With the Psoriasis Area and Severity Index (PASI) first introduced in 1978, and the Dermatology Life Quality Index (DLQI) developed in 1994 is now time to move on to a newer measure for patients with psoriasis? I made the Psoriasis Score a few years ago because I never felt the PASI was easy to follow, now there is a study that is suggesting it could be time for a change.

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Abstract:
In a non-life-threatening disease such as psoriasis, treatment goals should be referred to the improvement in severity and extent of the disease and their impact on patients’ perceived health-related quality of life (HRQoL), usually measured by the Dermatology Life Quality Index (DLQI).

The ultimate goal of therapy is blanching, and an improvement of 90% or better (PASI90 response) with respect to baseline Psoriasis Area and Severity Index (PASI) is considered as treatment success by the European Medicines Agency. PASI75 response has become accepted as a less stringent reasonable therapeutic goal, but absolute PASI values might provide a better benchmark, irrespective of baseline PASI.

Anyway, objective measures of psoriasis involvement are clinically meaningful only if they correlate with significant improvements in DLQI, and especially with the achievement of a DLQI = 0–1 status, corresponding to lack of effect of the disease on patient's HRQoL. Even though PASI75 response meets therapeutic expectations in most patients, PASI90 response or better has a significantly higher impact on DLQI improvement and is associated with significantly higher DLQI = 0–1 response rates.

The introduction of anti-IL17 drugs in clinical practice bears the promise of achieving PASI90 response or better in the majority of patients, and initial data suggest that the PASI90 benchmark provides better discriminatory value as regards achievement of DLQI = 0–1 response.

Further research is required to confirm the value of absolute PASI cut-offs as a measure of therapeutic success independent of baseline and duration of treatment, and to develop newer, more practical and more accurate measures of psoriasis severity.

For those of you with psoriatic arthritis the results will come as no surprise to you, but it's an interesting little study that set out determine the effects of psoriatic arthritis (PsA) on sleep quality.

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Aim:
The purpose of this study was to determine the effects of psoriatic arthritis (PsA) on sleep quality and investigate the association between sleep quality and clinical parameters of PsA, quality of life and psychological state in patients with PsA.

Method:
Forty-one patients with PsA and 38 healthy volunteers were included in this study. In both patients and healthy controls, sleep quality was assessed by means of the Pittsburgh Sleep Quality Index (PSQI) and anxiety and depression were assessed by means of the Hospital Anxiety and Depression Scale (HADS). In addition, PsA Quality of Life (PsAQoL) Index and Psoriasis Area and Severity Index (PASI) were used on patients. Generalized pain was assessed by means of a visual analogue scale (VAS).

Results:
Subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbance, daytime dysfunction and total PSQI scores were significantly higher in patients with PsA compared to healthy controls. Total PSQI scores significantly correlated with anxiety, generalized pain, PsAQoL scores, enthesitis and levels of C-reactive protein (CPR) and erythrocyte sedimentation rate (ESR) (P < 0.05). Also, multiple regression analysis indicated that ESR level was independently associated with total PSQI score (P <0.05, R2 = 0.325).

Conclusion:
Sleep quality is diminished in patients with PsA. Sleep disturbance is particularly associated with generalized pain, anxiety, enthesitis and levels of CRP and ESR in patients carrying the diagnosis of PsA.

Glycerine is in the skin layers. I use it as a moisturizer especially in winter. My Paloplanter and on hands and feet seem to always be seasonal.i STAY AWAY FROM WATER THAT IS NOT FILTERED. Wash with glycerine soap no itch after bath then moisturize.

I use it in many of my home made mixtures. Non alcohol watch hazel AND GLYCERINE.

SINCE using these my hands and feet P. R in remission for 4 years now. Also a spa with paraffin wax . I use at night night then add glycerine and occlusion over night. Really gets down thru the deep layers of my P. Skin.

JUST having to try DEMARDS To treat PSA. Were also talking about a new bio...

The DEMARDS really help the pain but make me too sick. I also have severe OA 2 THR. My hips r always cold . I'm probably worth more with all that metal in my hips and shoulders.

Some days during this time of year I really need the Tin Man's oil can...

So it's always trial and error. Some of us have different outcomes with meds than others.

