Science topic

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.
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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.
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Cytokine storm is an aggressive Inflammatory response with the release of large amounts of pro-inflammatory cytokines. This is a life threatening systemic Inflammatory response involving highly elevated levels of circulating cytokines with immune cell hyperactivation. All these can be triggered by pathogens,cancers,autoimmune diseases, various treatment modalities. Erythroderma/exfoliative dermatitis is a difficult to control scenarion in dermatology and demonstrates diffuse erythema and scaling of greater than 90% of the body surface area. The most common dermatologic causes like psoriasis/atopic dermatitis may cause cytokine flare-ups. The inflammation thus caused may account for its clinical picture/favorable response to systemic glucocorticoids.
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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?
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We have to see the skin (and not the scale) after scratching, for candle grease sign. After scratched, psoriatic scales fall off and if revealing a shiny candle-like surface, it should be considered as positive candle grease sign.
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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.
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Thank you Malcom Nobre
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lease suggest which kind of biochemical test to be performed after animal study in case of psoriasis?
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IL17/IL23 axis cytokines.
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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 ?
Kind Regards:
Carsten Sauer Mikkelsen
Specialist in dermato-venereology
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According to a recent paper published in "Nature" by Sarah Esther Chang et al. titled: "New-onset IgG autoantibodies in hospitalized patients with COVID-19", more than 50% of hospitalized Covid-19 patients have new-onset autoimmunity manifested by autoantibodies.
Nat Commun. 2021:14;12(1):5417.
doi: 10.1038/s41467-021-25509-3
There is increasing evidence worldwide that part of the late post-Covid syndrome includes a degree of new-onset autoimmunity.
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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.
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We categorize psoriasis on the signs we observe and symptoms, the patient experience, of skin on knees, elbows, lumbosacral region, nails, joints, stretch marks, scalp, body folds and genitals.
Onset of psoriasis presented with with papules, scales leading to other clinical types. Untreated cases have erythema, thickening and scaly with clear margins.
We categorize psoriasis as follows : 1 Congenital psoriasis, 2 Primary psoriasis, 3 Infantile psoriasis, 4 Childhood psoriasis, 5 Papular psoriasis, 6 Guttate psoriasis, 7 Plaque psoriasis, 8 Linear psoriasis, 9 Exfoliative psoriasis, 10 Erythrodermic psoriasis, 11 Herpetiform psoriasis, 12Inverse psoriasis, 13 Scalp psoriasis, 14 Nail psoriasis, 15 Psoriatic arthritis, 16 Pustular psoriasis and
17 Palmoplantar psoriasis.
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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?
Thoughts?
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One important consideration is it there are may be multiple ligands for the same receptor, depending on the receptor of course. Blocking the receptor may therefore potentially inhibit the signalling from multiple ligands, rather than just one.
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I am looking for skin images (cancer, normal skin, psoriasis, etc.) obtained with optical coherence imaging.
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My coworker are developing skin OCT images. Please feel free to contact with me if you need more data.
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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?
Thank you
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Thank you so much Nabodita Sinha for your help.
Actually I want to know that the triggers like IFN-γ, TNF-α, IL-1β, IL-6, IL-17/Th17 and so on. So as there any different trigger activator for each psoriasis types? because about 90% is Plaque psoriasis, so it has a different triggering cytokines for it's activation than other types? please clear me about it.
Thank you
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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.
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  • First of all assess for the cause of transaminitis; was the patient on Mtx at any point and when was the last dose taken? Repeat transaminase level, rule out viral hepatitis, take a drug history to look for hepatotoxic drugs, abdominal ultrasound if you're suspecting NASH etc.
  • Assess the severity (extent and disability) of the psoriasis
If not severe (Limited plaque psoriasis i.e. < 20% BSA or PASI<10,) prefer Topical agents.
