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 SYMPTOMSIBS 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

TYPES OF PSORIASIS – PLAQUE PSORIASIS

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Plaque psoriasis or Psoriasis vulgaris (common type) – affects between 58% and 97% of all psoriasis cases. The difference in prevalence can be explained by race and geographical placement.1

It is characterized by sharply demarcated erythematous (red), silvery (whitish/yellowish), scaling plaques which most commonly occur on the elbows, knees, scalp, chest, back, and groin regions. The lesions are well-defined round or oval plaques that differ in size and in chronic plaque psoriasis often coalesce to form very large lesions covering large areas of the body.  Other involved areas include the ears, glans penis, perianal region, and sites of repeated trauma.

The lesions vary in size from 0.5 cm in diameter to large confluent areas on the trunk and limbs. There is a sharp line of demarcation between a plaque and clinically normal, uninvolved skin. Longitudinal studies of individual plaques have demonstrated that plaques are dynamic with an active and expanding edge, sometimes to the extent that the advancing edge may become annular leaving clinically normal skin in the centre of the original plaque.2,3

Plaque psoriasis can present in several different ways.

plaque-psoriasis

Figure 1. Plaque Psoriasis – colour varies from pinkish red to deep red, shiny with minimal silvery scale. Multiple lesions often coalesce forming larger plaques. This patient would be classified has having sever psoriasis

rupioid-sub-type

Figure 2. Plaque Psoriasis –  Rupioid subtype  Deep violaceous annular (round) lesions with distinctive, thickened, silvery scale. Multiple small lesions can be seen to be coalescing.

The term rupioid relates to distinct morphological subtype of plaque psoriasis. Rupioid plaques are small (2–5 cm in diameter) and highly hyperkeratotic, resembling limpet shells (see Figure 2).

A white blanching ring, known as Woronoff’s ring, may be observed in the skin surrounding a psoriatic plaque.

Other morphological subtypes of plaque psoriasis:-

  • Psoriasis gyrate — Figure 3 – in which curved linear patterns predominate annular psoriasis (psoriasis annularis – see figure 7 & 8) )—in which ring-like lesions develop secondary to central clearing

gyrate-sub-type Figure 3

  • Psoriasis follicularis — Figure 4 – in which minute scaly papules are present at the openings of pilosebaceous (hair) follicles.

Psoriasis - Folicularis Figure 4

  • Ostraceous psoriasis (see Figures 5 & 6 below) refers to hyperkeratotic plaques –  extremely thick scaled plaques often resembling an oyster shell.

ostraceous-fig-6 Figure 5                ostraceous-fig-5 Figure 6

Plaque psoriasis (see Figures 7 & 8 below) with a discoid (circular or oval) appearance is called psoriasis annularis or annular psoriasis.

psoriasis-annularis-fig-8 Figure 7                  Psoriasis - Annularis Figure 8 

Scale is typically present in plaque psoriasis, is characteristically silvery white, but may appear a yellowish colour and can vary in thickness.

Removal of scale may reveal tiny bleeding points (Auspitz sign – See Figure 9). The amount of scaling varies among patients and even at different sites on a given patient. In acute inflammatory or exanthematic psoriasis, scaling can be minimal and erythema may be the predominant clinical sign.4

OLYMPUS DIGITAL CAMERA
Figure 9. Thickened, red lesions with fine silvery scale. Multiple lesions have coalesced to form a large plaque. Note the excoriations marks where the patient has scratched the surface of the plaque to reveal pinpoint capillary bleeding, known as Auspitz sign
  • Lichenified psoriasis (Figure 10 and 11) – thickened psoriasis caused by chronic scratching (eczematized)

lichenified-2 Figure 10        lichenified Figure 11

Elephantine psoriasis (Figure 12 and 13) – large persistent, leathery plaques 

Psoriasis - Elephantine 1  Figure 12                Psoriasis - Elephantine Figure 13

Presentation examples of Plaque Psoriasis

Plaque Psoriasis 11 plaque-psoriasis-10  Plaque Psoriasis 9

plaque-psoriasis-8 plaque-psoriasis-7 plaque-psoriasis-6 plaque-psoriasis-5

Plaque Psoriasis 4 plaque-psoriasis-3  plaque-psoriasis-2 plaque-psoriasis-1

Read also “Psoriasis – Severity and Types”

Nail Psoriasis – Part 2

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Various Presentations 1,2,3,4,5

Nail Pitting:

Pitting is the commonest symptom of nail psoriasis. Pits usually affect the fingernails more commonly than the toenails. They are superficial depressions in the nail plate that indicate abnormalities in the proximal nail matrix (where the nail grows from under the cuticle). Psoriasis affecting the proximal nail matrix disrupts the keratinization of its stratum corneum by parakeratotic cells. Keratinization is the process by which epithelial cells become filled with keratin protein filaments, die, and form tough, resistant structures such as the skin, nails and hair. Pitting results when the keratinization process has been disrupted and the structure of the nail has been compromised allowing some of the cells, as the nail grows and becomes exposed, to be sloughed off forming scattered and coarse pits. Pitting may be arranged in transverse (side to side) or longitudinal rows or it may be randomly scattered. They may be shallow or large to the point of leaving a punched out hole in the nail plate. This is known as elkonyxis.

nail_1nail_2nail_3

Clustered                          Scattered                         Linear  

  nail_4

   Punctate

Transverse grooves

Transverse grooves (also known as Beau lines) are formed in the same way as pits. This occurs when the psoriatic lesion affects a wider area of the nail matrix.

    nail_5 nail_6

Subungual hyperkeratosis (Nail plate thickening) and crumbling

An extensive involvement of the entire nail matrix affecting the toenails more frequently than the fingernails. It results from the lifting of the nail plate off the nail bed due to the build-up of cells that have not undergone desquamation (shedding). The resulting accumulated tissue is friable (soft and crumbling) which is susceptible to infection by fungal dermatophytes e.g. Candida albicans (C. albicans) and pseudomonas aeruginosa, leading to either yellow/green discoloration.