As most of us p.with know it can be so tricky. Does anyone use a dehumidifier in damp areas of the country for PSA.?
I've read it helps with cold weather to control the moisture in the air in homes.

New drug BI 655066 moves on to phase 11 trial after showing psoriasis clearance for 66 months after one single dose Dr. James G. Krueger reported at the annual congress of the European Academy of Dermatology and Venereology. Yes you heard it right 66 months that's 5.5 Years.

Quicky version:

Key clinical point: Up to 66 months after receiving a single subcutaneous injection of a biologic agent that selectively blocks interleukin-23, six patients with moderate to severe chronic plaque psoriasis at baseline remained PASI 100 responders with clear skin.

Major finding: The PASI 75 response rate 12 weeks after receiving a single dose of the investigational agent BI 655066 was 87%, and the PASI 90 rate was 58%.

Data source: This was a first-in-humans, proof-of-concept study involving 39 psoriasis patients.


Longer version:

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“For me, this is one of the most interesting features of this proof-of-concept study,” he added. “If this kind of activity is confirmed in the ongoing phase IIb trial, I think this represents the potential for very long-term disease modification. This could become an important agent in the future to treat psoriasis.”

BI 655066 is a monoclonal antibody that specifically targets the p19 subunit of interleukin (IL)-23. Unlike ustekinumab (Stelara), which blocks both IL-23 and IL-12, BI 655066 selectively blocks only IL-23, which Dr. Krueger believes is the central driving force in activating and sustaining the T-cell subsets responsible for the hyperproliferative and inflammatory reactions that define psoriasis.
“This study is all about testing for the specific pathogenic contribution of IL-23 to psoriasis in a first-in-humans study.

Our findings really emphasize the importance of IL-23 in driving the key pathways of psoriasis,” observed Dr. Krueger, professor of investigative dermatology and director of the Milstein Medical Research Program at Rockefeller University, New York.
The study included 39 patients with moderate to severe plaque psoriasis. Their baseline PASI was 18, and they averaged more than a 20-year history of psoriasis. Twenty-four patients were randomized 3:1 to a single intravenous injection of BI 655066 at various doses ranging from 0.01 mg/kg to 5 mg/kg or to placebo in order to get an initial sense of the agent’s safety and tolerability.
In the second part of the study, 15 other participants received a single subcutaneous injection: two got placebo and the rest were randomized to BI 655066 at either 0.25 mg/kg or 1.0 mg/kg. Safety and efficacy were assessed at weeks 0, 2, 4, 12, and 24. In addition, skin biopsies were obtained at weeks 0 and 8 for immunohistochemistry studies and RNA sequencing analysis.

By week 12, the PASI 75 response rate in subcutaneous BI 655066 recipients was 87% and the PASI 90 rate was 58%. At week 24, nine patients elected to continue structured prospective follow-up while remaining off treatment, including six PASI 100 responders. Those six PASI 100 responders remained PASI 100 at ongoing follow-up 48-66 weeks after receiving their single dose of the agent.

Biopsy specimens obtained at week 8 showed normalization of the epidermal psoriasiform hyperplasia which had been present at baseline. A normal-looking granular layer had been reestablished. “This looks essentially like the pattern of normal or nonlesional skin,” according to the dermatologist.

RNA sequencing analysis and gene profiling showed normalized production of the IL-23/IL-17-induced proteins that had been strongly overexpressed at baseline, including lipocalin, beta-defensin, and psoriasin.

“The immune axis is turned down. The number of immune cells is way down, although they’re not completely eliminated. With placebo, you still see a psoriasislike pattern of the disease. With blockade of IL-23, most cases have a gene profile like nonlesional skin. This represents a profound cellular and disease modulation,” Dr. Krueger said.

Among all 39 participants, the only serious adverse event deemed possibly treatment related was a 5-minute transient ischemic attack (TIA) episode in a patient on BI 655066. This caught Dr. Krueger’s attention as a possible red flag; however, he noted that more than 200 patients have since received the biologic agent in the ongoing phase IIb trial, with no reported major adverse cardiovascular events.

“I think that TIA may just be bad luck with small numbers,” he added.

Asked what he thinks might explain the remarkably lengthy disease remission seen following a single dose of the biologic, Dr. Krueger offered two possibilities.

