PSORIASIS and COMORBIDITIES – CARDIOVASCULAR DISEASE

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WHAT IS COMORBIDITY?

Comorbidity is a concurrence of multiple diseases or disorders in association with a given disease, in this case, psoriasis.

 INCREASED RISK

 The patient with psoriasis has an increased risk of developing one or more of a number of other diseases/conditions that share many immunological features with psoriasis.

 CHART 1: Comorbidities Associated with Psoriasis 1,2,3

Metabolic Syndrome – Cardiovascular Disease  

  • Arterial hypertension/ Atherosclerosis
  • Myocardial infarction (MI)
  • Dyslipidemia (Raised cholesterol)

The immunological abnormalities that lead to the development of psoriasis suggest that these patients may be at increased risk for other diseases associated with an inflammatory state. Research is yet to establish whether other diseases occur as a direct result of the systemic inflammation associated with psoriasis, as a consequence of genetically determined selection, or whether it is possible that the link between psoriasis and Cardiovascular disease and myocardial infarction (MI)  may be mediated by other factors beyond inflammation, such as psychological stress, sedentary lifestyle, or possibly poor compliance with management of cardiovascular risk factors.. 4.5

There is increasing evidence to suggest that the immune response, including activated T cells, antigen presenting cells, cytokines, and markers of systemic inflammation such as C-reactive protein, are important to the development of atherosclerosis (hardening and narrowing of the arteries) and ultimately, MI. 2 Research has shown that patients with psoriasis have a higher incidence of MI compared with control patients, with patients who have severe psoriasis as having the highest rate. The risk of MI associated with psoriasis is greatest in younger patients (under the age of 40) with severe psoriasis. This reduces with age but still remains an increased risk even after treatment for traditional cardiovascular risk factors that are associated with aging. 5

Psoriasis is also associated with hypertension (increased blood pressure). In one study researchers examined the association among hypertension, antihypertensive medication use, and risk of incident psoriasis using prospective data from a large cohort of US women. A total of 121,701 participants, of which 2477 participants were diagnosed with psoriasis, were followed for 11 years with 2 yearly questionnaires. Researchers found that a prior history of hypertension was associated with an increased risk of psoriasis among women with hypertension for 6 years or more. Specifically, hypertensive women without medication use and with current medication use were more likely to develop psoriasis compared with women who did not have hypertension. Among the individual antihypertensive drugs, only ?-blockers were associated with an increased risk of psoriasis after regular use for 6 years or more. 6

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In a United Kingdom study using a large (7.5 million patients from 415 practices) electronic medical records database (The Health Improvement Network (THIN), a random sample of patients with psoriasis between the ages of 25 and 64 years were identified. The identification parameters were a diagnosis of hypertension; confirmed psoriasis diagnosis and classified psoriasis severity. The severity classification was identified according to the National Psoriasis Foundation classification system 1) mild (limited disease with ?2% BSA affected), moderate (scattered disease with 3%-10% BSA affected), or 2) severe (extensive disease with >10% BSA affected). Blood pressure was compared to the UK National Institute of Health and Care Excellence clinical guidelines, with uncontrolled hypertension being defined as systolic blood pressure of 140 mm Hg or higher or diastolic blood pressure of 90 mm Hg or higher. 

All patients with psoriasis who met the inclusion criteria were included in the study, yielding 680, 469, and 173 patients with mild, moderate, and severe psoriasis, respectively. The researchers found a significant positive relationship between psoriasis severity and uncontrolled hypertension independent of potential risk factors for poor blood pressure control. The likelihood of uncontrolled hypertension in patients with vs without psoriasis was greatest among those with moderate and severe skin disease, representing nearly half of the psoriasis patients seen by GPs in the United Kingdom. The findings have important clinical implications, highlighting a need for more effective management of blood pressure in patients with psoriasis, especially those with more extensive skin involvement (i.e. ?3% BSA affected).7 

The precise mechanisms that underlie psoriasis and hypertension are unknown. One theory proposed is that adipose (fat) tissue in psoriasis patients serves as a major source of angiotensinogen, which is subsequently converted to angiotensin II. Angiotensin II not only promotes salt retention by kidneys; it also stimulates T-cell proliferation. Angiotensin II also appears to promote inflammation and the development of atherosclerosis. Other theories suggest that increased visceral adipose tissue in psoriasis patients may contribute to hypertension development. Increased visceral adipose tissue may be associated with accumulation of perivascular fat, which can serve as a reservoir for activated effector T cells that promote dysfunction in both hypertension and psoriasis. Or that endothelin-1 may play an important role in the development of hypertension among psoriasis patients. Endothelin-1 is a protein that constricts blood vessels and increase blood pressure, and it is produced by several different cell types including keratinocytes. While the level of endothelin-1 is usually regulated through various mechanisms, their expression appears to be altered in psoriasis patients. 8 The connection between obesity and psoriasis, when taken in light of the above theories, is further strengthened. It is always advisable for those with moderate to severe psoriasis who are overweight to try to lose weight through sensible eating – reducing fast and fatty foods and increasing the intake of vegetables, especially green vegetables.

The development of atherosclerosis and its increased prevalence may be partially explained by the presence of atherosclerotic risk factors, e.g., diabetes, hypertension, obesity, and hyperlipidemia (increased levels of lipids in the blood, including cholesterol and triglycerides) as well as by the chronic inflammatory processes that are commonly observed in psoriasis. 9 

Researchers have found that psoriasis patients have impaired endothelial function and greater thickness of the innermost two layers of the wall of the carotid artery which leads to increased arterial stiffness. 9

Atherosclerosis, the underlying process resulting in cardiovascular events, is caused by the build up of atheromatous plaques in the inner layer of the arteries. Atheromatous plaques are an accumulation of degenerative material in the inner layer of an artery wall. The material consists of mostly macrophage cells, or debris, containing lipids, calcium and a variable amount of fibrous connective tissue. The interaction between metabolic abnormalities such as diabetes, high cholesterol etc. and the systemic proinflammatory mechanisms operating involved in psoriasis and psoriatic arthritis may explain the accelerated atherosclerotic process in these patients. Patients with psoriatic disease display abnormalities in the innate and adaptive immune system that result in high serum levels of proinflammatory cytokines that may upregulate cell-mediated immunity, promote inflammatory cell migration through the vascular endothelium (tissue that lines the interior surface of blood vessels), resulting in endothelial dysfunction and thus causing plaque formation and build up. 10

Recent studies clearly demonstrated that inflammation impairs reverse cholesterol transfer (High-density lipoprotein (HDL) cholesterol efflux) in vivo, providing evidence that inflammation impairs HDL function. HDL is a complex lipoprotein particle with a broad variety of functions, exerting atheroprotective activity via effects on the endothelium and by potent anti-inflammatory capabilities. Functional impairment of HDL may contribute to the increased cardiovascular mortality experienced by psoriatic patients. HDL from psoriasis patients and healthy controls was assessed for changed HDL composition. Researchers found that there was a significant reduction in apoA-I levels of HDL from psoriatic patients, whereas levels of apoA-II and proteins involved in acute-phase response, immune response, and endopeptidase /protease inhibition were increased. Psoriatic HDL also contained reduced phospholipid and cholesterol. The researchers found that the compositional alterations impaired the ability of psoriatic HDL to promote cholesterol efflux from macrophages. Importantly, HDL cholesterol efflux capability was more impaired as the psoriasis area and severity increased. 11

Efflux is a mechanism responsible for moving compounds, like cholesterol out of the cells.  The efflux process is extremely important because cholesterol overloading, such as occurs in the cells of the arterial walls, leads to the development of atherosclerotic plaque.12

Chronic systemic inflammation associated with psoriasis and psoriatic arthritis induces endothelial dysfunction, altered glucose metabolism, and insulin resistance that plays a significant role in the development of obesity, diabetes mellitus, dyslipidemia (high cholesterol), and cardiovascular disease such as atherosclerosis and myocardial infarction.

Those with moderate to severe psoriasis should ensure that they visit their General Practitioner to have their blood pressure and cholesterol checked and to have an ECG regularly to ensure the health of their heart.

 

REFERENCES

  • Arzu K?l?ç, Seray Cakmak; PSORIASIS AND COMORBIDITIES; EMJ Dermatol. 2013;1:78-85.
  • Howa Yeung et al.;Psoriasis Severity and the Prevalence of Major Medical Comorbidity – A Population-Based Study; JAMA Dermatol. 2013;149(10):1173-1179. doi:10.1001/jamadermatol.2013.5015
  • Aurangabadkar SJ. Comorbidities in psoriasis. Indian J Dermatol Venereol Leprol 2013;79, Suppl S1:10-7
  • Elgendy A, Alshawadfy E, Altaweel A, Elsaidi A (2016) Cardiovascular and Metabolic Comorbidities of Psoriasis. Dermatol Case Rep 1: 106.
  • Gelfand JM, Neimann AL, Shin DB, Wang X, Margolis DJ, et al. (2006) Risk of myocardial infarction in patients with psoriasis. JAMA 296: 1735-1741.
  • Wu S, Han J, Li W, Qureshi AA. Hypertension, Antihypertensive Medication Use, and Risk of Psoriasis.JAMA Dermatol. 2014;150(9):957-963. doi:10.1001/jamadermatol.2013.9957
  • Takeshita J, Wang S, Shin DB, et al. Effect of Psoriasis Severity on Hypertension Control: A Population-Based Study in the United Kingdom.JAMA dermatology. 2015;151(2):161-169. doi:10.1001/jamadermatol.2014.2094.
  • Wang Armstrong A. et al; Psoriasis and Hypertension Severity: Results from a Case-Control Study; PLoS ONE 6(3):e18227 · March 2011
  • Kalkan G , Karada? A.s.:The Association Between Psoriasis and Cardiovascular Diseases: Eur J Gen Med 2013; 10 (Suppl 1):10-16
  • Eder L. and Gladman D.D.; Atherosclerosis in psoriatic disease: latest evidence and clinical implications; Ther Adv Musculoskel Dis 2015, Vol. 7(5) 187–195 DOI: 10.1177/ 1759720X15591801
  • Holzer M. et al.; Psoriasis alters HDL composition and cholesterol efflux capacity; Journal of Lipid Research Volume 53, 2012
  • Phillips M.C.; Molecular Mechanisms of Cellular Cholesterol Efflux; J Biol Chem. 2014 Aug 29; 289(35): 24020–24029.