nail_7 nail_8

Subungal                                                       Hyperkeratosis          

nail_9 nail_10  

Crumbling                                                 Nail Plate

Leukonychia

Leukonychia consists of areas of white nail plate due circumscribed focus of trapped parakeratotic cells within the body of the nail plate. Punctate Leukonychia is characterized by white spots 1-3 mm in diameter occurring singly or in groups and almost exclusively appear on the finger nails.

nail_11 nail_12

Transverse leukonychia                                      Punctate leukonychia

Subacute or chronic paronychia

Psoriatic paronychia usually develops when the periungual skin (around the cuticle) is affected by psoriasis, but it is also commonly seen in psoriatic arthritis with nail involvement. The chronic inflammation causes thickening of the free edge of the proximal nail fold with consecutive loss of cuticle and the attachment of the nail fold’s ventral surface to the underlying nail plate. This allows foreign material such as dirt, microorganisms, or allergenic substances to enter the space beneath the nail fold where they may aggravate inflammation.

nail_13 nail_14

   Subacute                                             Chronic

Acropustulosis

Acropustulosis is associated with pustular psoriasis and can involve one or all of the digits on the feet and hands. Pustulation of the nail bed and its growth site (matrix) may result in onychodystrophy (malformation) and anonychia (loss of nail). It may also occur as either a part of palmoplantar pustulosis, or acrodermatitis continua of Hallopeau. Usually, there is erythema (redness), swelling and severe discomfort of the entire digit or at the end of the digit. Resorptive osteolysis (resorption of the bone) of the finger or toes may also occur.

nail_15 nail_16

Mild                                                      Mild                                              

nail_17 nail_18

 Severe                                                  Severe

Splinter Haemorrhages and Salmon Spots

Splinter haemorrhages are small linear blackish streaks, about 2-3 mm long, arranged at the distal end of a nail plate. They are caused by the rupture of blood vessels and tracking of the blood along the longitudinal furrows beneath the nail plate. Salmon Spots, also known as “Oil Spots” are a translucent yellowish-red discoloration in the nail bed and can be a small rounded spot or a largish odd shaped spot. 

nail_19 nail_20

     Splinter Haemorrhages                   Salmon Patch

Onycholysis (separation of nail plate from nail bed)

It usually starts at the tip and/or the side(s) of the nail and works backwards. It normally appears white, but occasionally may also appear yellowish. Secondary fungal infections are common.

nail_21 nail_22

Onychomycosis

Secondary fungal infections, Onychomycosis, may cause a brownish, blackish or even greenish discolouration.

nail_23 nail_24

Onychomycosis is caused by dermatophytes, yeast (C. albicans) and moulds (e.g. Pseudomonas) and is the most common nail disease worldwide with between 6 -30% of the population affected, in PsN up to 70% of sufferers have a secondary fungal infection. Psoriasis often leads to abnormal morphology of the nails. Nails, damaged by psoriasis, lose their natural protective barrier and are therefore more susceptible to fungal infections. Researchers have found that dermatophytes more often cause toenail onychomycosis. Yeasts were isolated in a higher percentage from fingernails. The most common pathogens are Trichophyton rubrum, Trichophyton mentagrophytes and C. albicans. A correlation was observed between psoriatic change of fingernail plate – Nail Psoriasis Severity Index (NAPSI) and positive mycology.5

REFERENCES

  • Dogra A.and  Kaur Arora A.: Nail Psoriasis: The Journey So Far; Indian J Dermatol. 2014 Jul-Aug; 59(4): 319–333.
  • Sánchez-Regaña M. and Umbert P.; Diagnosis and Management of Nail Psoriasis; Actas Dermosifiliogr. 2008;99:34-43
  • Ghosal A, Gangopadhyay DN, Chanda M, Das NK. Study of nail changes in psoriasis. Indian J Dermatol. 2004;49:18–21.
  • Reich K. Approach to managing patients with nail psoriasis. J Eur Acad Dermatol Venereol. 2009;23(Suppl 1):15–21. [PubMed: 19686381]
  • Zisova L. et al. ; Onychomycosis in patients with psoriasis; Mycoses 55, 143–147 doi:10.1111/j.1439-0507.2011.02053.

Psoriatic Nails – Part 1

skinconditionsblogcategory

Psoriasis can affect both finger nails and the toe nails (Psoriatic Nails). The percentage of those with psoriasis who have nail involvement is thought to be 50%. For some unknown reason the finger nails are more often involved than toe nails. In most cases people with psoriasis have concurrent nail psoriasis; however, in 5- 10% of cases the nails only may be affected. In one study it was found that the frequency of nail changes in patients with Koebner’s phenomenon was 56%, whereas as in those without Koebner’s phenomenon it was only 29%. Nail psoriasis is approximately 10% more common in males than in females and is positively associated with higher bodyweight.1

Nail psoriasis is characterised clinically by manifestations on the fingernails and toenails. The mean delay of onset for nail dystrophies occurs in individuals with psoriasis between 9 and 11.5 years, explaining the lower prevalence of nail psoriasis in children.2 There may be involvement of only a single nail or of all nails and over time is associated with severe nail destruction or total nail loss.

Clinical Forms of Nail Psoriasis 3,4,5

  1. Psoriasis on the Nail Matrix and Plate
  • Pits or pitting, or dimples – Pitting is the result of the loss of cells from the surface of the nail. (see pictures 1-4 Part 2) Pitting occurs in approximately 70% of psoriatic nails.
  • Trachyonychia – rough (sandpapered) accentuated linear ridges (longitudinal striations) on the nails
  • Leukonychia – white nails or milk spots
  • Beau Lines – deep transverse (side to side) linear depressions, lines or trenches across the nails
  • Red lunulae – is the white half-moon–shaped area located at the base of fingernails and toenails; it is the only visible part of the nail matrix. The lunula becomes red when the capillaries under the nail are congested.