If the involvement is more extensive (>20% BSA or PASI>10), some of the systemic/other agents which (according the literature) are not hepatotoxic are:
  • Narrow band UVB: slower onset of action; good for long term maintenance
  • Cyclosporine: quick onset of action, good for quick induction of remission
  • Apremilast: hepatic impairment does not alter its pharmacokinetics hence no dose adjustmest is required (1) and no pre-treatment tests are required (2). It is indicated when other systemic agents are contraindicated (2).
Feel free to add inputs if anything important was missed.
(1) Zerilli T, Ocheretyaner E. Apremilast (Otezla): A New Oral Treatment for Adults With Psoriasis and Psoriatic Arthritis. P T. 2015;40(8):495-500
(2) Vujic I, Herman R, Sanlorenzo M, et al. Apremilast in psoriasis - a prospective real-world study. J Eur Acad Dermatol Venereol. 2018;32(2):254-259. doi:10.1111/jdv.14598
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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.
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I'm trying to make my own evidence based practice question for my research paper. Any suggestion for my question please?
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Sandhu K et al. in a study revealed the median time for marked improvement with methotrexate and cyclosporine was 5.3 weeks and 6.8 weeks respectively. Patients on methotrexate were found to have more rapid and complete clearance than those on cyclosporine. Both drugs were well tolerated. Side effects in both the treatment groups were minor, transient, and manageable. They concluded at doses with comparable safety profiles, methotrexate resulted in more rapid clearance of patients with severe psoriasis. Pl. have a look at the following link:
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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.
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Please go through the following RG link.
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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.
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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:
Smoking
Drinking alcohol
Stress, including that caused due to psoriasis
Hair dye
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
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The environmental risk factors in the causation of psoriasis include smoking, alcohol consumption, diet, overweight and physical inactivity, infection, drugs, and stressful life events.
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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
Nov. 2019
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
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.
I suggest reading this article-
Dinan TG, Cryan JF.The Microbiome-Gut-Brain Axis in Health and Disease. Gastroenterol Clin North Am. 2017 Mar;46(1):77-89. doi: 10.1016/j.gtc.2016.09.007. Epub 2017 Jan 4
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Psoriasis is a common skin condition that speeds up the life cycle of skin cells. It causes cells to build up rapidly on the surface of the skin.
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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.
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Yes
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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.
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Prof. Gheita, Thank You dear Prof
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Psoriasis ,lab animals chemical agent
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Imiquimod (e.g. Aldara ointment/cream - see https://www.drugs.com/international/imiquimod.html)
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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?
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Madame, actually we know TNF-alpha inhibitors make a latent tubercolosis infection blow up as well as omalizumab is associated to an increased incidence of arterial thrombotic events as reported by US Food and Drug Administration (FDA), after having collected the adverse events since January 2004 to January 2011 (see: Ali AK, Hartzema AG. Assessing the association between omalizumab and arterio-thrombotic events through spontaneous adverse event reporting. J Allergy Asthma 2012, 5: 1–9. Efalizumab was withdraw from market because causing drug induced aseptic meningitis and polyneuropathies, but it is too early to establish know other delayed side effects of biologics
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Hey I intend to induce in Psoriasis in human keratinocytes (Primary and HaCat cell line) ? Can anyone help me design one ? Can i use Imiquimod ?
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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
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Dear Ayush please share me your protocol and which type of psoriasis you are working, psoriasis are various types like Plaque psoriasis, guttate, inverse, pustular etc. Lots of therapy are there but for plaque psoriasis I will recommended you two medicinal plant's like Argemone mexicana and aloe vera. First you make protocol and focus plant extraction write down phytochemical property's then discuss with me. My mail I'd - rk981487@gmail.com.
I will 100% help you.
Thanks and best regards
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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?
Drug rash?
Psoriasis?
Any other disorders you might suggest?
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From point of view it could be Gardner-Diamond Syndrome, fixed drug rash or morphea. Not probably Lupus.
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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???
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Look to my last reply!