Itch + Psoriasis

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Itch (Pruritus)

is an important but underestimated symptom in psoriasis. However, there is limited published research data available on both its prevalence and characteristics. Some studies suggest that its prevalence in psoriasis sufferers, from different parts of the world, ranges from between 70% and 90%. In one Study Researchers found that 83% of psoriatic patients suffered from itching and in 45% of these patients pruritus was a daily occurrence (in 32% “often” and in 13% “always”) 1

Functional brain imaging studies have shown that the itch-scratch cycle in humans can be tracked to specific regions of the brain, including areas related to reward, pain sensation, and addiction.

The Itch-Scratch-Rash cycle is commonly used to describe this ongoing, never ceasing, always constant itch. The itchier a patient feels, the more scratching of the skin that occurs and which ultimately lead to skin damage and the appearance of a red rash. Often, in chronic presentations it becomes a completely unconscious habit and patients are often not even aware that they are scratching. When a patient scratches, their skin becomes inflamed, this inflammation then causes the skin to itch even more, thus making it even harder for the patient to resist the urge to scratch. This vicious circle can become so severe that it causes sleeplessness, irritability, anxiety and stress. In extreme cases it can lead to significant excoriations (open, bloody and deep scratch wounds) on the lesions and the surrounding normal skin. In chronic psoriasis it can even cause severe lichenification (thickening of the skin) and pain.

One study found that itching was the most frequent complaint (64%) among patients hospitalized for psoriasis. A National Psoriasis Foundation USA survey of its members in 2001, reported that for 79% of sufferers – itch was the second most troublesome symptom after scaling. Psoriasis sufferers have indicated that the severity of their itching on a scale from one to 10 VAS scale (from mild, moderate to severe pruritus where scratched plaques bleed). Most described pruritus (itch) as a sensation of stinging (20%) and burning (15%); the intensity reflected by VAS scale was scored as mild only in 13%, moderate in 37% and severe in 33% of those surveyed. 75% percent of itch patients had to scratch until they bled. Itch was also found to be more severe and frequent at night with 50% reporting difficulty in falling asleep. 2, 3

Itching/Scratching can lead to the hypertrophy (enlargement) of cutaneous (skin) nerve endings, which in turn become more sensitive. For those psoriasis sufferers that have as their Primary trigger, flare-ups caused by the “Koebner Phenomenon” (in which skin injury e.g. tattoos, surgical procedures, cuts, insect bites or sunburn etc. elicits a disease response) scratching can continually exacerbate and worsen their condition. The “Koebner Phenomenon” affects between 11% to 75%, depending on various study results. 4

Where constant and vigorous scratching has occurred and plaque scales have been removed, pin point bleeding, known as the Auspitz sign can be observed.

it_1

Studies have also shown that in people suffering from depression, and who suffer from itching due to a variety of causes, that there is a correlation between the severity of itchiness and the severity of depression. Itching therefore causes both a real serious physical and psychological suffering, similar to what chronic pain does.5 It has been noted that there is a direct positive relationship between the severity of pruritus and the severity of depression in patients with psoriasis.6 One study revealed that patients with psoriasis, that experienced intense pruritus, also reported significantly higher scores for depression and anxiety, and showed personality traits of somatic anxiety, embitterment, mistrust, and physical trait aggressiveness. It was also noted that approximately 30% of these patients experienced high-level pruritus, when the great majority of patients had very few skin lesions.7

Patients when answering the questions on “what was the aggravating factors of pruritus”, gave the following answers –  “when I was stressed out” (35.0%), followed by “in a hot environment” (18.8%), “when sweating” (17.5%), “during a change in the weather” (12.5%), and “in a cold environment” (10.0%). Of these patients, 32.5% complained of itching on the entire body, followed by the scalp and trunk (17.5%), the scalp only (16.3%), and the scalp and extremities (13.8%).8

Scratching, even for adults, is difficult to resist because it does give the impression of easing the itch – but this is only for the short-term. Eventually the sensation to itch comes back – even worse that before the patient scratched.

Basic tips to control the urge to itch:- 

  • Keep nails short to avoid tearing the skin when scratching. 
  • Keep cool. Over-heating can trigger the itch. Try to keep your body temperature as constant as you can, wear light layers of cotton clothes.
  • Avoid overheated rooms, keep ducted heating to a minimum, and at night keep the bedrooms cold.
  • Avoid heavy blankets and doonas – use cotton blankets (hospital style) if possible. 
  • Gently rub with the back of the fingers, place pressure on the area instead of scratching. 
  • Use a cold compress 

it_2

REFERENCES:

  1. Aerlyn D. “Treating Itch in Psoriasis.” Dermatology Nursing 18.32006 227-233. 20 Apr. 2008. http://www.medscape.com/viewarticle/541971.
  2. “Itch Relief.” Psoriasis.org. 9 Nov. 2001. National Psoriasis Foundation. 20 Apr. 2008.
    http://www.psoriasis.org/news/stories/2001/20011109_itch.php.
  3. Prigninao P. et al.; Itch in psoriasis: epidemiology, clinical aspects and treatment options.; Clinical, Cosmetic and Investigational Dermatology 2009:2 9–13
  4. Sampogna, F. “Prevalence of Symptoms Exerienced by Patients with Different Clinical Types of Psoriasis.”British Journal of Dermatology 151.3 Sep. 2004. 594-599. 20 Apr. 2008. http://www.blackwell-synergy.com/doi/abs/10.1111/j.1365-2133.20.
  5. Thappa, D.M. “The Isomorphic Phenomenon of Koebner.” Indian Journal of Dermatology, Venereology and Leprology 70.32004 187-189. 23 Apr.2008. http://www.ijdvl.com/text.asp?2004%2F70%2F3%2F187%2F11105.
  6. Gupta MA.et al. Pruritus in psoriasis. A prospective study of some psychiatric and dermatologic correlates. Arch Dermatol 1988; 124: 1052–1057.
  7. Remröd C. et al.; Psychological aspects of pruritus in psoriasis; Acta Derm Venereol 2015; 95: 439–443
  8. Tae-Wook Kim et al.; Clinical Characteristics of Pruritus in Patients with Scalp Psoriasis and Their Relation with Intraepidermal Nerve Fiber Density; Ann Dermatol Vol. 26, No. 6, 2014

Types of Psoriasis – FLEXURAL/INTERTRIGINOUS (INVERSE PSORIASIS) and GENITAL PSORIASIS

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Inverse psoriasis

 also known as flexural or intertriginous psoriasis is a rare form of psoriasis that occurs in the flexural skin folds. Plaque psoriasis is most commonly found on the trunk and extensor surfaces of the body, such as the knees, elbows, sacral (lower back) area, and scalp whereas Inverse psoriasis is found in the folds of the axilla (armpits), submammary (breast) folds, and groin (inguinal) and buttock folds. It can occur in any area where two skin surfaces meet. The inguinal fold is the most commonly affected area, followed by the axilla and the external genitalia. The skin at the inverse body sites differs from skin at extensor sites with less epidermal keratinization (thinner skin) and more sweat glands. The most evident difference between classical plaque-type psoriasis and inverse psoriasis is the lack of, or less, scaling. The lesions are usually well demarcated, erythematous (red), and are often shiny, appear moist, weepy and fissured. The irritation may be increased in inverse psoriasis as a result of the rubbing and sweating involved in the skin folds. 1, 2   

Approximately 3–7% of psoriasis patients present with inverse psoriasis and patients with palmar psoriasis have a greater chance of having inverse psoriasis as compared with plaque psoriasis. In one study of 170 psoriasis patients with palmar involvement, 5.3 times more patients had inverse psoriasis than patients with plaque psoriasis. Development of inverse psoriasis has been reported as a paradoxical side effect to treatment with infliximab for Crohn’s disease and hidradenitis suppurativa. Inverse psoriasis has been observed to be more common in the obese population possibly due to the rubbing of the skin folds. 1, 2

Inverse psoriasis affecting the genitalia seems to be underreported and undertreated; and approximately 35% patients with genital psoriasis never speak to their physician about their genital lesions. Nearly 70% of Physicians do not offer treatment for genital lesions. 3

Flexural Psoriasis 3

A study on the quality of life and sexual life in 487 patients with genital psoriasis concluded that3:

  • patients with genital lesions report even significantly worse quality of life than patients without genital lesions;
  • sexual distress and dysfunction are particularly prominent in women;
  • sexual distress is especially high when genital skin is affected;
  • the attention given to possible sexual problems in the psoriasis population by healthcare professionals is perceived as insufficient by patients.     

