinctoria extract, we noticed that food and drink additives and preservatives have adverse effect in the healing of psoriasis lesions.
During the period between 2010 and September 2017 We treated over 1500 psoriasis cases. There was disappearance of signs and symptoms of psoriasis in many cases after discontinuing Wrightia tinctoria herbal usage for a period of 5 to 7 years. The patients are advised to follow healthy dieting and healthy life style. No smoking, no drinking and no soft drinks or juices with preservatives,. Night fasting in sleep. No animal protein. Maintain regular physical activity preferably Yoga or exercise. Regular excretion of waste body metabolites through sweat, urine, stool and breathe. To keep positive emotions and to meditate.
I have a list of differentially expressed genes of two diseases and want to create diseasome network like this http://journals.plos.org/plosone/article/figure?id=10.1371/journal.pone.0149175.g002. Please, can anyone help? I have queried for protein interactions in HPRD site. am I doing right? for every gene, i am doing like same. As I am new for this, I have a doubt whether I am doing correct or not. after identifying the proteins, they have made graph Psoriasis diseaseome along with proteins common in AD and so on. have they taken only genes or genes and their interaction proteins also? which tools they have used for creating the figure.
are there are any online resources to learn diseasome construction, please send links.
What is Psoriasis. What leads have been acquired at investigating the cause of this ailment and its prevention.
We are designing a survey study on adolescent psoriasis, and are interested in collecting disease severity data of our sample. While we do not have the oppurtunity to do clinical examinations of all patients, we would highly appreciate your input or ideas on this matter. What are your thoughts on this issue? Do you have any suggestions as to how to best address this issue?
Thanks in advance!
e.g. eczema of nipple, pyoderma gangrenosum on breast, nipple piercing, tatoos on breast and their complications, complications in breast implants etc.
Would you like to contribute? You will be acknowledged.
The observations reveals that Vamana & Virechana Karma followed by Ayurvedic drugs is found beneficial in the patient of Psoriasis. Side by side, it also pacifies the other associated complaints of the patient. Thus, the therapeutic approach, which is used in this patient found to be very safe, cost effective and improve the overall health status of the patient. This observation is not finally conclusive but it is a lead for further study. In this regard provide us with a larger population based data on above study and give your views on the same.
I invented a creme with natural compounds, which may help to alleviate the syntoms of psoriasis and eczema too. But I need to test on volunteers for a clinical trial, then if succeed we can patent. Pleas if someone is interested please contact me.
Psoriasis is an inflammatory, chronic, common, worldwide autoimmune skin disorder characterized by T-cells mediated hyper-proliferation of keratinocytes. T-Cell population as well as Dendritic and Keratinocyte Cell population takes vital accountability for creating the disease Psoriasis. About 125 million populations are affected globally by the severity of the disease. A direct involvement of many cytokines in the pathogenesis of skin lesions in psoriasis is also well explored but the role of Enzyme is not well explored.
I am trying to induce psoriasis in a mice model. In the publication attached, imiquimod application for 6 days would induce formation of the lesion. However, i have discovered that this is not so in my case. There is only a slight redness of the skin with none of the other features of psoriasis (scaling, increase skin thickness etc) after 6 days of treatment. I would really appreciate some advice. Thank you.
Any case series/reports, recommendations or experiences appreciated.
There is wealth of information available on aromatherapy but not sure what to believe. It is difficult to find reputable research based information.
recent data have shown that treating patients with severe psoriasis may be better if an anti IL 12/23 strategy is firstly used instead of anti IL17. Does it make any sense for you?
Is it true that women in their 40s or older may develop psoriasis first, because they had a traumatic experience, e.g. notice that their partner suffer from stomach cancer, and second, they are the first case in their family with this disease? What is the explanation why this combination provoke psoriasis and what type of women would more likely suffer from this?
I am interested by bodily manifestations of depression. I have noticed the association of psoriasis with depresion and regression of cutaneous lesions paralleling with that of depressive signs under antidepressants.
Has anyone noticed this association and/or an idea about the mechanism of linking?
I found that the phase 3 clinical trial that supports Ustekinumab to get marketed with placebo. To me knowledge, in clinical trials the patients are usually allowed to take some background drugs, so the placebo control arms are actually background drugs plus placebo and the experimental arms plus drugs to be studied. However, in this Ustekinumab trial the participants were prohibited to take any other drug. I understand that because psoriasis is not a life threatened disease, even if the studied drug has no effect a short period of time without treatment is OK. Is it necessary to compare the new drugs with a standard treatment? How does the drug administration make the decision if the new drug is allowed on the market?
Clinically when one sees a case of psoriasis who has family history and and another who does not have a family history how would the two cases respond to the medication recurrence and severity. How should one align to such cases.. I don't know if I have framed my question properly. But will be glad if corrected too.
This is relating to erythrodermic psoriasis , when a patient is extensively red and scaly affecting almost the entire body. How does one differentiate if he has an ongoing flare of his erythroderma with constitutional symptoms and a possibility of an exanthematic drug rash to Vancomycin given for MRSA skin infection? Can this be guessed on a Skin examination?
about genetic markers could be useful to add the MTHFR polymorphism that involves about 30% of population and could cause demethylation issues and so istamin demethylation (psoriasis) deficiency but also thrombosis (cardiovascular risk)?
In very severe psoriasis patient with currently diagnosed squamous cell carcinoma,
should ignore the dermatological problem? because PUVA side effect is SCC and that patient is already resistant to other topical treatment.
I am doing research for my EBP question . Any suggestion please.
I would like to assess the acceptability of an economic analysis of the biologic therapy in moderate to severe psoriasis patients based on NNTs.
Ustekinumab binds IL-12 and IL-23, while anti TNF- alfa drugs bind TNF-alfa. Does TNF exerts more effect on the immune system than IL-12 and IL-23 or is it just less studied and understood?
Based on the evidence can any one suggest the best treatment option for this group of patients?