“It may be that IL-23 is necessary to sustain pathogenic clones of memory cells in the skin, and as we get rid of it those clones most likely apoptose. And if you’ve sufficiently removed the clones, then you don’t get the expansion. That’s guess one. Guess two would be that we’ve renormalized tolerance mechanisms in some way. Both of these hypotheses can be tested,” according to Dr. Krueger.

I started Humira on October 9. Ever since then I have been having some discomfort in my chest and a cough. I am suppose to take another shot on Thursday October 30. I am going to hold off till I talk to my dermatologist. Her office is closed on Thursday so I am going to call her Friday.

Has anyone on here that is on or have taken Humira have any side effects?

This study set out to determine for the first time whether the anti-TNF-α monoclonal antibody Humira (adalimumab) may improve insulin sensitivity in non-diabetic patients with psoriasis.

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Objective:
Psoriasis is a chronic inflammatory disease associated with increased risk of cardiovascular death. Several studies have shown a beneficial effect of anti-TNF-α therapy on the mechanisms associated with accelerated atherogenesis in patients with inflammatory arthritis, including an improvement of insulin sensitivity. In this study, we aimed to determine for the first time whether the anti-TNF-α monoclonal antibody adalimumab may improve insulin sensitivity in non-diabetic patients with psoriasis.

Methods:
Prospective study on a series of consecutive non-diabetic patients with moderate to severe psoriasis seen at the Dermatology Division of Hospital Universitario Marques de Valdecilla (Northern Spain) who completed 6 months of therapy with adalimumab (80 mg at week 0 followed by 40 mg every other week, starting 1 week after the initial dose). Patients with chronic kidney disease, hypertension or body mass index ≥ 35 kg/m[sup]2[/sup] were excluded. Metabolic and clinical evaluation including assessment of insulin sensitivity using the Quantitative Insulin Sensitivity Check Index (QUICKI) was performed at the onset of the treatment (time 0) and at month 6.

Results:
Twenty-nine patients (52% women; 38.6 ± 10.7 years) with moderate to severe psoriasis [body surface area (BSA) 37.9 ± 16.3%], Psoriasis Area and Severity Index [(PASI) 18.9 ± 7.8] were assessed. Statistically significant improvement (P=0.008) of insulin sensitivity was observed after 6 months of adalimumab therapy (QUICKI at time 0: 0.35 ± 0.04 vs. 0.37 ± 0.04 at month 6). Significant improvement of erythrocyte sedimentation rate, ultrasensitive C-reactive protein, BSA, PASI, Nail Psoriasis Severity Index, physician global assessment and psoriatic arthritis screening and evaluation questionnaire was also observed at month 6 (P < 0.05 for each variable).

Conclusion:
Our results support a beneficial effect of the anti-TNF-α blockade on the mechanisms associated with accelerated atherogenesis in patients with psoriasis.

It's been known for a long time there are other disorders (or diseases) co-occurring with psoriasis and psoriatic arthritis, this retrospective study was obtained from the Clinical Practice Research Datalink (CRPD) between 2006 and 2010.

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Background:
Previous studies have demonstrated that patients with psoriasis have higher rates of comorbidities compared to the general population. Despite the clinical and economic burden of psoriatic disease, there have been few large-scale observational studies focused on this condition.

Objective:
To assess rates of cardiovascular, autoimmune, infectious and other conditions in patients with psoriasis or psoriatic arthritis (PSA).

Methods:
The data for this retrospective study were obtained from the Clinical Practice Research Datalink (CRPD). Cohorts of patients with psoriasis (n = 27 672; mild, n = 22 174, severe, n = 5498) and PSA (n = 1952) were generated based on the diagnosis made by general practitioner or specialist recorded in CPRD between 2006 and 2010. Frequencies of comorbidities at baseline and incidence rate ratios (IRR) of medical conditions occurring during follow-up were calculated and compared between groups. Cox proportional hazard models were employed to compare hazard ratios (HR) of comorbidities across the same subpopulations previously described.