  

Blausen.com staff.

“Blausen gallery 2014”. Wikiversity Journal of Medicine. 

DOI:10.15347/wjm/2014.010. ISSN20018762

  1. Psoriasis of the Nail Bed
  • Onycholysis – the separation of the nail plate from the underlying nail bed and hyponychium (commonly known as the “quick”)
  • Subungal hyperkeratosis – excessive proliferation of the nail bed and hyponychium where a chalk like substance builds up.
  • Oil spots or salmon patches – these are the only lesions that are exclusive to nail psoriasis; they appear as round or oval yellowish brown/orange coloured areas in the centre of the nail plate
  • Splinter haemorrhages – small black lines that run from the tip of the nail to the cuticle as the result of the capillaries (very small blood vessels) between the nail and the skin bleeding.
  1. Paronychia

    An infection of the skin around the fingernails and toenails usually caused by a bacterial and/or fungal infection.

  1. Acropustulosis – characterised by pustular eruptions beginning in the tips of fingers and toes.

          Digits become swollen and malformed.

Psoriatic arthritis initially may present with only a few swollen joints. It is often common for just a single finger or toe to be noticeably swollen. Some people feel stiff when they wake up. As they move around, the stiffness fades. Sausage-like swelling in the fingers or toes (dactylitis), pain in and around the feet and ankles, especially tendinitis in the Achilles tendon or Plantar fasciitis in the sole of the foot and changes to the nails, such as pitting or separation from the nail bed are all indicative of Psoriatic Arthritis. More than 80% of patients with psoriatic arthritis will present with psoriatic nail lesions.

Researchers found that the nail and the enthesis (connective tissue – that directly attaches to the bone, via the distal interphalangeal (DIP) joint extensor tendon) are key players in the pathophysiology of nail psoriasis. Specifically, they found that the extensor tendon, at its enthesis, is able to send superficial fibres, which contribute to the formation of thick tissue surrounding the finger bones. This links the dense fibrous connective tissue from the nail plate to the tissue surrounding the finger bones and indirectly to the extensor tendon. The study suggested that there is an association between the DIP joint arthritis and nail disease due to the close interaction between the nail, joint and its associated tendons and ligaments. This is supported by the fact that although the nail system has no neural component, 50% of patients with nail psoriasis observe mild to severe pain and restricted mobility of the fingers.2

Many patients find that it becomes progressively more and more difficult and painful to use the fingers for gripping cutlery, pens and tools and performing tasks such as buttoning clothes, buttering toast, writing, typing etc., which are actions that we take for granted, become tasks that they can no longer do. As well as daily day to day activities many patients find that psoriatic nails also impact upon their sporting activities such as tennis, golf, swimming etc.

 

REFERENCES

  • Dogra A.and  Kaur Arora A.: Nail Psoriasis: The Journey So Far; Indian J Dermatol. 2014 Jul-Aug; 59(4): 319–333.
  • Tirant M. et al.; Nail Psoriasis In an Adult Successfully Treated With a Series of Herbal Skin Care Products Family – A Case Report; Journal Of Biological Regulators & Homeostatic Agents; 30, no. 2 (S3), 21-28 (2016)
  • Sánchez-Regaña M. and Umbert P.; Diagnosis and Management of Nail Psoriasis; Actas Dermosifiliogr. 2008;99:34-43
  • Ghosal A, Gangopadhyay DN, Chanda M, Das NK. Study of nail changes in psoriasis. Indian J Dermatol. 2004;49:18–21.
  • Reich K. Approach to managing patients with nail psoriasis. J Eur Acad Dermatol Venereol. 2009;23(Suppl 1):15–21. [PubMed: 19686381]

 

PSORIASIS AND COMORBIDITIES – Occular Inflammation

blog-7

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

Occular Inflammation –

Iritis

Uveitis

Episcleritis

Conjunctivitis

1, 2, 3

Ocular Inflammation

eye-1516983  episcleritis-eye

Overall, ophthalmological manifestations occur in about 10% of the cases of psoriasis and include blepharitis, conjunctivitis, keratitis, xerophthalmia (a medical condition in which the eye fails to produce tears), corneal abscess, cataract, orbital myositis (inflammation of the eye muscles), symblepharon (adhesion of the eyelid to the eyeball), chorioretinopathy (detachment of the retina), uveitis and ectropion with trichiasis (inwardly growing eyelashes) and madarosis (loss of eyelashes) secondary to eyelid involvement. 1,2

Uveitis

Although the etiology of psoriasis and its association with ocular disease remains unknown, it has been suggested that activated neutrophils in peripheral blood may be responsible for the attacks of anterior uveitis associated with psoriatic arthritis. Uveitis tends to develop more often in patients with arthropathy or psoriasis pustulosa rather than the other forms of psoriasis. Psoriasis patients with uveitis tend to be older than those without psoriasis. 1,2

Uveitis is characterized by an intraocular inflammatory process resulting from various causes. Individual forms of uveitis may be differentiated as a function of the location of the inflammation within the eye, symmetry and continuity of the inflammation, associated complication and distribution of cells along the corneal endothelium. 1,2

schematic_diagram_of_the_human_eye_en-edit

The uvea is the mid-portion of the eye. Its anterior portion includes the iris and the ciliary muscle, and its posterior portion consists of the choroid. Anterior uveitis or iritis is the inflammation of the anterior uveal tract. When the adjacent ciliary body is also affected, the process is known as iridocyclitis. Anterior uveitis is four times more common than posterior uveitis.