Flexural Psoriasis 2

Results of several questionnaire-based surveys show that involvement of the genital skin region occurs in 29–40% of patients with psoriasis. The genital area may frequently be involved in cases of inverse psoriasis. Of 48 patients with inverse psoriasis, the external genitalia were involved in 38 (79.2%). 4

Flexural Psoriasis 1

In another report researchers stated that patients with genital psoriasis have significantly worse quality of life (QoL) scores compared with patients without genital lesions. In addition, numerous patients with psoriasis have sexual dysfunction. Between 25–40% of patients reported a decline of sexual activity since the onset of psoriasis, mainly due to diminished sexual desire, embarrassment of physical appearance and inconvenience caused by scaliness of the skin or topical therapy. Particularly in women with genital psoriasis, sexual distress is higher and sexual function is more significantly impaired compared to those without genital lesions. 4

Inverse psoriasis is often misdiagnosed for bacterial or fungal intertrigo. Intertrigo is inflammation of opposed skin folds caused by skin-on-skin friction that presents as erythematous, macerated (moist, broken, soft skin) plaques. Secondary bacterial and fungal infections are common because the moist, denuded skin provides an ideal environment for growth of microorganisms. Candida is the most common fungal organism associated with intertrigo. Intertriginous candidiasis also presents as well demarcated, erythematous patches but with tell tale satellite papules or pustules at the periphery (around the edges). Candida, Staphylococcus aureus and Malassezia furfur have been shown to colonize psoriatic skin lesions so diagnosis for flexural psoriasis is sometimes not easy. Candida species have been isolated from the skin of 15% of psoriasis patients compared to only 4% in the control group. 5, 6 However, some studies have also suggested that Candida is not commonly found in psoriatic lesions of inverse of genital psoriasis.

Application of topical treatment in the intertriginous areas is considered as treatment under occlusion due to enhanced hydration and increased skin absorption. However, the inverse areas are considered more sensitive and prone to side effects from topical steroids (i.e. due to thinner skin at these locations). 2

 

REFERENCES

  1. Syed Z. U. and Khachemoune A.; Inverse Psoriasis Case Presentation and Review; Am J Clin Dermatol 2011; 12 (2): 1-4 1175-0561/11/0002-0001/$49.95/0
  2. Silje Haukali Omland  and Robert Gniadecki; Psoriasis inversa: A separate identity or a variant of psoriasis vulgaris?; Clinics in Dermatology (2015) 33, 456–461
  3. Meeuwi  K.A.P. et al.; Genital Psoriasis: A Systematic Literature Review on this Hidden Skin Disease;  Acta Derm Venereol 2011; 91: 5–11
  4. Meeuwis KAP, et al.; Genital Psoriasis Awareness Program: Physical and Psychological Care for Patients with Genital Psoriasis. Acta Derm Venereol. 2015, 95, 211–216
  5. Wilmer E.N. et al.; Resistant “Candidal Intertrigo” ”: Could Inverse Psoriasis Be the True Culprit?; doi: 10.3122/jabfm.2013.02.120210
  6. Taheri Sarvtin, et al.;. Evaluation of candidal colonization and specific humoral responses against Candida albicans in patients with psoriasis. International Journal of Dermatology. Dec2014,Vol.53Issue12, pe555-e560. 6p.

Psoriasis and Fatigue

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Fatigue is a common and often disabling symptom that occurs in patients with chronic inflammatory and autoimmune diseases, cancer, neurological diseases and a number of other conditions in which inflammation and/or cellular stress occurs. Fatigue may be defined as ‘an overwhelming sense of exhaustion, tiredness, languidness, languor, lassitude, and listlessness. It is a subjective feeling which is distinct from weakness, and has a gradual onset.  Fatigue can be Acute and/or Chronic (ongoing state of tiredness), that leads to mental or physical exhaustion, or both, and prevents people from functioning within normal boundaries.

There is emerging evidence that points to the innate immune system as an important ‘fatigue generator’, brought on by invading pathogens, autoimmune diseases, cancer or other ‘danger-signals’, as well as cellular stress responses. Many dermatological diseases and conditions demonstrate inflammatory or autoimmune features, suggesting that fatigue can be a common symptom in a number of chronic skin diseases. Also, psoriasis shares common pathways of immune signalling with other inflammatory diseases including psoriatic arthritis and rheumatoid arthritis (RA).1

The reduction of productivity and work capacity caused by fatigue has been studied by industrial psychologists. In these studies, the importance of physical or mental motivational factors has been clearly demonstrated. Real muscular weakness, however, cannot be detected in most individuals who complain about fatigue. The individual affected by fatigue is often unable to handle complex mental problems and tends to be less reasonable. Inferiority complexes may surface. In neurologic and psychiatric departments, anxiety and depression are frequently diagnosed in fatigued patients. 2

In one study stressed psoriasis patients, responding to a comprehensive series of questionnaires had the following physical and psychological symptoms: constant sensation of exhaustion (78.54%); memory problems (72.54%); constant fatigue (70.58%). In another study constant and excessive fatigue and the inability to work occurred in 56.86% (F) and 43.13% (M) of respondents. 3

In one clinical study researchers wanted to determine the relationship between fatigue and disease-related and psychosocial variables in psoriatic arthritis (PsA). They interviewed 499 patients attending the University of Toronto PsA Clinic using a modified fatigue severity scale (mFSS) questionnaire.  Results showed that moderate fatigue occurred in 49.5% of PsA patients and severe fatigue in 28.7%. 4

In another clinical study in plaque psoriasis patients, researchers found nearly 50% of psoriasis patients suffered from substantial fatigue. The fatigue severity was also associated with smoking, pain, and depression, but not with psoriasis severity. 5

Because fatigue is a perceived phenomenon, researchers and clinicians rely on subjective measures to indicate the patients’ level of fatigue and impact on their quality of life. It gives an overall picture of the patient and where they are at and plays a roll in determining the need for intervention or effectiveness of treatment. The 9-item Fatigue Severity Scale (FSS) is one of the most commonly used self-report questionnaires to measure fatigue. 6

The FSS questionnaire contains nine statements that attempt to explore severity of fatigue symptoms. Read each statement and circle a number from 1 to 7, depending on how appropriate they felt the statement applied to them over the preceding week. A low value indicates that the statement is not very appropriate whereas a high value indicates agreement (1 disagree to 7 agree).

FSS Questionnaire 7

During the past week, I have found that: Score
  1. My motivation is lower when I am fatigued.
1 2 3 4 5 6 7
  1. Exercise brings on my fatigue.
1 2 3 4 5 6 7
  1. I am easily fatigued.
1 2 3 4 5 6 7
  1. Fatigue interferes with my physical functioning.
1 2 3 4 5 6 7
  1. Fatigue causes frequent problems for me.
1 2 3 4 5 6 7
  1. My fatigue prevents sustained physical functioning.
1 2 3 4 5 6 7
  1. Fatigue interferes with carrying out certain duties and responsibilities
1 2 3 4 5 6 7
  1. Fatigue is among my three most disabling symptoms.
1 2 3 4 5 6 7
  1. Fatigue interferes with my work, family, or social life.
1 2 3 4 5 6 7

Circle closest to how you feel – (1 disagree, 7 agree).

FSS Scoring: Add up the circled numbers and divide by 9. ________

A Fatigue Severity Scale (FSS) score of 4 – defined as the patient is suffering from “Fatigue” and >?5.1 as suffering from “Severe Fatigue”.

Compare results with the following scores:

  • People who do not experience fatigue score about 2.8
  • People with Lupus score about 4.6
  • People with Lyme Disease score about 4.8
  • People with fatigue related to Multiple Sclerosis score about 5.1
  • People with Chronic Fatigue Syndrome score about 6.1

NOTE: The FSS might have difficulties distinguishing fatigue from depression (the influence of pain may influence scores on the FSS).

For those that have scored 5 or more it is seriously recommended that you see your practitioner and discuss the possibility as to whether you may also be suffering from depression.

References:

  • Skoie I.M. et al.; Fatigue in psoriasis: a phenomenon to be explored; British Journal of Dermatology (2015) 172, pp1196–1203
  • Carneiro C. et al.;  Fatigue in Psoriasis With Arthritis; SKINmed. 2011;9:34–37
  • Leovigildo E. S. et al.; Stress level of people with psoriasis at a public hospital; An Bras Dermatol. 2016;91(4):446-54.
  • Husted JA, Tom BD, Schentag CT, et al.; Occurrence and correlates of fatigue in psoriatic arthritis Annals of the Rheumatic Diseases 2009;68:1553-1558.
  • Skoie I.M. et al.; Fatigue in psoriasis – a controlled study; British Journal of Dermatology; 2017; DOI: 10.1111/bjd.15375
  • Valko PO, Bassetti CL, Bloch KE, Held U, Baumann CR. Validation of the Fatigue Severity Scale in a Swiss Cohort. Sleep. 2008;31(11):1601-1607.
  • Krupp LB, et al The Fatigue Severity Scale. Application to patients with multiple sclerosis and systemic lupus erythematosus. Arch Neurol 1989; 46:1121– 3.

PSORIASIS – Kidney Disease

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The patient with psoriasis has an increased risk of developing one or more of a number of other diseases/conditions that share many immunological features with psoriasis.