Results:
Significant differences in the unadjusted risk of cardiovascular disease, hyperlipidaemia, diabetes, skin cancer and autoimmune diseases were observed between patients with differing severity of psoriasis or between PSA and psoriasis patients. The adjusted HR analyses confirmed patients with severe psoriasis had significantly higher rates of several conditions including diabetes (1.23; 95% CI: 1.01–1.51) and rheumatoid arthritis (2.88; 95% CI: 2.25–3.67) compared to patients with mild psoriasis. Patients with PSA had significantly higher adjusted rates of hypertension (1.30; 95% CI: 1.01–1.68), rheumatoid arthritis (6.93; 95% CI: 5.45–8.80) and ankylosing spondylitis (6.98; 95% CI: 2.37–20.58) compared to those with severe psoriasis.

Conclusion:
Patients with mild psoriasis are less affected by comorbid conditions than those with severe psoriasis, and patients with psoriasis are less affected by comorbidities than those with PSA. Given the differences observed across severities of psoriasis and between psoriasis and PSA, each patient subgroup should be taken into consideration in clinical practice and future research.

This study looked at different patterns of bone spur formation in psoriatic arthritis (PsA) and hand osteoarthritis (OA), using high-resolution peripheral quantitative computed tomography (QCT).

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Methods:
The study group comprised 70 subjects (25 patients with PsA, 25 patients with hand OA, and 20 healthy controls). The 2 patient groups were similar with regard to age and sex distribution and clinical involvement of the metacarpophalangeal (MCP) joints. All patients underwent high-resolution peripheral QCT scanning of the second, third, and fourth MCP joints of the dominantly affected hand. Demographic and disease-specific data were recorded, and the number, size, and distribution of bone spurs were assessed and compared between patients with PsA and patients with hand OA.

Results:
The overall number and size of bone spurs were similar in patients with PsA and patients with hand OA. However, localization of lesions within individual joints was substantially different between patients with PsA and those with hand OA. In PsA, bone spurs dominated the radial sides of the joints (for the metacarpal head of the second joint, P < 0.001 versus hand OA; for the base of the second phalangeal joint, P < 0.001 versus hand OA), whereas the palmar and dorsal quadrants were the predilection sites in hand OA. Detailed anatomic analysis showed that bone spurs in the entheseal regions were prominent in patients with PsA but rare in patients with hand OA, and that bone spurs in patients with hand OA typically emerged at the cartilage–bone interphase and the joint margins.

Conclusion:
Our findings show that the overall number and size of bone spurs are similar in patients with PsA and patients with hand OA. Nonetheless, the anatomic sites of bone proliferation are different between these 2 groups of patients.

It's been known for a long time that our nails play an important part in the detection of psoriatic arthritis (PsA) and this study looks like it confirms that.

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Background:
Patients with psoriatic arthritis (PsA) suffer from increased burden of disease and impairments in quality of life. Early detection and treatment of PsA could contribute to the prevention of clinical and radiological progression.

Objectives:
To analyse the predictive value of clinical and patient-reported outcomes for concomitant PsA in a population-based cohort of patients with psoriasis.

Methods:
We performed a retrospective analysis of data from three independent national cross-sectional studies on health care in psoriasis and PsA, conducted in Germany in the years 2005, 2007 and 2008. Patients with psoriasis were included in the study by dermatologists (n = 3520) and via the German patient advocacy group for psoriasis (n = 2449). In all studies, psoriasis history, clinical findings, PsA, nail involvement, health care and patient-reported outcomes were collected with standardized questionnaires.

Results:
In the regression model on 4146 patients the strongest predictors for concomitant PsA were nail involvement [odds ratio (OR) 2·93, 95% confidence interval (CI) 2·51–3·42, P < 0·001] and inpatient hospital treatment (OR 1·63, 95% CI 1·38–1·93, P < 0·001). By contrast, scalp involvement was not a significant predictor.

Conclusions:
Patients with psoriasis seen by dermatologists and those in patient advocacy groups show clinical indicators of PsA, the most predictive being nail disease. In practice, a comprehensive assessment of clinical findings associated with PsA is needed.

The University of California, Irvine may have found a new way of tackling psoriasis by discovering that a gene called grainyhead, known to be important in epidermal development and wound healing triggers a repair pathway for psoriasis lesions.

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A UC Irvine-led study has revealed the underlying genetic factors that help repair skin lesions caused by psoriasis, which could engender new methods of controlling the lingering condition.


Dr. Bogi Andersen, professor of biological chemistry and endocrinology at UCI, and colleagues discovered that a gene called grainyhead – known to be important in epidermal development and wound healing – triggers a repair pathway for psoriasis lesions. Conversely, they found that deletion of this gene increased the severity and longevity of the disfiguring patches.