Uveitis can be divided into four main subgroups according to the etiology of the inflammation – infectious disease, immune-mediated disease, syndromes limited to the eyes or idiopathic forms. Of the patients with uveitis, around 40% of cases are secondary to an immune-mediated disease; around 30% of the cases of uveitis do not fit into any well-defined etiology. 1,2

Uveitis may occur in 7-20% of the patients with psoriasis. In a cross-sectional study researchers found a prevalence of uveitis of 2% in patients with psoriasis irrespective of the severity of the dermatosis. The association between uveitis and chronic plaque psoriasis has also been found, and in these patients uveitis tends to be bilateral affecting both eyes), prolonged and more severe. Uveitis, particularly anterior uveitis, has also been associated with the arthropathic form of the disease and approximately 7% of the patients with psoriatic arthritis may develop uveitis. Some cases of uveitis have been reported to occur even before psoriatic skin disease, and uveitis has been reported as the first presenting sign of Spondyloarthropathies (SpAs – a family of long-term (chronic) diseases of joints) in up to 11.4% of cases. The severity of ocular inflammation does not necessarily correlate with extent of joint findings but may correlate with skin disease. 1,2

Stephen Bafico

Conjunctivitis is a commonly occurring eye condition that can be caused by psoriasis, but it is more commonly due to allergies, bacterial infection, or viral infection. The most common presentation is generalized conjunctival injection with mild photophobia, gritty discomfort, and possible discharge. Thick purulent (pus-like) discharge is a hallmark of bacterial infection and watery discharge is characteristic of viral infections. Increased rates of obstructive meibomian (tarsal – sebaceous gland at the rim of the eyelids) dysfunction were noted in psoriatic patients. Published articles have suggested conjunctivitis prevalence rates in psoriasis patients as high as 64.5%.4

allergicconjunctivitis

Dry eye (Keratoconjunctivitis sicca – Dry Eye Syndrome) has been cited at a prevalence rate of 2.7% of psoriatic arthritis patients. Studies have suggested prevalence rates of dry eyes as high as 18.00% of psoriasis patients.4

 Facial psoriasis can of course present on the eyebrows and on the eyelids.

psoriasis-eye-before psoriasis-eye-after

      Facial Psoriasis – Before                                 Facial Psoriasis – After

When psoriasis affects eyelids or eyelashes, these may become covered with fine plaques and the rims of the eyelids may become red and crusty. If the rims of the eyelids are irritated for long periods of time, the rims of the lids may turn up or down (Ectropion). If the rims turn down, the lashes have a tendency to rub against the surface of the eye and cause further irritation and possibly damage to the surface of the eye.

Psoriatic eye manifestations, uveitis in particular, can lead to serious consequences, including vision loss. It is important at the first sign of occular redness, weeping, blurred vision, for psoriasis sufferers to see their Practitioner immediately, as they may need to be referred to an Ophthalmologist depending upon the severity of the symptoms.

 

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
  • Shiu-chung Au et al.; Psoriatic Eye Manifestations; FALL 2011; psoriasis forum, Vol. 17, No. 3; https://www.psoriasis.org/files/pdfs/forum/Psoriatic-Eye-Manifestations-Forum_Fall_11_WEB.pdf
  • Naiara Abreu de Azevedo Fraga et al.; Psoriasis and uveitis: a literature review; An Bras Dermatol. 2012;87(6):877-83. http://www.scielo.br/pdf/abd/v87n6/v87n6a09.pdf

 

PSORIASIS – Severity and Types

skinconditionsblogcategory

Psoriasis is one of the most common immune-mediated diseases world-wide. It is a chronic condition that waxes and wanes. Importantly it is not contagious but it can be an extremely painful, disfiguring and disabling condition for which there is no cure.

The exact causes of psoriasis have yet to be determined, however impairment of the immune system and genetics are known to play major roles in its development. When the immune system is somehow triggered it speeds up the growth cycle of skin cells among other immune reactions leading to a thickening of the skin, inflammation and excessive scaling.1

The prevalence of psoriasis in different populations varies between 0 and 12%, with estimates between 2 – 3% in most western populations. The prevalence in the northern most regions of the Russia and Norway ranges between 5–10% of the population and the highest 12% prevalence is found in the arctic population.2  In the U.S., prevalence ranges from 2.2% to 3.15% and the prevalence among African Americans is 1.3%. There is a low prevalence among North American Indians, Asians and Western Africans (0.3%). In Japan it is 0.1-0.2% of the population, in China 0.3% and is virtually undetected in Native South American Indians.3, 4, 5 Estimates of the prevalence of psoriasis in Australia ranges from 2.3% to 6.6% and in the U.K., the range was 1.3% to 2.6%.4,6  In Australia in the indigenous population it  occur rarely, with two recent Australian studies reporting small numbers of Indigenous patients in both the urban and rural environment presenting with psoriasis.7

What triggers psoriasis is a complex question and a large number of factors are involved. Genes are important: numerous family studies have provided compelling evidence of a genetic predisposition to psoriasis, although the inheritance pattern remains unclear. The condition will develop in up to 50% of the siblings of persons with psoriasis when both parents are affected, but prevalence falls to 16% when only one parent has psoriasis and falls further to only 8% percent if neither parent is affected.8 Environmental risk factors also play a role: bacterial and viral infections, stress, skin trauma, smoking and obesity have all been associated with the onset and exacerbation of psoriasis.9

The classification of severity is based on several dermatological markers. It often is a combination of a PASI (Psoriasis Area and Severity Index) score and a BSA (Body Surface Area) coverage factor.