CHART 1: Comorbidities Associated with Psoriasis

    Renal Disease

 

    Chronic Kidney Disease

1, 2, 3

Numerous case reports have described the coexistence of psoriasis and kidney disease (Glomerulonephritis – acute inflammation of the glomeruli, which are structures in the kidneys that are made up of tiny blood vessels). Various types of kidney disease have been discussed in case studies and clinical research papers, including:-

  1. IgA nephropathy

    Berger’s disease, is a kidney disease that occurs when an antibody called immunoglobulin A (IgA) lodges in the kidneys causing inflammation.

  1. Focal segmental glomerulosclerosis

    a rare disease that attacks the kidney’s filtering units (glomeruli) causing serious scarring which leads to permanent kidney damage and even failure.

  1. Membranous nephropathy

    thickening of a part of the glomerular basement membrane.The glomerular basement membrane is a part of the kidneys that helps filter waste and extra fluid from the blood, and

  1. Proteinuria

    the presence of excess proteins in the urine.

  1. Urinary albumin excretion (UAE)

    the presence of excess albumin in the urine.

The exact causative relationship between Psoriasis and kidney disease is unknown; however, over several decades the incidence of the disease occurring in psoriasis patients has been well documented and researched. It has been suggested that given the strong relationship of the metabolic syndrome with psoriasis and kidney disease, it is perhaps not surprising that these diseases may coexist within a psoriasis sufferer.  Some mechanisms that have been put forward include immunologic mechanisms such as defects in T cell function as well as increased levels of immune complexes that underlie glomerular injury in psoriasis and tubular injury induced by raised uric acid concentrations in people with psoriasis. When the mechanisms that cause the systemic and kidney/renal disorders are analyzed, the systemic inflammatory process appears to play a fundamental role.1

Immunoglobulin A Nephropathy (IgAN)  – is the most common type of glomerular disease in psoriasis patients presenting with hematuria (presence of blood in the urine), a variable degree of proteinuria and occasionally also with a decreased glomerular filtration rate. Several cases of IgAN-accompanied psoriasis have been described in the literature. In one case study of a psoriasis patient with IgAN, the researchers found that the diffuse mesangioproliferative glomerulonephritis was accompanied by vascular nephrosclerosis (hardening of the small blood vessels in the kidneys) and tubulointerstitial nephritis (swelling caused by tubulointerstitial injury) with diffuse fibrosis and tubular atrophy. 2

IgAN is sometimes present in association with seronegative spondyloarthropathies, including psoriatic arthritis. All of the seronegative spondyloarthropathies are associated with mucosal or skin inflammation, which may lead to an increased production of IgA and elevated serum IgA levels. One clinical study found that 14 patients (67%) from a group of 21 patients had evidence of IgA-containing circulating immune complexes at some time in the course of their psoriasis. 2

In a large population based cohort study the risk of moderate to advanced kidney disease in patients with psoriasis was extensively studied. Some 136,529 patients with mild psoriasis and 7354 patients with severe psoriasis based on treatment patterns were compared with 689,702 healthy patients. The researchers reported that “The combined results indicated that, although no association is seen in patients with truly mild disease (less than 2% body surface area affected), as consistent with other previous studies, associations were seen in moderate and severe psoriasis, which are estimated to affect over 20% of patients with psoriasis worldwide. The relative risk of chronic kidney disease was especially increased in younger patients, however, the clinical relevance of the absolute risk of chronic kidney disease attributable to psoriasis increases with age. In patients aged 40-50 with severe disease based on treatment patterns, psoriasis accounts for one extra case of chronic kidney disease per 134 patients per year, and in those aged 50-60, it accounts for one additional case per 62 patients per year.” 3

Urinary albumin excretion (UAE) (Microalbuminuria) is considered to be a marker of glomerular damage and can be used to predict diabetic or hypertensive nephropathy. Early detection of glomerular damage, when it is minimal and/or at a reversible stage is extremely important. Studies performed in patients with psoriasis have found increased UAE in psoriatics compared with healthy controls. Study results have also revealed a significant correlation between UAE and PASI scores (severity of lesions). 4

The researchers strongly recommended that “Closer monitoring for renal insufficiency should be considered for patients with moderate to severe psoriasis (those with 3% or more body surface area affected), and nephrotoxic drugs should be used with caution in this at risk population. 3

Commonly-used drugs which can affect renal function

  • Diuretics
  • Beta blockers Acebutolol (Sectral), Atenolol (Tenormin); Bisoprolol (Zebeta)
  • Vasodilatorshydralazine (Apresoline) and minoxidil (Loniten)
  • ACE inhibitorsincluding Capoten (captopril), Vasotec (enalapril), Prinivil, Zestril (lisinopril), Lotensin (benazepril), Monopril (fosinopril), Altace (ramipril), Accupril (quinapril), Aceon (perindopril),  Mavik  (trandolapril), Univasc (moexipril)
  • Aminoglycosides including gentamicin, tobramycin, amikacin, streptomycin, neomycin, and paromomycin 
  • Contrast Dye used in some diagnostic tests such as MRIs.
  • Compound analgesics NSAIDs (e.g. aspirin, ibuprofen, diclofenac. paracetamol)
  • Antiviral agentsincluding acyclovir (brand name Zovirax)
  • Lithium
  • Antibiotics including ciprofloxacin, methicillin, vancomycin, sulfonamides.
  • Chemotherapy drugsincluding interferons, pamidronate, cisplatin, carboplatin, cyclosporine, tacrolimus, quinine, mitomycin C, bevacizumab; etanercept, methotrexate and anti-thyroid drugs, including propylthiouracil, used to treat overactive thyroid.

Signs and symptoms of chronic kidney disease include:

  • high blood pressure
  • changes in the amount and number of times urine is passed
  • changes in the appearance of your urine (e.g. colour is extremely dark, frothy or foaming urine)
  • blood in your urine
  • puffiness in your legs, ankles or around your eyes
  • pain in your kidney area
  • tiredness
  • loss of appetite
  • difficulty sleeping
  • headaches
  • lack of concentration
  • itching
  • shortness of breath
  • nausea and vomiting
  • bad breath and a metallic taste in your mouth
  • muscle cramps
  • pins and needles in your fingers or toes.

As you can see these symptoms are very general and may be caused by other illnesses, however, it is extremely important to seek medical advice if you know that you may be susceptible to kidney disease (i.e. runs in the family) or you know that you are taking medication that could cause kidney disease.

References:

  • Wan, Joy et al. “Risk of Moderate to Advanced Kidney Disease in Patients with Psoriasis: Population Based Cohort Study.”The BMJ 347 (2013): f5961. PMC. Web. 22 Mar. 2017.
  • Zadražil et al.; IgA nephropathy associated with psoriasis vulgaris: a contribution to the entity of “psoriatic nephropathy”; J NEPHROL 2006; 19:382-386
  • Wan J. et al.; Risk of moderate to advanced kidney disease in patients with psoriasis: population based cohort study; 2013; 347: f5961., Published online 2013 Oct 15. doi:  10.1136/bmj.f5961; PMCID: PMC3805477
  • Dervisoglu E. et al.; The spectrum of renal abnormalities in patients with psoriasis; Int Urol Nephrol; DOI 10.1007/s11255-011-9966-1

PSORIASIS AND COMORBIDITIES – Psychological and Psychiatric Disorders – PART 3

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The last in our 3 part series addressing psychological and psychiatric disorders associated with psoriasis.

   Psychological and Psychiatric Disorders –

   Sleep Disorders

   Somatoform Disorders

   Substance dependence of abuse

1, 2, 3

Sleep Disorders

It is thought that psoriasis has a direct effect on the development of sleep disorders due to the cutaneous (skin) symptoms of the condition. The skin is the primary circadian mediator of core body temperature (CBT), and a decrease in CBT in the late evening is an important mechanism for sleep initiation. Psoriasis has been associated with problems with thermoregulation and researchers have indicated that the reduced ability to dissipate heat is one factor in the inability to initiate sleep. Pruritus (itch) is another contributor to sleep disturbance and it is also regulated by circadian mechanisms. The threshold for pruritus is lowered in the evening due to complex circadian-mediated factors such as lower cortisol levels, decreased epidermal barrier function, and increased distal-to-proximal (distant limbs-to-body centre) gradient in skin temperature. Thus pruritus in psoriasis typically manifests or exacerbates mainly in the evening and worsens at night. 4,5,6

 so-tired-1440121-1600x1200

The inflammatory biological mechanism(s) that lead to initiation and exacerbation of psoriasis, also contribute to the development of systemic diseases e.g. depressive disease, hypertension (blood pressure), adverse cardiac events, diabetes, metabolic syndrome and obesity. All of these conditions are known to indirectly give rise to sleep-disordered breathing. The heightened pro-inflammatory state in conditions such as obstructive sleep apnoea syndrome (OSAS) and insomnia could in turn lead to exacerbations of psoriasis.4,5,6

A systematic review of the literature on the relationship between psoriasis, PsA, and formal sleep disorders identified an increased prevalence of OSAS with a 36-81% prevalence in psoriasis versus 2% for women and 4% for men in the general population.4,5  In one study researchers found that some patients with chronic psoriasis and concurrent OSAS showed improvement of their psoriatic lesions while on nasal continuous positive airway pressure (CPAP).6 OSAS leads to severe physical and, possibly, psychological stress to the body, e.g., by hypoxemia (low blood oxygen levels), increased blood pressure, tachycardia (fast or irregular heart rate), sleep fragmentation, reduction of deep sleep, reduction of REM sleep, hypersomnia (excessive sleepiness), and insomnia. It is known that OSAS also dysregulates the function of the patient’s autonomic nervous system and hormone system. It is felt that this might alter the homeostasis of the immune neuroendocrine network in the skin and may cause the initiation of psoriasis in the genetically predisposed individuals.4,5,6

Somatoform Disorders – psychosomatic symptoms

Somatization is the manifestation of psychological distress by the presentation of bodily symptoms such as feeling nausea due to anxiety, stress headaches, falling ill after a trauma and inability to cope with a disease. 