“Our research suggests that targeting this mechanism of healing may lead to pharmaceutical products that limit the itchy, painful lesions all psoriasis sufferers must endure,” Andersen said.

The researchers learned that in psoriasis a compound called grainyhead-like 3 – which binds to DNA to control the rate of transcription of genetic information from DNA to messenger RNA – orchestrates the activation of an epidermal repair pathway. (The grainyhead gene was initially discovered in fruit flies, where it’s important for wound healing.)

They also found it easier to induce psoriasis-like lesions in mice lacking the GRHL3 gene. Furthermore, these lesions did not resolve properly and persisted even in the face of active immune suppression treatments currently being studied for the disease.

“Our study indicates that an evolutionarily ancient epidermal repair pathway is activated in psoriasis lesions and that this pathway suppresses disease severity and helps heal the lesions,” Andersen said. “We speculate that abnormalities in this pathway might contribute to disease severity and that in the future this mechanism could be targeted to help treat psoriasis.”

My new dermatologist recommend I start with Stelara treatments. I have it a patch around my bellybutton, behind, scalp and a starting with a small spot on my face. I am concerned with the health risks. I am a 20 year old male college student. Very self conscious about my looks. Not sure what to do. Scared of the side effects. Any advice would be great.

This study looked at the efficacy and safety of Stelara (ustekinumab) (UST) treatment in elderly patients with psoriasis, and suggests it is the preferable agent for the elderly.

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The ratio of the elderly among psoriasis patients has been increasing. However, satisfactory long-term management of psoriasis for the elderly is challenging because of the more frequent presence of comorbidities, and the higher risk of adverse events from systemic therapeutic agents than younger patients.

The use of ustekinumab (UST) appears to be an appropriate systemic treatment because it is considered less likely to cause adverse events than other systemic treatments, as well as necessitating fewer hospital visits.

Our retrospective study aimed to evaluate the efficacy and safety profile of UST in elderly patients with psoriasis. The study included 24 patients aged over 65 years (range, 65–88 years; mean, 73.1 years) with moderate to severe plaque psoriasis with impaired quality of life.

Efficacy and safety were assessed over a 1-year period using the Psoriasis Area and Severity Index (PASI) and the Dermatology Live Quality Index (DLQI).

The efficacy was evaluated by the proportion of subjects who achieved ≥75% reduction in PASI score (PASI 75). PASI 75 responses were 56.5% at week 16, 59.1% at week 28, and 60.0% at week 52.

None of the patients developed any serious infection during the 1-year treatment. The mean DLQI score at weeks 0, 16, 28, and 52 was 7.8 ± 6.0, 2.5 ± 3.4, 1.4 ± 1.7, and 1.2 ± 1.7, respectively.

UST showed sufficient efficacy for elderly patients with psoriasis without any serious infection over the 1-year treatment. Our results suggest that UST is the preferable agent for the treatment of elderly patients with psoriasis.

None of us like visiting our doctor but getting early diagnoses can pay off in the long run, this study looked at psoriasis patients getting a diagnoses of psoriatic arthritis (PsA) it suggests it may not be a good idea to put off a proper diagnoses longer than 6 months.

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Objectives:
To investigate the demographic and clinical characteristics contributing to the delay from symptom onset to the first visit to a rheumatologist; to compare clinical, radiographic and patient-reported outcome measures of those who saw a rheumatologist early in their disease course with those who were diagnosed later.

Methods:
All psoriatic arthritis (PsA) patients, fulfilling CASPAR criteria, with an average disease duration of >10 years were invited for detailed clinical evaluation. The total lag time from symptom onset to their first rheumatological encounter was studied. The data were extracted from the referral letters and medical records. Patients were classified as early consulters or late consulters depending on whether they were seen by a rheumatologist within or beyond 6 months of symptom onset.

Results:
283 PsA patients were studied. Median lag time from the disease onset to the first rheumatological assessment of the cohort was 1.00 years (IQR 0.5–2). 30% (n=86), 53% (n=149) and 71% (n=202) of the cohort were seen by a rheumatologist within 6 months, 1 and 2 years of symptom onset, respectively. PsA patients with low education status (OR 2.09, p=0.02) and Body Mass Index (OR 0.92, p=0.01) were significantly more likely to have a diagnostic delay of >2 years. On multiple stepwise regression analysis, the model predicted significant association of late consulters with the development of peripheral joint erosions (OR 4.25, p=0.001) and worse Health Assessment Questionnaire scores (OR 2.2, p=0.004).