Thomas
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I am searching for a clinical trial or studies which shows medicinal effect of Ganoderma lucidum on treatment of Psoriasis.
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Dear Samira,
Attached link may help you.
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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.?
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Still needs more trials though. But I think it's a good start to find molecular evidence behind this;)
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Dear colleague
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 !
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Creative Bioarray provides in vitro psoriasis model for research.
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Need based selection of research topic is good
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Medicinal Plants to Calm and Treat Psoriasis Disease
March 2017
DOI: 10.5772/67062
In book: Aromatic and Medicinal Plants - Back to Nature
Azadeh IzadyariAzadeh IzadyariAzim Akbarzadeh Khiavi
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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.
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Did you try asking if it available as a galenic formulation at hospital and local pharmacies? Otherwise contact Meda pharm directly, they might be interested in the study and thus provide you with the cream .
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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?
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Dear Michael after reading your answer i did look up to the internet and started reaading bout flouride in water.
I am now able to get some insight about the big problem the humans are facing.
Lets hope that the council for water management will take up the issue in a more seroius manner.
It also has made a difference to my understnading of the disease patterns of autoimmunity.
Thank you for the insights.
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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.
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Good Morning Sir,
I am from Trichy, Tamilnadu.
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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.
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Till date we treated 1715 cases of psoriasis with Wrightia tinctoria herbal extract laying emphasis on keeping healthy life style, healthy diet, healthy fluids. The following have adverse affect on healing of psoriasis lesions.
  • Smoking and drinking
  • Animal protein including egg, fish and flesh
  • Soft drinks, reconstituted or other wise, containing chemical and preservatives
  • Foods and drinks containing chemical preservatives
  • Consumption of salted pickles, mango and others
  • Constipatiopn
  • Failure to excrete the body waste metabolites, sweat, urine, carbon dioxide and stool.
  • Lack of exercise
  • Negative emotions, anger, mental stress
  • lack of adequate rest and sleep in the night
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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.
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Professeur honoraire Faculté Libre de Médecine de Lille.
La manifestation clinique comme la disparition du psoriasis dépendent de si nombreux facteurs, qu'on simplifie l'étude de son étiologie en évoquant "l'environnement", "la prédisposition" les "HLA...", quel qu'en soit la clinique, puisqu'il peut être cutané et/ou arthropatique, sa définition anatomo-pathologique étant l'abcès de Munro et Sabouraud.
Il en est de même pour l'eczéma, ou "les eczémas" qui ont pour caractère commun la spongiose, alors qu'il est lui aussi en équation avec une pathologie "interne", l'asthme...
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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.
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Hi Rajasekar,
You can use STRING or GeneMania database to extract the interaction in desired format (tab delimited or csv).
The cytoscape itself has plugins like StringApp & GeneMania. Network can be created directly by giving input as list of genes
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What is Psoriasis. What leads have been acquired at investigating the cause of this ailment and its prevention.
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Good morning Dr. I think this thesis was very important for your work so it shows son correlations of psoriasis pathogenesis parameters that proved its contribution in psoriasis severity.
Thanks Mukhtar, but please do not associate the term pathogenesis with psoriasis. In ur comment above.
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Relation between methotrexate and wound healing
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Wait until she is no remission with psoriasi. There is no need to performe abdominoplasty under MTX. Better wait and push the surgery for a while. Otherwise pause mtx two weeks before and after.
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Hi
 please tell me the relation between the Psoriasis and heart function
and in any part and which type 
Thanks ...
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Thanks Aldona Pietrzak
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Hi everyone,
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!
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No response
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Please suggest me that in Psoriasis cytokine determination in skin homogenate, How much dilutions should i need to prepare for cytokine detection in ELISA.
What is the correct way to induce psoriasis in mice with imiquimod?. 
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Dear Sir,
I have not yet performed the cytokine estimation for skin samples obtained from the diseased animals so I am unable to share the protocol. I am planning to conduct the cytokine estimation in sequential studies. I will be in touch with you.