Patients with psoriasis exhibit higher scores of hypochondriasis, hysteria, and somatization. As previously exposed hypochondriasis and hysteria may be connected with specific personality traits of patients with psoriasis of late-onset. Psychosomatic factors, namely stressful life events, lack of social support, and attachment insecurity, may explain why patients with psoriasis have greater scores of somatization. Moreover, the presence of depression in psoriasis may modulate itch perception and then exacerbate symptoms of pruritus.7 (Refer to Part 1 of this series) A systematic review of the psychosocial burden of psoriasis found that social stigmatization, high stress levels, physical limitations, depression, employment problems and other psychosocial co-morbidities experienced by patients with psoriasis are not always proportional to, or predicted by, other measurements of disease severity such as body surface area involvement or plaque severity. Some psoriasis patients had, even when their lesions were small and mild, levels of stress and loss of confidence that was not in keeping with the severity of their condition – which leads to the conclusion that they had maladaptive coping mechanisms in play e.g. self blame, blaming parents, social phobia, avoidance behaviours, substance and alcohol abuse etc. 9

Substance – Dependence of Abuse

In our previous blog Psoriasis and Alcohol (ethanol), we stated that patients with psoriasis experience considerable emotional distress, depression and social isolation due to the visibility of skin lesions, especially when the lesions are widespread and severe. Whilst it would be demeaning to state that all psoriasis patients with mild to severe psoriasis suffer from alcoholism, it has been confirmed in several Quality of Life studies that the percentage of psoriasis patients who admit to having a drinking problem may be as high as 32%. Research indicates that men are more likely to use alcohol excessively as a coping mechanism with the psychosocial burden of psoriasis. Consequently they are at a higher risk of developing depression – with the alcohol misuse and psoriasis as underlying causes. 4 Another study indicated that for women, excessive alcohol intake above a certain threshold (?30.0 g/d), may be associated with a significantly increased risk of Psoriatic Arthritis (PsA).5

have-a-drink-1-1510449-640x480-1

Alcohol is known to inhibit inflammation and immune responses; however acute and chronic alcohol consumption have opposite effects on inflammatory cell activation. Results indicate that acute alcohol exposure is inhibitory, whereas chronic alcohol exposure leads to an increase in inflammatory cell responses.6

Research has confirmed that alcoholics are more susceptible to infections, as streptococcal infections are trigger factors for psoriasis, this increased susceptibility may be involved in the onset and progress of the disease. It is also known that measurable quantities of ingested ethanol are secreted through human skin. Transdermal ethanol derives from two processes: active secretion by eccrine glands, primarily sweat glands, and passive diffusion through the lipid layers of the skin. Ethanol disrupts the dermal barrier enhancing skin permeability for numerous chemicals and increases the solubility of penetrating chemical compounds.6

Research into the the use of illicit drugs and psoriasis is extremely limited. Methylenedioxymethamphetamine (MDMA), also called Ecstasy, has been reported to initiate Guttate Psoriasis. The researchers theorized that “While MDMA [the main ingredient in ecstasy] is taken for its psychomimetic effect, pharmacologically it increases the level of noradrenaline, serotonin and dopamine by inhibiting the reuptake mechanism. It is known that Patients with psoriasis already have increased levels of noradrenaline.”7 There are also anecdotal stories on support websites where psoriasis sufferers have spoken about the exacerbation of their psoriasis with the use of “meth” (Methamphetamine, Ice). Within our clinic we have had several patients whose psoriasis was initiated and exacerbated by the use of cannabis (street not medicinal), once they ceased the use of cannabis their psoriasis resolved. As long as they did not use cannabis they remained free of any psoriatic lesions.

REFERENCES

  • Susskind W. and McGuire R.J.: The Emotional Factor in Psoriasis; Scot. med, J., 1959,4:503
  • Kessler R. C. et al.; Epidemiology of Anxiety Disorders; M.B. Stein and T. Steckler (eds.), Behavioral Neurobiology of Anxiety and Its Treatment, Current Topics in Behavioral Neurosciences 2, DOI 10.1007/7854_2009_9, # Springer?Verlag Berlin Heidelberg 2009, published online 3 September 2009
  • Nasreen S. et al.; Frequency and Magnitude of Anxiety and Depression in Patients with Psoriasis Vulgaris; Journal of the College of Physicians and Surgeons Pakistan 2008, Vol. 18 (7): 397-400
  • Brenaut E. et al.; Alcohol consumption and psoriasis: a systematic literature review. J Eur Acad Dermatol Venerol. 2013 Aug;27 Suppl 3:30-5. doi: 10.1111/jdv.12164.
  • Shaowei Wu et al.; Alcohol Intake and Risk of Incident Psoriatic Arthritis in Women; J Rheumatol. 2015 May ; 42(5): 835–840. doi:10.3899/jrheum.140808.
  • Farkas A, Kemény L.; Psoriasis and alcohol: is cutaneous ethanol one of the missing links?; • British Journal of Dermatology 2010 162, pp711–716
  • Tan B., Foley P.; Guttate psoriasis following Ecstasy ingestion; Australasian Journal of Dermatology45(3):167-9 September 2004?

PSORIASIS AND COMORBIDITIES – Psychological and Psychiatric Disorders – PART 2

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WHAT IS COMORBIDITY?

Comorbidity is a concurrence of multiple diseases or disorders in association with a given disease, in this case, psoriasis.

 INCREASED RISK

 The patient with psoriasis has an increased risk of developing one or more of a number of other diseases/conditions that share many immunological features with psoriasis.

 CHART 1: Comorbidities Associated with Psoriasis

    Psychological and Psychiatric Disorders –  

   Personality Traits and Personality Disorders

   Schizophrenia and other psychoses

   Sexual Dysfunction

1, 2, 3

Personality Traits and Personality Disorders

It has also been proposed by a number of researchers that patients with skin disease usually present with certain psychological traits that makes them vulnerable to stress. Although a specific personality structure for psoriasis patients has not yet been defined, psoriasis patients are reported to have more obsessive compulsive, avoidant, schizoid and passive-aggressive properties than healthy controls, however the research surrounding personality and psoriasis is still controversial. 4

The term personality represents the different behavioural styles that individuals present in their habitual habitats or environments.4 In one study of male psoriasis patients and a control group the psoriasis group scored significantly higher scores than the control group in Extravagance (NS3), Disorderliness (NS4), Novelty Seeking (NS), Anticipatory Worry (HA1), Shyness with Strangers (HA3), Fatigability and asthenia – weakness – lack of energy and strength (HA4), Harm Avoidance (HA), Dependence (RD3), Reward Dependence (RD), Self-forgetfulness (ST1), Transpersonal Identification (ST2), Spiritual Acceptance (ST3) and Self-Transcendence – the ability to focus attention on doing something for the sake of others (ST).5

Another study found that the severity of pruritus (itch) and the severity of psoriasis was associated with significantly higher scores for depression and anxiety, and showed the personality traits of somatic anxiety (physical reactions to anxiety e.g. sweating, nausea etc.), embitterment, mistrust, and physical trait aggressiveness. However, the researchers also found that the severity of itch was not associated with the severity of psoriasis from a PASI score perspective. In fact they found that there was a higher severity of itch reported in 30% of psoriasis patients in which the greater majority of these had very few lesions.6

Psoriasis Patients often report felt or perceived stigma, referring to the negative attitudes and responses that they perceive to be present in society and the sense of shame and fear of being discriminated against because of being ‘flawed’ due to the physical appearance of their lesions. The actual experiences of stigmatization range from –  people showing disgust or aversion, making negative comments or totally avoiding contact.6

Stigmatization contributes considerably to disability, depression and reduced quality of life in psoriasis patients, and can be considered a stressor. As distress can be a trigger for psoriasis exacerbation, this can become a vicious self-perpetuating cycle. The Type D personality has previously been associated with increased risk of cardiovascular morbidity and mortality and impaired health behaviour e.g. smoking and alcohol dependence, which are both frequently reported in psoriasis. The two main features – SI (social inhibition) and NA (negative affectivity) – may both increase the impact of perceived stigmatization. SI refers to conscious or subconscious avoidance of a situation or social interaction because of the possibility of others disapproving of their feelings or expressions.  Whilst NA refers to negative emotions, including anger, contempt, disgust, guilt, and fear, and nervousness. Furthermore, individuals with high levels of NA may be more likely to perceive social interactions as negative, due to the associated cognitive bias to negative feedback. In one study researchers found that perceived stigmatization was particularly predicted by disease impact, as well as by lower age, lower education, greater disease severity and visibility, longer disease duration, higher levels of SI, having a type D personality and being single. 6