Conclusions:
Even a 6-month delay from symptom onset to the first visit with a rheumatologist contributes to the development of peripheral joint erosions and worse long-term physical function.

When logged in and on the front page you will see in the green menu bar "View Unread Posts" beside it you will see two brackets ( ) inside those brackets are the number of posts that you have not read. For example (3) (72) Etc.

Now when you first try this you may need to set it to Zero. To do this go to the front page of the forum, scroll down to the bottom and click "Mark All Forums Read" which you can find on the right hand side of the bottom dark green bar. Now you will see (0) next to View Unread Posts.

When a new post is made by someone it will change once you refresh the front page and will tell you how many posts you have not read, so click the link again and you should now see only a few threads listed. So it's now set and ready to go.

To find the post you have not go to the thread and look for Unread post on the right hand side next to Post: # once you leave the thread the system will assume you have read it and it will no longer show in the brackets.

Tip: When you click "View Unread Posts" there may be some you're not interested in. No problem just click the little box on the left it will change to White and be marked as read, or visit the ones you want then get rid of the others by clicking "Mark all threads read"

If you log out and have not read all posts listed they will show up again when you log back in, so you won't miss any.

Any questions or feedback please post here.

*Thank you to Caroline for this suggestion.

Though not mentioning the products by name in the study I assume it is about treating adolescent scalp psoriasis with Dovobet (Daivobet) and Dovonex (Daivonex) as it was sponsored by LEO Pharma.

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Objectives:
The primary objective was to assess the safety of once-daily application of fixed-combination calcipotriol plus betamethasone dipropionate gel in adolescent scalp psoriasis. Assessment of efficacy was a secondary objective.

Methods:
This phase II, multicentre, single-arm, open-label, 8-week trial included patients aged 12–17 years with moderate-to-very severe scalp psoriasis according to Investigator's Global Assessment (IGA) (≥ 10% of the scalp area affected).

Results:
Seventy-eight patients received treatment. Twenty-seven patients (35%) reported a total of 64 adverse events (AEs); most were mild (33/64) or moderate (22/64) in severity and there were no serious AEs. No cases of hypercalcaemia were reported, and the mean changes from baseline to end of treatment in albumin-corrected serum calcium (0·00 mmol L−1), 24-h urinary calcium excretion (−0·03 mmol per 24 h) and urinary calcium-to-creatinine ratio (−0·12 mmol g−1) were not considered clinically relevant. At the end of treatment 66 patients (85%) were clear or almost clear according to IGA. There was an 80% improvement in mean Total Sign Score from baseline to end of treatment. In total, at the end of treatment, 87% of patients rated their scalp psoriasis as clear or very mild, and 75 (96%) had no or mild pruritus compared with 14 (18%) at baseline.

Conclusions:

Once-daily calcipotriol plus betamethasone dipropionate gel is well tolerated and efficacious for scalp psoriasis in adolescents.

Hello all - My name is Cheryl and i live in manchester, I am married with four children (well one teenage girl and 3 younger boys) i was diagnosed with aih about 3 and half years ago and apart from the fatigue have been managing quite well! I just want to make a quick confession first - i think i may have psoriasis - have been to the gp with odd looking lesions on my skin mainly on my legs and she said she didnt think it was anything really to worry about but if it didnt clear up she would refer me to skin specialist - however on showing them to a couple of people they have said psoriasis straight away and i have googled images and found a couple that look exactly like what i have got. The reason for joining is i wanted to ask a couple of questions, I have an appt with the doctor in a couple of weeks but cannot get hold of her on the phone, even after leaving messages, the lesions dont itch themselves but for the past few days i have been itching all over, does anybody suffer with this before the lesions come up and also does anybody get them round their eyes, i have really sore eyes (like when youre really tired?) and i have just got rid of one off my left eye only to notice that there may be another coming up just a little further along. Sorry if i broke any rules here lol just desperate to try and find out what is going on! Thanks for reading and if anybody can offer any advice i would be most grateful

There are a lot of threads here on Psoriasis Club that discus the link with hypertension and psoriasis, and this study from the UK suggests a need for more effective blood pressure management, particularly among patients with severe psoriasis.