Thanks.
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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.
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Dear Ranthilaka, I may provide you with accessory nipples,eczema, psoriasis, clear cell acanthoma, BCC et cetera. Please notify me how connect with you. Sincerely. Carlo.
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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.
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Dear all,
In our clinical practice, after proper bio-purification regimens, we found promising results of Bhasma based prescriptions, e.g. Mall Sindura, Hartala etc along with suitable herbal adjuvants in Psoriasis. Nevertheless, appropriate diet & life style must be followed by patient, else recurrence is often the common failure found in therapy.
The below mentioned report on Researches conducted at Gujarat Ayurved University, Jamnagar may add some knowledge in regard to its Ayurvedic management (achievements or failures of trials).
Regards
Dr Rohit
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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.
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I am already studying effect of diffrent plant extracts in psoriasis. Would be interested for inteacting & may be collaborative work in due course.
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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.
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Hi Amit,
There is a plethora of enzymes known to be involved in skin diseases including psoriasis, that's why I asked whether you had a specific type or family in mind. A major group of enzymes are the ADAM metalloproteinases, cell surface expressed enzymes which regulate activity and/or expression of other cell surfaced proteins including cytokine receptors (e.g. IL-6 receptor), adhesion molecules (e.g. L-selectin) or even cytokines by a process sometimes referred to as 'shedding', i.e. proteinase-mediated cleavage od protein domains from the cell surface. One of the most important examples in the context of inflammation is the conversion of membrane-bound (inactive) TNF-alpha into its soluble (active, proinflammatory) form by the ADAM17 proteinase, also known as TACE. TACE and several other ADAMs have been shown to be upregulated in lesion of psoriatic skin, resulting in enhanced inflammation. Selective therapeutic targeting, however, is challenging due to the high homology between the family members and also due to other functions for cell homeostasis. I attached a paper for your interest.
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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.
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 I am working extensively on the imiquimod model with different protocols to induce psoriasis. I must mention that to check efficacy of a antipsoriatic drug, systemically or topically, 62.3mg per mice is enough. But this is highly schedule (pretretreatment followed with imiquimod or imiquimod followed with drug therapy) and dose dependant. For topical study, 62.3 mg is fine, since imiquimod is such a potent inducer of immune system, this much dose is enough to get to know the difference in treated group (testing compund) and imiquimod control group
While for severe psoriatic phenotype, 81.5 mg is also used, but this is good only if you need to study long term effects.
However, in both cases, you cant get to trace the cytokine levels. As this is an acute model and activation of cytokine is transient. Thus if your study emphasis on cytokine levels, day 3 or maximum day 4 is good timepoint to detect cytokines. At later timepoint you cant get detectable levels.
Hope this will be helpful.
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is there any other methods possible to induce psoriasis in rats other than the exposure of the rat's skin to UV radiation?
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This article may be helpful for you: Preclinical models of psoriasis. Danilenko DM. 
Vet Pathol. 2008 Jul;45(4):563-75
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Thanks in advance.
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Thanks @Jon Holmes
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I can only found generic instruments as the WLQ and the WPAIQ. Thanks
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You might want to refer to:
Wordsworth S, Thompson S. , An annotated cost questionnaire for patients: results of piloting, HERU Discussion Paper, 2001, Discussion Paper 03/01,
... Chapter 6 provides some useful guidance on measuring productivity loss in both chronic and acute conditions. Full description here: http://www.dirum.org/instruments/details/28#
DIRUM (Database of Instruments for Resource Use Measurement) also have details of certain instruments for 'skin'
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Any case series/reports, recommendations or experiences appreciated. 
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High IgE and eosinophilia point towards allegic phenomenon. Has the patient applied some creams like framycetin, silver sulphdizine etc? Oral cyclosprin can be strted as 5 mg/kg in psoriatic erythroderma in 2 divided doses /day and taper by 1 mg/kg depending upon clinical response over 2-4 weeks. Of course, monitor blood pressure and Renal function parameters.