The researchers concluded that it seems likely that patients with psoriasis who are prone to feelings of helplessness regarding the disease may also experience a larger impact of psoriasis and magnify negative reactions of others. Type D personality and its subcomponent SI were found to be significant predictors of perceived stigmatization. The fear of disapproval that leads individuals to inhibit emotions or behaviour in SI may explain its relation to perceived stigmatization. They stated that socially inhibited individuals may be more sensitive to the reactions of others and may therefore perceive themselves to be stigmatized more readily. They found that not only was SI in itself, but also the combination of higher levels of SI and NA (type D personality) was a significant predictor of perceived stigmatization, which  corresponded with previous studies that suggested that type D was associated with social impairments. 6

It was suggested that Practitioners should screen for feelings of Stigmatization and related problems, and implement with the patient, targeted interventions that may focus on the impact of the condition on daily life, considering that this was the largest predictor. Therapy, such as Cognitive Behavioural Treatment, which should include social skills training, has shown promise as an intervention treatment. Previous research indicates that it can decrease perceived stigmatization in skin conditions, improve psychological and disease-related outcomes in psoriasis patients, and decrease feelings of helplessness, which shows high correlations with disease severity and impact. 6

It is extremely important that psoriasis sufferers do not cut themselves off from social interactions and it is highly recommended that they join a support group that is not only internet based but one that meets socially on a face to face basis. 

frustrated

Schizophrenia and other psychoses

 The psychiatric morbidity in psoriasis is considered an important indicator of the disability experienced by the patient than the dermatologic aspects of the disorder, sometimes more so than the physical aspect of the lesions. Some studies have found a possible connection between psoriasis and psychosis, including schizophrenia. Schizophrenia is a polygenic (involvement of 2 or more genes), multifactorial disorder and recent neuroanatomical and neurobiological being related to the nervous system as well as environmental and genetic studies have suggested that inflammatory pathways are also involved in its pathogenesis. Because psoriasis is also considered a state of chronic systemic inflammation involving several genes and is a related immune processes might explain the link between psoriasis and its comorbidities.7

In a systematic review researchers reviewed the published clinical papers on the link between psoriasis and Schizophrenia and other psychoses. The results of the systematic review found that there is some evidence of a relationship between schizophrenia and/or disorders with psychotic features and psoriasis. In one case-controlled study the authors concluded that schizophrenic patients have a higher probability of having a diagnosis of psoriasis whilst other studies highlighted that psoriasis patients have a higher risk of having schizophrenic traits. The main characteristics of schizoid character are social isolation, intimacy avoidance and restricted affections. Although for a long time was considered that a schizoid character was related to schizophrenia, this has been found to be not always true. Nevertheless, schizoids may be more susceptible to psychosis. This personality shares with schizophrenia, although with its own subtleties, the problem of the distinction between the “self” and the “other”. Several studies have reported on the occurrence of psoriasis in schizophrenia patients being treated with cyclosporine A and olanzapine. And other schizophrenia patients with existing psoriasis found that treatment with haloperidol and levomepromazine actually also improved the patients psoriasis.7

 For some psoriasis patients it was found that whilst they were experiencing a worsening of their skin lesions their existing psychotic condition also worsened, and as their skin improved so too did their psychotic condition.7 The hypothesis is that psoriasis, schizophrenia and other psychotic conditions share similar pathways.

Sexual Dysfunction

Sexual health is an important part of general health and sexual dysfunctions can negatively affect self-esteem, confidence and interpersonal relationships. The impact of psoriasis upon sexual function seems to be substantial and it has a significant impact in quality of life. One study found that when compared to a control group, the psoriasis group showed significant impairment of all the components of sexual function: sexual interest, sexual arousal, orgasm, erection and sexual satisfaction. “Sexual interest” and “global sexual satisfaction” were the most negatively affected components. Male patients with psoriasis showed an increase in erectile dysfunction compared to controls. The prevalence of sexual dysfunction was 53.7% in patients with psoriasis vs. 17.5% in the healthy control group. The researchers also found that psoriasis lesions on the genitals, buttocks, abdomen or lumbar (back) region were significantly linked to sexual dysfunction and those psoriasis patients with sexual dysfunction had higher scores for depression (32.5%) and anxiety (50%). 9

Certain components of sexual response, such as sexual interest, depend primarily on psychological factors, and are impaired by conditions such as anxiety and depression, while others such as erection and orgasm can be affected by psychological and physical causes.

It has also been suggested that the sexual dysfunctions might not be as a direct result of depression, but rather of low self-esteem or other emotional problems. As sexual impairment in psoriasis patients was seen to occur in all components of the sexual response, the researchers concluded that this suggested that sexual dysfunction in psoriasis must be a consequence of several combined factors.9,10

If you have a concern about depression, bipolar, schizophrenia or sexual dysfunction please discuss your concerns with your General Practitioner.

Read also PSORIASIS AND COMORBIDITIES – Psychological and Psychiatric Disorders – Part 1

REFERENCES

  • Susskind W. and McGuire R.J.: The Emotional Factor in Psoriasis; Scot. med, J., 1959,4:503
  • Kessler R. C. et al.; Epidemiology of Anxiety Disorders; M.B. Stein and T. Steckler (eds.), Behavioral Neurobiology of Anxiety and Its Treatment, Current Topics in Behavioral Neurosciences 2, DOI 10.1007/7854_2009_9, # Springer?Verlag Berlin Heidelberg 2009, published online 3 September 2009
  • Nasreen S. et al.; Frequency and Magnitude of Anxiety and Depression in Patients with Psoriasis Vulgaris; Journal of the College of Physicians and Surgeons Pakistan 2008, Vol. 18 (7): 397-400
  • Martín-Brufau R. et al.; Personality in Patients with Psoriasis; Chapter 11 rfrom the book Psoriasis Downloaded from: http://www.intechopen.com/books/psoriasis
  • Ak M. et al.; Temperament and character properties of male psoriasis patients; Journal of Health Psychology; pg 1-8; 2011; DOI: 10.1177/1359105311423863
  • Remröd ;  Pruritus in Psoriasis: A Study of Personality Traits, Depression and Anxiety; Acta Derm Venereol 2015; 95: 439–443;
  • Ferreira BR, Pio Abreu JL and Figueiredo A.; Psoriasis, Schizophrenia and Disorders with Psychotic Features: Are They Linked?; J Schizophr Res. 2015;2(1): 1006.
  • Molina-Leyva A. et al.; Distribution pattern of psoriasis, anxiety and depression as possible causes of sexual dysfunction in patients with moderate to severe psoriasis; An Bras Dermatol. 2015;90(3):338-45
  • Sarbu, Maria Isabela; Tampa, Mircea; Sarbu, Alexandra Elenda; and Georgescu, Simona Roxana (2014) “Sexual Dysfunctions in Psoriatic Patients,” Journal of Mind and Medical Sciences: Vol. 1: Iss. 1, Article 5.

PSORIASIS and COMORBIDITIES – PSORIATIC ARTHRITIS

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WHAT IS COMORBIDITY?

 Comorbidity is a concurrence of multiple diseases or disorders in association with a given disease, in this case, psoriasis.

 INCREASED RISK

 The patient with psoriasis has an increased risk of developing one or more of a number of other diseases/conditions that share many immunological features with psoriasis.

Psoriatic Arthritis

Spondyloarthropathies

CHART 1: Comorbidities Associated with Psoriasis 1,2,3

Psoriatic arthritis (PsA) is an inflammatory arthropathy, which is associated with psoriasis in approximately 25% of patients. It is characterized by stiffness, pain, swelling, and tenderness of the joints as well as the surrounding ligaments and tendons. It affects men and women equally and typically presents at the age of 30 to 50 years. Skin lesions usually precedes the onset of PsA by an average of 10 years in the majority of patients but 14– 21% of patients with PsA develop symptoms of arthritis prior to the development of skin lesions.4

human_hand_bones-en The Foot

                  The Hand                                                                                             The Foot

The presentation of PsA is variable and can range from a mild, non-destructive arthritis to a severe, debilitating, erosive arthropathy.

There are various classifications for PsA:-

• Monoarthritis of the large joints – inflammation and arthritis in one joint.

PsN 1 Finger

          Swelling evident in the joint between the Intermediate and Proximal Phalanges in the index finger

  • Distal interphalangeal arthritis – affecting the joint between the Distal and Proximal phalanges.
  • Spondyloarthritis – affecting the spine and, in some people, the joints of the arms and legs.

Symmetrical deforming polyarthropathy – similar to that of rheumatoid arthritis

PsN all Distal Joints

Deformity of the Distal interphalangeal joints with varying degrees of severity seen across all of the fingers from severe to mild.

If PsA is left untreated, a percentage of patients may develop chronic inflammation with progressive deforming joint damage which leads to severe physical limitations and disability. So it is very important for a patient with psoriasis who is experiencing joint swelling or pain to be reviewed by a Rheumatologist as soon as possible. However, as there is no specific test for PsA, the diagnosis of PsA is based on clinical judgement. The main aspect is the absence of rheumatoid factor (91-94%), this key finding together with the specific presentation of joint pain and inflammation plus the presence of psoriasis skin lesions all combine to lead the Practitioner and the Rheumatologist to diagnose PsA. X-rays may aid diagnosis and can show the extent and location of joint damage. Other types of scans such as MRI or CT scans can also be used to look at the joints in more detail.