A PASI score is used by dermatologist to measure the dermatological markers to determine the severity and extent of psoriasis, especially during a clinical trial. Four body areas, the head, the arms, the torso and the legs, are measured according to redness (erythema), thickness (Induration/Infiltration) and scaling (Desquamation) from 0 to 4. (See Chart)

% coverage of the body affected is also involved in the classification of the severity of psoriasis. The classification of mild psoriasis is made when symptoms affect less than 3% of the body surface. Moderate psoriasis covers 3% – 10% and the classification of severe indicates that symptoms affects more than 10% of the body, also the involvement of the hands, feet, facial, or genital regions, by which, despite involvement of a smaller BSA, the disease may interfere significantly with activities of daily life. This of course does not take into account the emotional impact that the condition has on the sufferer.9

Absent MildModerateSevereVery Severe
Redness / Erythemasevere_1

None


Score 1
severe_3
Score 2
severe_4

Score 3

Sev_1
Score 4
Thickness/

Hyperkeratosis

sev_2
None
sev_3
Score 1
Sev_4
Score 2
Sev_5
Score 3
Sev_6
Score 4
Scaling/DesquamationSev_7
None
Sev_8
Score 1
Sev_9
Score 2
Sev_10
Score 3
Sev_11

Score 4

Sev_12

Psoriasis can have a devastating impact on psychological well-being and social functioning, similar to that of cancer, arthritis, hypertension, heart disease, diabetes or depression. Most people with psoriasis suffer feelings of stigmatization because of their highly visible symptoms. This leads to feelings of social discrimination and alienation which compounds the feelings of anxiety and depression.9

Almost 90% of psoriasis sufferers have feelings of shame and embarrassment, 62% feel depressed, 58% suffer from anxiety, 44% feel that they have problems at work with most feeling that they are rejected for promotions, not accepted as part of the work group etc., 42% suffer from a lack of self-confidence due to their self-consciousness and 40% have difficulties in sexual relationships.10 

TYPES OF PSORIASIS

Psoriasis has been classified into several different types10, depending upon presentation, including:-

  • Plaque psoriasis or Psoriasis vulgaris (common type) – comprises approximately 90 percent of cases. Characterized by sharply demarcated erythematous silvery scaling plaques which most commonly occur on the extensor surface of the elbows, knees, scalp, sacral, and groin regions. The lesions are well-defined round or oval plaques that differ in size and in chronic plaque psoriasis that often coalesce to form very large, oddly shaped lesions covering large areas of the body.  Other involved areas include the ears, glans penis, perianal region, and sites of repeated trauma.
  • Scalp psoriasis is plaque psoriasis that is confined to the scalp, nape, forehead, sideburns, ears) the scalp lesions rarely extend > 2 cm beyond the hairline. Compared with plaque psoriasis elsewhere on the body, scalp involvement is frequently asymmetrical.
  • Guttate psoriasis – numerous small, red or salmon pink, drop-like spots which cover a large portion of the skin. Spots have fine, slivery scale. Lesions are usually located on the trunk, arms and legs. Usually proceeded by a bacterial streptococcal infection (strep throat, chronic tonsillitis) or a viral respiratory infection.
  • Flexural/intertriginous (Inverse psoriasis) – is located in the skin folds: i.e. armpits, under the breasts, skin folds around the groin and between the buttocks and in the skin fold of the obese. It is particularly subject to irritation from rubbing and sweating because of its location in the skin folds and tender areas. The plaques are thin, have minimal scale and a shiny surface commonly accompanied by secondary fissuring and/or maceration (the softening and breaking down of skin resulting from prolonged exposure to moisture). It is also prone to secondary infections such as tinea and candida.
  • Palmoplantar psoriasis – presenting as hyperkeratotic (thickened), red or yellowish, scaly plaques on the central palm or weight-bearing areas of the soles. The lesions are well demarcated and often accompanied by painful cracking and fissuring.
  • Palmoplantar pustulosis (PPP): is characterized by hyperkeratosis and clusters of pustules over the palms, and soles of hands and/or feet. These sterile pustules can remain as discrete pustules or may become confluent, producing lakes of pus which dry out, and the skin subsequently peels off, leaving a glazed, smooth erythematous surface. Quite often new crops of pustules will then appear.
  • Pustular psoriasis or Generalized Pustular psoriasis (von Zumbusch type) – Pustular psoriasis may be localized clusters of pinhead sized sterile pustules or as in the Generalized presentation – the skin becomes very red and tender and within hours, pinhead-sized pustules appear studding the erythematous back? These painful, sterile pustules may become confluent, producing lakes of pus. Subsequently, the pustules dry out, and the skin peels off, leaving a glazed, smooth erythematous surface on which new crops of pustules may appear. This is usually accompanied by a fever and systemic symptoms e.g. nausea, and may require the patient to be hospitalized.
  • Erythrodermic psoriasis – characterized by erythema, severe scaling, itching, and pain. This unstable psoriasis may some? times evolve to whole-body involvement that can lead to the inability to maintain homeostatic functions and often requires the patient to be hospitalized.
  • Nail psoriasis – affecting the nails of the fingers and/or toes, may affect only one or several nails. The most frequent signs of nail psoriasis are pitting and distal onycholysis. Clinical manifestations range from pitting, yellowish discoloration, and paronychia, to subungual hyperkeratosis, onycholysis, and severe onychodystrophy.
  • Psoriatic arthritis (PsA) a chronic inflammatory joint disease occurs in up to 39 % of patients with psoriasis. This type of arthritis can be slow to develop, with only mild symptoms or it can develop rapidly with extreme pain and characterized by focal bone erosions. PsA can be a severe form of arthritis with prognosis similar to that of rheumatoid arthritis

For more information on each classification of psoriasis refer to posts on each individual type.