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There is wealth of information available on aromatherapy but not sure what to believe. It is difficult to find reputable research based information.
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The best allopathic therapy with promissing results and distantly relapsing is Methotrexate 10-20mg / weekly stratum doses. The adjuvant of Folic acid 5mg should be given evry day except on the day of taking Methotrexate. It can be combined with phototherapy also. 
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What are the results, What are the kidney problems and how long do you usually use it  ?
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Dear Amerigo,
I had some patients that needed a long term CyA treatment, because they do respond to a short term one but immediately they relapsed. Dose was usually 5 mg/kg QD. Of course it is needed to control blood pressure and lab analysis, particularly creatinine clearance, cholesterol, triglycerides  etc . If one year treatment was not enough to control and avoid immediate recurrences, I asked opinion of nephrologist before to continue and evaluated the risk/benefice of another therapy. I had no problems in my private patients, not so many, I treated as I mention. When they had a pathological background I preferred to refer them to our department where we treated them with help of other specialists. There is an updated short version guidelines of systemic treatment of psoriasis in the JEADV 2015; 29, 2277-94.
Warmest regards from your old friend Jose.
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how frequent are the existence of RA and psoriasis.  Is HCQS or hydroxychloroquine justified in the condition?
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Dear Satyaprasad,
I think you are asking for the frequency of coexistence of true rheumatoid arthritis with psoriasis, rather than psoriatic arthropathy? There may be literature on this but the problem is that ascertaining the existence of true RA in the presence of psoriasis is not straightforward. Rheumatoid factors and ACPA occur in a small percentage of normals so could occur alongside psoriatic arthropathy. 
The only time I have been convinced that I knew that an arthritis was true RA in the presence of psoriasis was in a case with typical rheumatoid nodulosis and RF. I only saw the one case in thirty odd years.
In practical terms relating to hydroxychloroquine, I think you are entitled to go on probabilities. If an inflammatory arthritis is associated with RF and or ACPA and does not have DIP involvement then if you feel hydroxychloroquine is a reasonable choice for RA (I was never very convinced) then it is probably still reasonable if the patient also has psoriasis. Without autoantibodies or nodules the chances must be that you are dealing with psoriatic arthropathy and I know of no theoretical or practical evidence for hydroxychloroquine being useful there.
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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?
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Paulo, read  carefully the Nature Med´s paper:
IL-23 induces spondyloarthropathy by acting on ROR-γt+ CD3+CD4-CD8- entheseal resident T cells.
 
Nat Med. 2012 Jul 1;18(7):1069-76. doi: 10.1038/nm.2817.
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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?
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Dear Glatz
It was found that seventy-five per cent  of psoriatics had disease onset before the age of 46 years, males and females are equally affected by psoriasis. Considerable clinical evidence exists for the role of stress in onset and exacerbation of psoriasis. In a recent UK study, over 60% of a sample of psoriasis patients believed stress. Gupta  reported that several psychocutaneous characteristics, including more exacerbations and worse disease, correlated with stress reactivity. The early onset of psoriasis in women, with a peak around puberty, changes during pregnancy and provocation
of psoriasis by high-dose oestrogen therapy potentially indicates a role for hormonal factors in the disease.
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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?
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Thanks. In my experience of internist, I noticed by chance that psoriasis of my depressed patients disappeared with the other signs, psychic and somatic as well, owing to the algorithm of treatment I had developed. 
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I found that the phase 3 clinical trial[1] 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?
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Our article published in peer-reviewed Journal "Communicative & Integrative Biology". A few major points discussed in the paper:
(1) Brain is not the source of consciousness.
(2) Consciousness is ubiquitous in all living organisms, starting from bacteria to human beings.
(3) The individual cells in the multicellular organisms are also individually cognitive entities.