In many patients articular patterns change or overlap in time. Enthesitis, inflammation at the sites where tendons or ligaments insert into the bone, may occur at any site, but more commonly at the insertion sites of the plantar fascia (the fibrous band of tissue (fascia) connecting the heel bone to the base of the toe bones), the Achilles tendons, and ligamentous attachments to the ribs, spine, and pelvis. PsA is unusual in that it can affect joints on only one finger or toe, several joint on one side or on affect joints on both sides of the body. PsA symptoms often resemble those of rheumatoid arthritis. Both diseases cause the joints to become inflammed, painful, swollen and warm to the touch.4

The most common symptoms are:-

  • Swollen fingers and/or toes.  PsA can cause a painful, sausage-like swelling of the fingers and/or toes. Swelling and deformities in the hands and feet before having significant joint symptoms may occur.

  • Foot pain. Psoriatic arthritis can also cause pain at the points where tendons and ligaments attach to the bones — especially at the back of the heel or in the sole of the foot.
  • Lower back pain.Some sufferers develop a condition called spondylitis as a result of PsA which causes inflammation of the joints between the vertebrae of the spine and in the joints between your spine and pelvis (sacroiliitis).

Skin lesions in patients with PsA and psoriasis may vary from a mild to a severe presentation and the skin activity is commonly not indicative of the severity of the arthritis symptoms. It is important to note that skin lesions and symptoms normally precede arthritic signs and symptoms in 80% of psoriatic arthritis patients. Whilst simultaneous onset of arthritic and psoriatic symptoms will occur in approximately 13% of patients, only 3% of patients will have joint involvement preceding the development of skin lesions.5

People with PsA often experience pain, stiff joints and muscle weakness and often this is due to lack of use so a regime of light exercise is very important to improve overall health and to keep the joints as flexible as possible. It may be of benefit for people with PsA to consult with an exercise physiologist / remedial therapist who can give advice as the most suitable exercises that are patient specific, including how to get started safely, so that the potential to aggravate the joints are kept to a minimum.

Some of the types of exercise that should be discussed with your physiologist / therapist are:-

  • Aerobic exercises – walking, swimming or gentle water aerobics
  • Muscle-strengthening exercises – light weights
  • Muscle-stretching exercises
  • Hydrotherapy – supervised structured exercises of specific extremities and joints in warm water.

Use of Assistive Devices

An assistive device is a tool or implement that makes a particular function or action easier or possible to perform, e.g.:-

Clothing Aids

  • Velcro on clothes and shoes or elastic shoelaces.
  • Button and zipper hooks.
  • Leg-Up Leg Lifter allows users with limited mobility to avoid having to bend down or hold onto clothing to lift their leg.
  • Long handled shoe horns.

Grooming Aides

  • Fit Combs, brushes and toothbrushes with easier-to-hold handles for ease of use.
  • Or use Long handled brushes and combs that have anti-slip handles.
  • Use a toothpaste dispenser that automatically dispenses a set amount of toothpaste onto a brush.

Bathing and Showering Aides

  • Use a long handled hair washer that can be used to apply shampoo and massage the user’s scalp while reducing strain on the hands, shoulders, or arms.
  • Long handled foot wash brush to assist people with limited access to their feet.
  • Long handled sponge or cloth body washers.
  • Long handled lotion or ointment applicators.

Cooking and Cleaning Aides

  • Finger loop utensils.
  • Oven knob turner.
  • Cut resistance gloves and Finger protector (slicing) guard.
  • Easy glide plastic bag opener.
  • Jar “pop” openers.
  • Tin pull top openers.

Walking Aides

  • Walkers, canes, knee and ankle braces.

Remember there are many websites available where you can purchase any number of assistive devices.

It is important not to lock oneself away and use immobility as an excuse not to socialize. Use group exercise classes to not only improve one’s fitness and mobility but also use the opportunity to talk to other class member’s, or join a support group ….. just the act of talking and sharing can be enough to ensure that you do not become depressed.

 

 

REFERENCES

  • Arzu K?l?ç, Seray Cakmak; PSORIASIS AND COMORBIDITIES; EMJ Dermatol. 2013;1:78-85.
  • Howa Yeung et al.;Psoriasis Severity and the Prevalence of Major Medical Comorbidity – A Population-Based Study; JAMA Dermatol. 2013;149(10):1173-1179. doi:10.1001/jamadermatol.2013.5015
  • Aurangabadkar SJ. Comorbidities in psoriasis. Indian J Dermatol Venereol Leprol 2013;79, Suppl S1:10-7
  • Lloyd P. et al.; Psoriatic Arthritis: An Update; Hindawi Publishing Corporation Arthritis Volume 2012, Article ID 176298, 6 pages doi:10.1155/2012/176298
  • Gottlieb A.B. et al.; Clinical characteristics of psoriatic arthritis and psoriasis in dermatologists’ offices; Journal of Dermatological Treatment. 2006; 17: 279–287

 

 

Christmas and the Holiday Season with Skin Conditions

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So now the Christmas and New Year holiday season is upon us and for those of you who suffer from a skin condition, this time of the year can be challenging.

We all know that the intake of alcohol can be a trigger for many skin conditions such as psoriasis, eczema, urticaria etc. It is dehydrating and dehydration impairs the skin barrier. Alcohol also has the potential to weaken one’s immune system, this makes people with skin conditions more susceptible to bacterial infections and injuries, which in turn can trigger and exacerbate their condition.

For those of you who are yeast sensitive, the intake of drinks such as beer and champagne, both of which contain yeast, most certainly will aggravate their skin condition and could cause a major flare up. Those that are gluten sensitive or suffer from Celiac disease also have to be careful with their alcohol intake as some types of liquors e.g. vodka, bourbon etc. may use a starch-source for fermentation and these starch sources e.g. barley contain gluten.

This time of the year can be emotionally challenging, if you are experiencing family or relationship difficulties, you may be experiencing considerable emotional distress, depression and even social isolation. Try to reach out to friends and support groups for support during this time. It is important that you do not isolate yourself and allow your stress levels to escalate.

If tasks such as shopping or getting the house ready cause you stress, then make sure you plan ahead and allow yourself extra time.

Food of course is a big deal at this time of the year. Catching up with friends for barbecues, lunches, dinners at restaurants or at homes is an important tradition and catch up time for all of us.

 Control on what is on the menu is often out of your hands, therefore it is important to choose your food wisely. So avoid all spicy foods or at least keep it to a minimum – if you eat spicy food at one sitting try to avoid another serve for a few days.

Avoid or at least keep to a minimum intake of tomatoes (including chutneys), smoked foods, red and processed meats. Try to select green vegetables, chicken, turkey, fish and moderate all other intake. Remember if you do have a food sensitivity, be it seafood, gluten, yeast, sugar then try to avoid it as much as possible. The golden rule is “If you ate it during one meal wait a few days before having it again”  if you can’t avoid eating it then moderation is key.

If you are eating at the home of family member or friend then don’t be afraid to tell them of your eating requirements. Most people will be only too happy to oblige by either offering an alternative that you can eat or by modifying the dishes that they are preparing.

As mentioned earlier dehydration impairs the skin barrier so drink plenty of water. It is important to try to drink between one and a half litres to two litres of water a day and critical if you are drinking alcohol.  

The most important thing is to try to enjoy your time with family and friends, don’t overdo the alcohol or food intake. Remember moderation and alternatives, drink your water, get plenty of rest. If you find yourself feeling stressed, make some time to chill out, meditate or listen to music.

 So Check List:

  • Drink water
  • Eat Greens, chicken, turkey, fish
  • Avoid tomatoes, spicy, red and processed meats, smoked foods, sugar
  • Avoid your trigger foods
  • Moderate alcohol intake 
  • Keep stress to a minimum, plan ahead & get support 

PSORIASIS and COMORBIDITIES and INFLAMMATORY BOWEL DISEASE

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WHAT IS COMORBIDITY?

 Comorbidity is a concurrence of multiple diseases or disorders in association with a given disease, in this case, psoriasis.

INCREASED RISK

The patient with psoriasis has an increased risk of developing one or more of a number of other diseases/conditions that share many immunological features with psoriasis.

CHART 1: Comorbidities Associated with Psoriasis

Inflammatory Bowel Disease (IBD) –

Crohn’s Disease

Ulcerative Colitis

Irritable Bowel Syndrome (IBS)

1, 2, 3

Gastro Intestinal (GI) disorders are present in 28% of patients with psoriasis. Common abnormalities in psoriasis patients include changes in the mucous membrane of the duodenum. Psoriasis may cause dermatogenic enteropathy and intestinal inflammation.

Irritable bowel syndrome (IBS) is one of the most common ‘functional’ gastrointestinal disorders accounting for 3% of all primary care consultations, with a strong female predominance. The main features are recurrent abdominal pain and/or discomfort, whose clear relationship to changes in stool frequency or consistency and its relief by defecation implies that they originate in the colon. In addition to these gastrointestinal (GI) symptoms, patients commonly report non-GI symptoms of lassitude, headache, backache, dysmenorrhoea (painful periods/menstruation), and dyspareunia (painful intercourse). Symptoms characteristically wax and wane. IBS patients, in common with other sufferers with functional GI disorders, are more anxious than healthy controls, showing greater anxiety and depression. Many patients believe that stress induces their symptoms.10

Inflammatory Bowel Disease (IBD) are a group of inflammatory conditions in which the body’s own immune system attacks parts of the digestive system. The two major types of IBD are ulcerative colitis (UC) and Crohn’s disease (CD). UC is limited to the colon and/or rectum (normally continuous lesions in the rectum and colon), and affects only the inner lining (mucosal and submucosal layers) of the gut. In contrast, CD can affect any part of the gut from mouth to anus as non-continuous or skip lesions (a majority of cases start in the terminal ileum), and affect the whole thickness of the bowel wall.4

stomach_etc_diagram-en-wikkip

Within the IBD group is also Microscopic Colitis, an inflammation of the colon that can only be detected with a microscope. There are two types of microscopic colitis – collagenous colitis and lymphocytic colitis. Under a microscope an increase in the number of lymphocytes, a type of white blood cell, can be seen in the epithelium—the layer of cells that lines the colon.15

The two types of colitis affect the colon tissue in slightly different ways:

  • Lymphocytic colitis – The number of lymphocytes is higher, whilst the tissues and lining of the colon are of normal thickness.
  • Collagenous colitis – The layer of collagen, a threadlike protein, underneath the epithelium builds up and becomes thicker than normal.