REFERENCES

  • Višnja Milavec-Pureti?  et al.; Drug Induced Psoriasis; Acta Dermatovenerol Croat 2011;19(1):39-42
  • Bhalerao A., Bowcock A. M. ; The Genetics of Psoriasis: A Complex Disorder of the Skin and Immune System; Mol. Genet. (1998) 7 (10): 1537-1545 doi:10.1093/hmg/7.10.1537
  • Kuchekar A.B. et al.; Psoriasis: A comprehensive review; Int. J. of Pharm. & Life Sci. (IJPLS), Vol. 2, Issue 6: June: 2011, 857-877 857
  • Parisi R et al. Global epidemiology of psoriasis: A systemic review of incidence and prevalence. J Invest Dermatol 2012 Sep 27; [e-pub ahead of print]. (http://dx.doi.org/10.1038/jid.2012.339)
  • Menter A., Stoff B.; Psoriasis – Chapter 1 History, Epidemiology and Pathogenesis; 2010; Manson Publishing UK.
  • Parisi R. et al. Global Epidemiology of Psoriasis; Journal of Investigative Dermatology (2013), Volume 133
  • Heyes C. et al.; Non-infectious skin disease in Indigenous Australians; Australasian Journal of Dermatology (2014) 55, 176–184
  • Farber, E.M., Nall, L. and Watson, W. (1974) Natural history of psoriasis in 61 twin pairs. Arch. Dermatol., 109, 207–211.
  • Pelle Stolt, Maglia Rotta; Bringing Psoriasis into the Light; International Federation of Pharmaceutical Manufacturers & Associations; http://www.ifpma.org/fileadmin/content/Publication/2014/Psoriasis_Publication-Web.pdf
  • https://www.statista.com/statistics/409255/psoriasis-impact-on-individuals-physical-and-social-functioning/
  • Zangeneh F.Z., Shooshtary F.S.; Psoriasis — Types, Causes and Medication – Chapter 1; http://cdn.intechopen.com/pdfs-wm/44173.pdf

PSORIASIS and DIET – Part 1

Integrative Dermatology Blog Image

For many years Dermatologists, General Practitioner’s and many researchers considered that patients who stated that eating certain foods made their psoriasis  worse as being utterly mistaken or delusional. However, over the last several years there has slowly been a change of thought and we are now seeing the results of several recent studies and clinical trials on various nutritional and dietary therapies for psoriasis. And the results have made it clear that diet may influence the health outcome for patients.

A study of some 20,000 eczema and psoriasis patients by the Department of Medical Nutrition, Donau University Krems in Austria, found that the patients showed, besides allergic reactions to foods, an increasing number of pseudo allergic reactions caused by toxic-irritative pollutants (formaldehyde, exhaust particles, food additives, nicotine, wood preservatives, pesticides, heavy metals) which are responsible for the inflammatory process behind the complex symptoms. The Researchers found that 60% of all patients had raised concentrations of circulating immune complexes with food-specific IgE- and IgG responsible for the delayed (Type III) allergic reactions. They found that both in atopic eczema and in psoriasis patients had pseudo allergic  reactions against biogenic amines and had constantly raised serum histamine levels. Previously published results showed significantly reduced DAO activities in  thrombocyte rich plasma of atopic eczema and psoriasis patients explaining their intolerance reactions to histamine, tyramine and octopamine rich foods.1 Diamine oxidase (DAO) is an essential enzyme in the body that breaks down histamine. The body then takes the break-down products (called imidazole compounds) and excretes them through the kidneys into the urine.

Biogenic amines play important role in human body such as: regulation of body and stomach pH, gastric acid secretion, the immune response and cell growth and differentiation. At the same time, amines are important for the growth, renovation and metabolism of every organ in body and are also essential for maintaining the high metabolic activity of the normal functioning and immunological system of the gut. Despite these roles, the consumption of foods with high content of biogenic amines can cause adverse reactions such as nausea, headaches, cardiac palpitation, hot flushes, oral burning, gastric intestinal problems, renal intoxication, rashes and changes in blood pressure. Different biogenic amines can cause different side effects such as: excess tyramine intake could cause hypertension whereas serotonin is a vasoconstrictor. People having deficient natural mechanisms for detoxifying biogenic amines due to genetic defects or due to the intake of antidepressant medicines such as monoamine oxidase inhibitors may experience allergen-type reactions characterized by difficulty in breathing, itching, rash, vomiting, fever and hypertension. 2

Histamine is found in fermented alcoholic beverages, especially wine, champagne and beer,

bacon, salami, luncheon meats and hot dogs,  sour cream, sour milk, buttermilk, sour dough  bread, etc., dried apricots, prunes, dates, figs, raisins, citrus fruits, aged cheese – camembert, brie, blue vein and including goat cheese, walnuts, cashews, and peanuts,  avocados, eggplant, spinach, and tomatoes and smoked fish and certain species of fish: mackerel, tuna, anchovies, sardines.

Psoriasis is considered to be an autoimmune disease and in severe, uncontrollable psoriasis histamine antagonists are of value in reducing disease activity. Histamine formation and release raises the possibility, that histamine is one of the molecules involved in pathogenesis  of autoimmune diseases. 3,5

Tyramine is found in fava beans and tomatoes, broad beans, concentrated yeast extract spreads and bouillons, salamis and mortadella, beer as well as the above foods.

Tyramine, derived from tyrosine, mimics the effects of adrenaline, causing increased heart activity and raising blood pressure. Research has suggested that psychological stress can induce exacerbation of psoriasis. It is further hypothesized that these stress effects on the course and outcome of psoriasis are caused by neuroendocrine modulation of immune functions.4 Excess levels of tyramine releases adrenaline from storage vesicles.4,5 When chronic illness is involved and the body is in a state of chronic stress the adrenal glands begin to work overtime. Over a period of  time the adrenal glands begin to suffer from adrenal fatigue. Impaired adrenal function is associated with the incidence of autoimmune diseases such as skin conditions and arthritis.6

Octopamine is found in green bean, edamame (soybeans), avocados, bananas, pineapple, eggplants, figs, red plums, raspberries, peanuts, Brazil nuts, coconuts, processed meat, yeast as well as the above foods