(4) Proposals like “artificial life”, “artificial intelligence”, “sentient machines” and so on are only fairytales because no designer can produce an artifact with the properties like internal teleology (Naturzweck) and formative force (bildende Kraft).
(5) The material origin of life and objective evolution are only misconceptions that biologists must overcome.
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tongue lesion in oral psoriasis
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It is still questionable whether oral psoriasis exists or not. I have seen psoriasis on lips, male and female genitals, but usually in conjunction with nearby skin changes. However, since malignancy and other conditions, like for example HIV, are excluded, acitretin seems the most siutable option for your patient. It would be interesting to know which histopathology clues  were determining for the diagnosis of psoriasis in this case.
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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.
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Dear Venkata;
There is overwhelming evidence that psoriasis has an important genetic component. Lomholt’s classic epidemiological study of psoriasis in the Faroe Islands (1963), in which he examined more than 10 000 inhabitants, made the key observation that the incidence of psoriasis was much greater amongst first- and second-degree relatives of patients than unaffected control subjects. A further large-scale study performed in Sweden supported these data, showing the prevalence of psoriasis to be 7.8% in first-degree relatives, compared with a prevalence of 3.14% in matched controls and 1.97% in the overall population . Based on population data, several investigators have calculated the risk for a child to develop psoriasis. In a German study, the risk was 14% if one parent was affected, 41% if both parents affected and 6% if one sibling affected, compared to 2% when no parent or sibling was affected. Henseler and Christophers demonstrated that the bimodal peak in disease onset (see above) could be taken as evidence for the existence of two pathogenetically distinct forms of the disease, similar to the model for diabetes mellitus. Thus, type 1 is hereditary, strongly HLA associated (particularly HLA-Cw6), early onset and more likely to be severe. Type 2 is sporadic, HLA unrelated, of late onset and usually mild.
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Also if what about if a patient has villus atrophy and psoriasis what would be the best intervention?
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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?
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FERNANDES NC. Erythroderma : a clinico- laboratorial and histopathological study of 170 cases .An Bras Dermatol .2008 ; 83 ( 6 ):526-32 .The main cause of erythroderma was psoriasis; three simultaneous skin biopsies can enhance the accuracy of the histopathologic diagnosis .Reaction TO INTERNAL DRUGS in 37 cases (21,77%).
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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)?
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It sounds convincing that MTHFR polymorphism a genetic marker for Cadiovascular disease in psoriasis. A review on MTHFR is enclosed.
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please give me suggestion.
with thanks.
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Yes, the combined therapy  has better efficacy, expecially in periferic arthritis and cutaneous involvement, and not only due to a reduction in anti-drug antibodies vs Anti TNF drugs.
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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. 
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I think you could try, after surgical excision of the SCC, acitretin or methotrexate.
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I would like to assess the acceptability of an economic analysis of the biologic therapy in moderate to severe psoriasis patients based on NNTs.
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ISSUE: Economic analysis of therapeutic treatment using NTT as the basis for treatment efficacy.
NEED TO TREAT: The idea of NTT is the determination of how many number of patients needed to be treated in order to maintain status quo, i.e. what is the number of replacement need in order to maintain the same number of patients compared to the control group. This is one way of verifying whether the treatment is efficient. Can this method be used as the basis for “economic analysis” for therapeutic treatment regime? NTT is given by:
(1)   NTT = 1 / (C - T)
… where C = control group, i.e. infected patients without treatment; and T = treatment group, i.e. patients receiving the treatment. For example if both groups are 50 each and after treatment, the treated group had 5 patients died. What is NTT? Answer: 1 / (C - T) = (1/50 - (50-5)) = (1/(50 – 45) = 1/5 = 0.20 or 20%; Twenty percent of 50 is 10. The number of patients need for replacement to maintain the status quo is 10. Can this number be used for “economic analysis”? This may mean “economic efficiency of the treatment.”