 The most common symptom of microscopic colitis is chronic, foul smelling, watery, non-bloody diarrhoea. Episodes of diarrhoea may last for weeks, months, or if chronic, even years, however, there may be intermittent periods without diarrhoea. During these periods the patient may even experience bouts of constipation.

Other signs and symptoms of microscopic colitis include15:-

  • A strong urgency to have a bowel movement.
  • Faecal incontinence – accidental passing of stool or fluid from the rectum – especially at night.
  • Pain, cramps, or bloating in the abdomen – that is usually mild but can be incapacitating.
  • Weight loss/gain
  • Nausea – usually without vomiting.
  • Dehydration – as a result from not drinking enough liquids to replace fluids lost through diarrhoea.
IBD SYMPTOMS IBS SYMPTOMS
Frequent and/or Urgent Bowel Movements

Diaorrhea

Bloody Stools

Abdominal Pain & Cramping

Fatigue

Weight Loss

Lack of Appetite

Joint, Skin or Eye Problems

Abdominal Pain & Cramping

Diaorrhea

Bloating

Gas

Mucus in Stools

 

As far back as 1968 studies reported a prevalence of 2-3% of psoriasis in first-degree relatives of patients with CD compared to 0–3% of controls. Later studies found psoriasis in 7–11% of the IBD population compared to 1–2% of general population. In one study, psoriasis was found to be more prevalent in CD (11.2%) than UC (5.7%). 5

In one study5 the Researchers studied the presence and characteristics of psoriasis were recorded and further classified as follows: sebopsoriasis, scalp psoriasis, plaque type psoriasis [trunk, arms], palmo-plantar psoriasis, nail psoriasis, inverse psoriasis, psoriatic arthritis, guttate psoriasis, and pustular psoriasis. Psoriasis that developed after anti-TNF? treatments was also reported. Severity of psoriasis was defined as mild, moderate or severe [not applied to psoriatic arthritis]. The study involved some 251 IBD patients, there were 158 patients with CD [63%] and 93 with UC [37%]. These 251 IBD patients were referred to the dermatologist and psoriasis was detected in 62 [25%], including 36 [58%] with CD and 26 [42%] with UC. The non-IBD group included 62 patients with psoriasis. Mild psoriasis was more frequent in IBD vs non-IBD, whereas moderate and severe psoriasis were more frequent in non-IBD vs IBD. Plaque-type psoriasis was the most common phenotype in both IBD and non-IBD. The frequency of plaque-type, nail psoriasis and psoriatic arthritis was lower in IBD vs non-IBD.

Other researchers analyzed the health records of 174,646 participants from the Nurses’ Health Study (NHS) and NHS II in an effort to also determine whether IBD was associated with specific psoriasis phenotypes. In this study they found 4,400 cases of psoriasis and of these 423 participants had developed CD or UC with a prevalence of psoriasis that was four to six times greater in IBD patients than the estimated prevalence in the general public.6

Several neutralizing anti-TNF agents, such as etanercept and infliximab, have been successfully used to treat autoimmune diseases, including inflammatory bowel disease. However, paradoxically, Infliximab and adalimumab-induced psoriasis in Crohn’s disease has been identified as a side effect of TNF-alpha inhibitor therapy. Researchers reviewed 142 case articles of new-onset psoriasis with infliximab, adalimumab, and etanercept therapy and of these confirmed eighty-one cases of infliximab induced psoriasis.7 In another study the researchers found that the vast majority of the cases (76%) developed psoriasis while on infliximab, and the rest (24%) after switching to adalimumab or certolizumab, indicating that this phenomenon is not drug specific, but rather a pharmacological group effect 12

 In another systematic literature review Researcher reviewed 222 cases. Of the 222 patients, 78.38% were diagnosed with Crohn’s disease, and 48.20% were female. The mean patient age was 26.50 years, and 70.72% of patients had no prior history of psoriasis. Infliximab was the anti-TNF-? therapy that caused the cutaneous reaction in most patients (69.37%). Clinical presentation varied; psoriasis-form lesions were the most common form of psoriasis (55.86%), followed by typical plaque type lesions (20.72%), and pustular-type lesions (3.60%). Six patients (2.70%) concomitantly presented with alopecia, one patient (0.45%) presented with palmoplantar pustulosis, and another patient (0.45%) presented with palmoplantar pustulosis and psoriatic arthritis.9

 Celiac disease is defined as a disease of the small intestine characterized by mucosal inflammation, villous atrophy, and crypt hyperplasia upon exposure to dietary gluten. Several studies have found that psoriasis patients are at an increased risk for celiac disease. A retrospective cohort study compared 25,341 psoriasis patients to over 125,000 matched controls in the U.S. The comparison data showed an odds ratio of 2.2 for the association of psoriasis with celiac disease. They also examined whether patients with celiac disease also have increased risk of psoriasis. A cohort of 28,958 biopsy-confirmed celiac disease patients from Sweden was evaluated for risk of future psoriasis compared to 143,910 age and sex-matched controls. The authors found a positive correlation between celiac disease antibody positivity and an increase in the severity of psoriasis or psoriatic arthritis. Interestingly, in the psoriasis patients, elevated celiac disease antibodies did not necessarily correspond to a biopsy-confirmed diagnosis of celiac disease, suggesting that psoriasis may be associated with gluten “sensitivity” (marked by antibody positivity) but not necessarily fully developed Celiac disease.10

In summary both Psoriasis and IBD and IBS are related inflammatory diseases. The skin and bowel represent both barrier and connection between the inner and the outer sides of the body. On average approximately 25% of patients who experience some form of bowel complaint will be diagnosed with psoriasis. It is also interesting to note that smoking in both IBD/IBS and psoriasis is considered an exacerbating trigger.

REFERENCES

  • Arzu K?l?ç, Seray Cakmak; PSORIASIS AND COMORBIDITIES; EMJ Dermatol. 2013;1:78-85.
  • Howa Yeung et al.;Psoriasis Severity and the Prevalence of Major Medical Comorbidity – A Population-Based Study; JAMA Dermatol. 2013;149(10):1173-1179. doi:10.1001/jamadermatol.2013.5015
  • Aurangabadkar SJ. Comorbidities in psoriasis. Indian J Dermatol Venereol Leprol 2013;79, Suppl S1:10-7
  • Huang B.L. et al.; Skin manifestations of inflammatory bowel disease; Frontiers in Physiology; www.frontiersin.org February 2012 | Volume 3 | Article 13 | 1
  • Skroza et al.; Correlations between Psoriasis and Inflammatory Bowel Diseases; Hindawi Publishing Corporation BioMed Research International Volume 2013, Article ID 983902, 8 pages ; http://dx.doi.org/10.1155/2013/983902
  • Lolli E. et al.; Psoriasis Phenotype in Inflammatory Bowel Disease: A Case-Control Prospective Study; Journal of Crohn’s and Colitis, 2015, 699–707 doi:10.1093/ecco-jcc/jjv068 Advanced Access publication April 23, 2015
  • Li W.Q. et al.; Psoriasis, psoriatic arthritis and increased risk of incident Crohn’s disease in US women; Ann Rheum Dis. 2013 July ; 72(7): 1200–1205. doi:10.1136/annrheumdis-2012-202143
  • Famenini S. and Wu J.J.; Infliximab-Induced Psoriasis in Treatment of Crohn’s Disease-Associated Ankylosing Spondylitis: Case Report and Review of 142 Cases; J Drugs Dermatol.2013;12(8):939-943.
  • Denadai R .et al.; REVIEW ARTICLE Induction or exacerbation of psoriatic lesions during anti-TNF-? therapy for inflammatory bowel disease: A systematic literature review based on 222 cases; Journal of Crohn’s and Colitis (2013) 7, 517–524
  • Bhatia B.K. et al.; Diet and Psoriasis: Part 2. Celiac Disease and Role of a Gluten Free Diet; J Am Acad Dermatol. 2014 August ; 71(2): 350–358. doi:10.1016/j.jaad.2014.03.017.
  • Spiller R.C.; Irritable bowel syndrome; Published Online March 14, 2005; British Medical Bulletin 2004; 72: 15–29
  • Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC. Functional bowel disorders. Gastroenterology. 2006 Apr. 130(5):1480-91.
  • Bercik P. et al.; Is irritable bowel syndrome a low-grade inflammatory bowel disease?; Gastroenterol Clin North Am.2005 Jun;34(2):235-45, vi-vii.
  • Gionata Fiorino , Paolo D. Omodei; Psoriasis and Inflammatory Bowel Disease: Two Sides of the Same Coin?; Journal of Crohn’s and Colitis, 2015, 1–2
  • Microscopic colitis. Mayo Clinic website.mayoclinic.org/diseases-conditions/microscopic-colitis/home/ovc-20192308