Octopamine is closely related to the hormone norepinephrine, Researchers studying patients with psoriasis whose psoriasis is associated with increased levels of psychological stress, found that in the psoriasis patients there were significantly increased norepinephrine blood levels compared with non-psoriasis controls. The researchers concluded that there was a positive correlation between the severity of psoriasis and high levels of norepinephrine. 7

There has been a known correlation between Irritable Bowel Diseases such as Crohn’s Disease, Colitis and Irritable Bowel Syndrome (IBS or Leaky Gut), since the 80s. Some researchers have concluded that Psoriasis and IBD are strictly related inflammatory diseases, probably sharing immune-pathogenetic mechanisms. Skin and bowel represent, at the same time, barrier and connection between the inner and the outer sides of the body share similar immune processes which play a key role in maintaining homeostasis and in sustaining pathological processes. 8

 

Solanine is a glyco alkaloid  poison found in species of the nightshade family (solanaceae), e.g. potatoes, tomatoes and eggplant. It can occur naturally in any part of the plant, including the leaves, fruit, and tubers. It is very toxic even in small quantities. Research has shown that the disruption of epithelial barrier integrity is important in the initiation and the cause of inflammatory bowel disease (IBD). Solanine has been found to permeabilize cholesterol-containing membranes, thus leading to the disruption of epithelial barrier integrity. Altered intestinal permeability is believed by some researchers to play a key role in the initiation and propagation of the inflammatory process in conditions other than IBD.9,10  Solanine and related glycoalkaloids are classified as acetylcholinesterase inhibitors leading to increased levels of neurotransmitters which cause prolonged muscle contractions, pain, tenderness, inflammation and stiff body movement. Swollen joints are a clinical manifestation of synovitis and the acute-phase response act as bio marker of pro-inflammatory cytokine production. Solanine may also induce oxidative stress leading to generation of free radicals and alterations in antioxidant and scavengers of oxygen free radicals. 11 There is the potential for solanine to have an adverse effect on psoriatic arthritis. The percentage of arthritic patients who are sensitive to the solanine family of plants might be significantly greater than 10%. A 1982 study published in the Journal of the International Academy of Preventive Medicine demonstrated significant improvements in over 70% of 5,000 (> 3,500) arthritic patients after having eliminated solanine-containing foods from their diets.12

Also read our blog “PSORIASIS and COMORBIDITIES, PSORIASIS and ALCOHOL and PSORIASIS and WATER INTAKE”.

 

REFERENCES

  • Ionescu JG, Constantinescu R, Constantinescu AT; Personalized Anti-Inflammatory Nutrition For Atopic Eczema And Psoriasis Patients; EPMA Journal (2011) 2 (Suppl 1):S157–S165 DOI 10.1007/s13167-011-0118-6
  • Songül ?ahin Ercan, Hüseyin Bozkurt and Çi?dem Soysal ; Significance of Biogenic Amines in Foods and Their Reduction Methods; Journal of Food Science and Engineering 3 (2013) 395-410
  • Nielsen HJ,Hammer JH.; Possible role of histamine in pathogenesis of autoimmune diseases: implications for immunotherapy with histamine-2 receptor antagonists.; Med Hypotheses. 1992 Dec;39(4):349-55.
  • Schmid-Ott G. et al.; Stress-induced endocrine and immunological changes in psoriasis patients and healthy controls. A preliminary study.; Psychother Psychosom.1998;67(1):37-42.
  • Maintz and Novak N.; Histamine and histamine intolerance; Am J Clin Nutr 2007;85:1185–96
  • Physiology of Stress; Chapter 2; http://www.jblearning.com/samples/0763740411/Ch%202_S eaward_Managing%20Stress_5e.pdf
  • Ionescu G,Kiehl R; Increased plasma norepinephrine in psoriasis.; Acta Derm Venereol. 1991;71(2):169-70.
  • 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
  • Patel B. et al.; Potato glycoalkaloids adversely affect intestinal permeability and aggravate inflammatory bowel disease; Volume 8,Issue 5, pages 340–346, September 2002
  • Shah S. Dietary Factors in the Modulation of Inflammatory Bowel Disease Activity.Medscape General Medicine. 2007;9(1):60.
  • Ayad S.K.; Effect of Solanine on Arthritis Symptoms in Postmenopausal Female Albino Rats; Arab Journal of Nuclear Science and Applications, 46(3), (279-285) 2013 27
  • Prousky J. E.; The use of Niacinamide and Solanaceae (Nightshade) Elimination in the Treatment of Osteoarthritis; Journal of Orthomolecular Medicine Vol 30, No 1, 2015

PSORIASIS and SMOKING

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Tobacco smoke contains numerous chemicals that exert inflammatory effects on the human body. Recent studies suggest that cigarette smoking may trigger the development of psoriasis through oxidative, inflammatory and genetic mechanisms. Smoking initiates formation of free radicals that stimulate cell signalling pathways active in psoriasis. Smoking damages the skin by increasing formation of reactive oxygen species (ROS) and decreasing the gene expression of antioxidants. Nicotine also stimulates innate immune cells integral to the pathogenesis of psoriasis. This perpetuates a cycle of chronic inflammation. Smoking also enhances expression of genes known to increase the risk of psoriasis.1,2,5

Research has found that increased smoking intensity corresponds to a higher risk of developing severe psoriasis whilst  longer cumulative duration of smoking (pack-years) increases the likelihood of developing psoriasis. The study also demonstrated a graded increase in psoriasis risk with increasing exposure to passive smoke.                              