ECONOMIC ANALYSIS: NTT may be used as the basis. However, for economic analysis of the treatment “efficacy;” one must go beyond NTT, i.e. NTT must be combined with the utility function. One possible utility function at hand may be that introduced by Kahneman-Tversky who received Nobel Prize in 2004 for their contribution in this area. The Kahneman-Tversky utility function is given by:
(2)   U = sum(PiUiVi)
…where P = probability of x-event; U = weight of the event; and V = function that best fitted in modeling the event occurrence. In the present case, V(function) is NTT. The weight (U) must be specified by the analyst; and the probability is the actual observations that show improvement (success) in the treatment divided by the total treatment counts. The probability is given in a form of binomial distribution in a Bernoulli trial & Laplace Rule of Succession fashion as expounded by Laplace, thus:
(3)   P = (s + 1) / (N + 2)
… where s = successful treatment counts among all treatment counts; and N = total treatment counts.
   In case of a single batch of patients, say, 50 patients we can divide them into 5 groups of 10 and them count the number of success in each group. Adhering to the same example given above where there are 5 patients failed, the remaining 45 are classified as successful cases, thus:
P = (45 + 1) / (50 + 2) = 46/52 =0.8846 or 88.46% probability of positive response to the treatment. Recall that V = function and that function is NTT and the value of NTT is 0.20. The only value missing is the weight. In the original function NTT, there are two groups: treatment and control, assume that each is assign equal weight then the weight is 0.50. Now all variables are complete: P = 0.8864; U = 0.50; and V = 0.20. The Kahneman-Tversky utility function calculation follows:
U = PUV = 0.8864(0.50)(0.20) = 0.08864
   Note that NTT speaks in the “negative language,” i.e. it counts the number of “failure” not success. Therefore, the utility yield by the Kahneman-Tversky is actually the obverse of the answer, which is 1 – U. It is necessary to obtain 1 – U; thus: 1 – 0.08664 = 0.91136 or 91.14%. Note further that the Kahneman-Tversty requires a summation which entails series of data in a set. Therefore, the original treatment must be a series of runs of i treatments from i = 1, 2, … Therefore, the value for NTT must be in a form of NTT1, NTT2, … from treatment1, treatment2, … respectively.
APPLICATION TO THE ECONOMICS OF THERAPY COST: Assume that the cost for psoriasis treatment is $1,000 per patient per year. There are 50 patients. The total cost for the treatment is $50,000 per year. Assume further that the physician fixed the target for the return on treatment at X%. The worst case scenario is the treatment completely fails; the total loss would have be ($50,000 in treatment cost + suffering and inconvenience which may be difficult to place a value). However, in the example, the treatment had 20% failure and yields 91.14% efficacy with 50% weight. What the economic benefits of the treatment? We know the efficient rate (91.14%) of the treatment, i.e. 50,000(0.9114) = $45,570. This means that with an investment of $50,000, the sunk cost is $4,430 and $5,570 is considered savings. This still does not answer the question of “economic benefit of the treatment.” In order to answer that question two pieces of information are required: (i) economic production of the patient after treatment, and (ii) economic production of patients without treatment.
   Assume now that patients are gainfully employed and earning $5,000 per month per person. With the effect of psoriasis, patients have to be absent from work and take a pay cut of $1,000 per month. With the treatment, patient can return to normal work schedule and earn a full $5,000 without any cuts. What are the economic benefits of the treatment? Recall there are 50 patients. The total monthly earning of the group is $50,000(50) = $250,000. There was an investment of $50,000 in the treatment out of which $4,430 is a sunk cost. The following scenario follows: (i) without treatment, there would be a loss of $1,000 per person per month X 50 people = ($50,000) loss due to psoriasis; (ii) if the treat fails (which is not the case, but IF …), then the loss is loss from work ($50,000) + loss of treatment cost ($50,000) = ($100,000) total loss; and (iii) if the treatment works (in the example this is the case), then normal monthly gainful employment earnings $50,000(50) + $45,570 savings from treatment cost + emotional well being – cost of capital of $50,000 treatment cost = $250,000 + 45,570 + emotional well being – cost of capital of $50,000 treatment cost. Note 95,570/100,000 = 95.57% economic benefit and 91.14%(100,000) = 91,1400 efficacy of treatment under Kahneman-Tversky equation are not the same thing. Assume now that the cost of capital is 10% then the total cost of capital is $50,000(0.10) = $5,000; the revised figure: [($250,000 + 45,570) – 5,000] = 295,570 -5,000 = 295,070.