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Importance:
Hypertension is prevalent among patients with psoriasis. The effect of psoriasis and its severity on hypertension control is unknown.

Objective:
To determine the association between uncontrolled blood pressure and psoriasis, both overall and according to objectively measured psoriasis severity, among patients with diagnosed hypertension.

Design, Setting, and Participants:
Population-based cross-sectional study nested in a prospective cohort drawn from The Health Improvement Network (THIN), an electronic medical records database broadly representative of the general population in the United Kingdom. The study population included a random sample of patients with psoriasis (n = 1322) between the ages of 25 and 64 years in THIN who were included in the Incident Health Outcomes and Psoriasis Events prospective cohort and their age- and practice-matched controls without psoriasis (n = 11 977). All included patients had a diagnosis of hypertension; their psoriasis diagnosis was confirmed and disease severity was classified by their general practitioners.

Main Outcomes and Measures:
Uncontrolled hypertension was defined as a systolic blood pressure of 140 mm Hg or higher or a diastolic blood pressure of 90 mm Hg or higher based on the blood pressure recorded closest in time to the assessment of psoriasis severity.

Results:
There was a significant positive dose-response relationship between uncontrolled hypertension and psoriasis severity as objectively determined by the affected body surface area in both unadjusted and adjusted analyses that controlled for age, sex, body mass index, smoking and alcohol use status, presence of comorbid conditions, and current use of antihypertensive medications and nonsteroidal anti-inflammatory drugs (adjusted odds ratio [aOR], 0.97; 95% CI, 0.82-1.14 for mild psoriasis; aOR, 1.20; 95% CI, 0.99-1.45 for moderate psoriasis; and aOR, 1.48; 95% CI, 1.08-2.04 for severe psoriasis; P = .01 for trend). The likelihood of uncontrolled hypertension among psoriasis overall was also increased, although not statistically significantly so (aOR, 1.10; 95% CI, 0.98-1.24).

Conclusions and Relevance:
Among patients with hypertension, psoriasis was associated with a greater likelihood of uncontrolled hypertension in a dose-dependent manner, with the greatest likelihood observed among those with moderate to severe psoriasis defined by 3% or more of the body surface area affected. Our data suggest a need for more effective blood pressure management, particularly among patients with more severe psoriasis.

So, finally after lots of running around, I collect my prescription of Furmederm today. The process will start and I will keep posting, daily if I can, to let you all know how it's going.

Just for reference, I have had psoriasis for 22 years. I have tried uv treatment, steroid creams, methotrexate, tar treatment and loads I have forgotten! I am hopeful that furmederm will, although might be difficult at first, help me with the process of not worrying about my skin anymore.

Fingers crossed!

More soon......

Hi all,
I'm obviously new to this interesting forum.
I've had mild psoriasis for over 30 years.
I got mild PsA 5 years ago but has got worse lately.
I have just started methotrexate last week.
After reading some other posts I don't think I have to much to worry about.
My psoriasis is mild but the PsA is really starting to affect my work (I'm a tradesman with lots of lifting).
Good luck to everyone looking for a pain free life.
Is anyone out there from New Zealand?

Hi everyone,

I'm new to this site after suffering from psoriasis since my teenage years. It is only in the last two years, however, that it turned from a few spots on my fingers when stressed to coverage over all of my body with guttate, scalp and inverse psoriasis after what I was told was a bacterial sinus infection (I now believe that it could have been strep throat).

I did topical treatments, like dovobet, before UVB treatment. I did 27 sessions and while I wasn't compltely cleared, it was almost. This lasted two months before it started to come back.

After a visit with my dermatologist yesterday, I was told that perhaps it was time to start oral treatments. I was given information on Methotrexate and Fumaderm, and told to consider my options. I'm back in 6 weeks so I have to decide by then.

Has anyone had experience with both of these treatments? Any advice would be helpful. I was leaning towards Methotrexate, but my worry is that as I work in a Creche with 2 year olds, who constantly have colds. Furmaderm seems to have a lot of nasty side affects, which makes me wary.

Thanks in advance