In one study, researchers investigated the associations between smoking status, quantity,duration, and cessation and exposure to environmental tobacco smoke and the risk of incident psoriasis in a total population of 185,836 participants from the Nurses’ Health Study (NHS), the Nurses’ Health Study II (NHS II), and Health Professionals’ Follow-up Study (HPFS). They reported that in the NHS, 20% of the cases of incident psoriasis might have been prevented by the elimination of smoking. Similarly, the population-attributable risk was 15% in the NHS II and 19% in the HPFS. For all participants, 17.5% of the incidents of psoriasis were attributable to having ever smoked. Evidence from past association studies seemed to indicate a stronger association between smoking and psoriasis in women than in men.3

Research has also shown that the risk increases with the number of cigarettes smoked daily. Studies have shown that smoking more than 10 cigarettes per day by men who are psoriasis patients may be associated with a more severe expression of disease in their extremities. In addition, smoking among both men and women who are psoriasis patients has been shown to reduce improvement rates and hence difficulty in achieving remission during treatment.4 In a multicentre case-control study of 404 psoriasis patients and 616 controls, the risk for psoriasis was higher in smokers compared with non-smokers, and the association with smoking was stronger and more consistent among women than men. A particularly strong association was also found between smoking more than 15 cigarettes per day and Palmoplantar Pustular Psoriasis (PPP). Several observational and case-control studies have demonstrated up to 94% prevalence of tobacco use in patients with PPP.6 

Smoking

As tobacco smoking also interferes with the bodies immunity by allowing colonization by perio -dontopathic bacteria and by acting as a local irritant, researchers have hypothesized that smoking may act as a trigger or permissive factor of periodontal disease in patients suffering from psoriasis. In order to test this hypothesis, the prevalence and severity of periodontal disease, Researchers assessed a group of smoking and non-smoking psoriasis patients and a group of smoking and non-smoking psoriasis-free controls. In this study it was statistically shown that psoriasis patients who smoke are at an approximately sixfold higher risk of developing severe periodontal disease, as compared to psoriasis patients who do not smoke.7

Another interesting observation was the frequent coexistence of a smoking habit and alcohol consumption in patients with psoriasis. In the literature, alcohol consumption has been described as a factor responsible for triggering psoriasis, but it is said that smoking increases the risk of the onset of the disease. Previous studies have indicated that smokers who drink are twice as likely to develop the disease as non-smokers and non-drinkers.8,9

It is well recognized that stress and anxiety acts in both the initiation and exacerbation of psoriasis. Psychosocial stressors include acute negative life events or chronic strains and have been implicated as risk factors for tobacco use. Psychological stress may influence smoking behaviour (e.g., initiation, maintenance, and relapse) through a number of mechanisms. Specifically, smoking may function as a coping behaviour, whereby nicotine is used to self-medicate in response to stress; it is also possible that exposure to stress may result in diminished self-regulation to control the urge to smoke. Previous observational studies illustrate that acute stressful events and greater exposure to chronic stressors (e.g., related to work, finances, or relationships) are associated with higher smoking prevalence compared to persons who did not experience these stressors.10

So in summary, studies suggest that cigarette smoking may trigger the development of psoriasis through oxidative, inflammatory and genetic mechanisms. Furthermore, smoking is associated with the clinical severity of psoriasis. Smoking also contributes to higher morbidity and mortality from smoking related disorders in these patients. It is, therefore, advisable, if possible to quit smoking, or at the very least, keep your smoking to a minimum, preferably under 10 cigarettes a day. Try to adopt other mechanisms to cope with your stress and anxiety and it is suggested that you read our other blogs on “Simple Physical and Mental Relaxation Techniques”.  Using these techniques you may be able to reduce your stress and anxiety levels and this may allow you to cut down on the number of cigarettes you smoke.

Also read our blog “Psoriasis and Alcohol Intake”, “Stress, Anxiety, Depression and Psoriasis”, “Stressed about Psoriasis – Identify Your Stressors and Yours Stress Responses”, “Simple Physical Relaxation Techniques for Psoriasis Patients” and  “Simple Mental/Mind Relaxation Techniques Part 1 and Part 2”

REFERENCES

  • Armstrong AW, Armstrong EJ, Fuller EN, et al. Smoking and pathogenesis of psoriasis. Br J Dermatol 2011; 165: 1162-8.
  • Al-Rubaii A, Al-Ward N, Al-Waiz M. The age of onset of psoriasis and its relationship to smoking habits and stressful life events. Saudi Med J2003; 24:108.
  • Wenqing Li et al.; Smoking and Risk of Incident Psoriasis Among Women and Men in the United States: A Combined Analysis; American Journal of Epidemiology Advance Access published January 12, 2012; http://aje.oxfordjournals.org/content/early/2012/01/11/aje.kwr325.full.pdf+html
  • Behnam SM,Behnam SE, Koo JY.; Smoking and psoriasis.; Skinmed. 2005 May-Jun;4(3):174-6.
  • Armstrong AW, ; Psoriasis and smoking: a systematic review and meta-analysis; British Journal of DermatologyVolume 170, Issue 2, Article first published online: 18 FEB 2014
  • Freiman A. et al.; Cutaneous Effects of Smoking; Journal of Cutaneous Medicine and Surgery Volume 8 Number 6 December 2004
  • Antal M. et al.; Smoking as a Permissive Factor of Periodontal Disease in Psoriasis; PLOS ONE | www.plosone.org; March 2014 | Volume 9 | Issue 3 | e92333
  • Agnieszka B. Owczarczyk-Saczonek , Roman Nowicki; The association between smoking and the prevalence of metabolic syndrome and its components in patients with psoriasis aged 30 to 49 years; Postep Derm Alergol 2015; XXXII (5): 331–336 DOI: 10.5114/pdia.2015.54743
  • Naldi L, Peli L, Parazzini F. Association of early-stage psoriasis with smoking and male alcohol consumption: evidence from an Italian case-control study. Arch Dermatol1999; 135:1479–84.
  • Slopen N. et al.; Psychosocial stress and cigarette smoking persistence, cessation, and relapse over 9–10 years: a prospective study of middle-aged adults in the United States; Cancer Causes Control DOI 10.1007/s10552-013-0262-5