   The economic gain is [(295,070 – (250,000 + 5000 + 5,000)/250,000 = (295,070 – 260,000)/250,000 = 235,070/250,000 = 0.94028 or 94.03%. Compared to economic loss of no treatment (250,000 – 50,000)/250,000 = 200,000/250,000 = 0.80 where the loss is 20%. Compared to a failed treatment: (250,000 – (50,000 + 50,000)/250,00 = (250,000 – 100,000)/250,000 = 150,000/250,000 = 0.60 or a loss of 40%.
REFERENCE:
(1) Kahneman, Daniel, and Amos Tversky. “Prospect Theory: An Analysis of Decision Under Risk.” Econometrica. XLVII (1979): 263–291.
(2) Tversky, A. and Kahneman, D. (1992). “Advances in Prospect Theory: Cumulative Representation of Uncertainty.” Journal of Risk and Uncertainty, 5, 297-323.
(3) Laplace, A Philosophical Essay, New York, 1902.
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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?
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As a future patient who will use Ustekinumab, I do hope both doctors are right about the impressive clinical efficacy of this treatment: indeed, in my case no TNF alpha blocker worked to stop my psoriatic arthritis. 
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Based on the evidence can any one suggest the best treatment option for this group of patients?
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elderly females with PPP will do better with phototherapy using Narrow band UVB.
Topical steroid with salicylic combination.
It may be difficult to consider methotrexate, but fatty liver should not be a problem, if The LFT is within normal limits and it may be tried for a short duration.
but yes Phototherapy helps. 
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Methotrexate and psoriasis: have you problems with this drug?
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Satyaprasad: it. is not necessary a complete renal study before the treatment. As we use 2.5 to  3  mg/ kg, this dose is generally very well supported by the kidney.
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Some evidence suggests that it may, but clinical trials to confirm this are lacking.
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to my knowledge this remains an answered but very interesting question . As chronic inflammation can induce endothelial damages , and some cytokines can enhance atheroma formation, at the opposite , antiinflammatory action of some biologc therapy for psoriasis could have a favorable effect , but it is only speculation at the moment and must be proved ,
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Will there be a coexistence of PLC and psoriasis in some patients and if so how do they present?
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In my very long personal clinical experience I have never seen coexistence of PLC and psoriasis. However PLC may sometimes look like psoriasis guttata and this would be possibly misinterpreted as an association or overlap. It is always possible that two different diseases could be present in the same subject but, before to conclude that PLC and psoriasis are present in the same individual, it is important to note that both could mimic the other.
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This is a case of third trimester pregnancy with psoriasis, extensive involvement, possibility of caesarian section. How does one manage the case when there is involvement of the abdominal region, arms? Which are the safe drugs? Are steroids indicated?
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Thank you Dr Jon, In this case the mother has not been given any steroid as systemic treatment nor cyclosporin. Psoriasis has affected all her limbs, abdominal area. there is erythema over the skin of abdomen.all her parameters ar normal. she has had 2 abortions hence this case has been considered precious.
My concern is of the following days post delivery.
1. if the delivery is normal then c section may be avoided.
2. precious baby hence probability of c section is high.
3. nsaids post delivery pose a risk to psoriasis.
4.extensive invovement of skin leads to topical steroids being absorbed.
5.methotrexate and phototherapy may be tried post delivery after advising against mothers milk.
6. very few studies are avalable for the management of psoriasis and pregnancy.