World Vitiligo Day

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Since inception in 2011, the World Vitiligo Day has been observed annually on the 25th of June.

Born from the determination of non-profit organizations VR Foundation (USA) and VITSAF (Nigeria), and their supporters across the world, the event was created in order to bring this ‘forgotten’ disease into the public eye, and to shine a light on challenges faced by those suffering from Vitiligo. 

The event has been growing bigger and bolder each year. And with it, recognition of Vitiligo grows, particularly since Winnie Harlow, supermodel and vitiligan, walked the Victoria’s Secret Fashion show – one of the hottest fashion tickets on the planet – last fall.  

What’s more, six U.S. State governors and numerous city mayors have now declared June ‘Vitiligo Awareness Month.’

Why World Vitiligo Day is Important

  • More than 100 million people around the world suffer from Vitiligo. The campaign helps disseminate important information that can help ease the pain of those living with Vitiligo.
  • Through events such as runs and walks, the campaign brings together Vitiligo sufferers along with their friends and family to show demand for specialized treatments. The day is also marked by educational seminars designed to share the latest scientific and medical research.
  • Through outreach to potential supporters, the campaign raises funds for local support groups, medical centres and academic researchers.

What and Where

This year, the international headquarters are set in beautiful Hanoi, Vietnam. The Honorary Chairman of the World Vitiligo Day 2019 is Prof. Nguyen Van Thuong, MD. The international theme of this year is “The Quality of Life of a Vitiligo Patient.” A panel of renowned speakers will cover a whole range of topics in Vitiligo: from novel herbal treatments by Prof. Torello Lotti to Viruses and Superantigens by Prof. Michael Tirant, and many others.

Support for the event is huge and well over 500 thousand people from across the world have now signed a petition that asks the UN Secretary General to officially designate June 25th as World Vitiligo Day. However, there is still much work to be done. Campaign organizers aim to persuade major healthcare providers and Big Pharma to give Vitiligo the attention it deserves and develop effective treatments for this disease. 

Vitiligo – The Latest Research

The founder of the Psoriasis Eczema Clinic, Professor Michael Tirant, will be in Vietnam on World Vitiligo Day to present some of his latest research in Vitiligo.

Professor Tirant will be presenting his research on viruses, superantigens and vitiligo as well as discussing the importance of diet, lifestyle and nutrition in vitiligo management.   Prof. Tirant, in conjunction with the Dr Michaels Skin Clinic in Vietnam, will also be launching the Vitilinex product range for Vitiligo prone skin.

For more information see https://vitiligo.clinic/

Rosacea- The Condition and its Triggers

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Rosacea is a condition affecting the face where the skin becomes persistently red, often with visible tiny blood vessels and acne-like bumps and pimples. There may be intermittent burning, stinging or mild itching. The skin may be may also be dry and mildly swollen. As the disease progresses, there may also be associated with eye symptoms, such as burning, irritation, redness and flaking of the eyelashes. Over many years the nose may become damaged and scarring may occur due to the acne-like lesions on the skin.

It is often preceded by episodes of facial flushing, which may last for years. It typically starts after the age of 30. The genetic component of this disorder is not well understood. However, a possible genetic origin in Northern European descendants, family inheritance, twin concordance, and genetic associations with autoimmune disorders attest the genetic predisposition to rosacea.

In addition to these factors, there are certain factors which may trigger off the condition. These are known as Primary Triggers.

These include

  • Emotional stress
  • Trauma – for example sun or wind burn
  • A pre-existing skin condition, for example, eczema of the face
  • Hormonal triggers, for example, the menopause
  • Excessive alcohol consumption

Secondary triggers are those which contribute to the condition once it already exists. There are many of them, but below are a few examples:

  • Hot beverages
  • Alcohol
  • Emotional stress
  • Air conditioning

The practitioners at Psoriasis Eczema Clinic are very experienced in the treatment of this condition and can help you identify and manage your triggers and improve your skin condition.

Phillip Bayer

Senior Practitioner, Psoriasis Eczema Clinic.

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Understanding the Triggers in Vitiligo

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What is Vitiligo?

Vitiligo is the most common of depigmentation disorders. It is an acquired pigmentation disorder of the skin and mucous membranes, in which there is a loss of melanocytes or pigmentation, producing irregular white spots and or white patches.

Initially, the white spots or white patches are small but enlarge over time. In some people, the white spots or white patches spread slowly while in others the spread is rapid.

 The Triggers in Vitiligo

Both genetic and non-genetic factors are believed to be involved in the onset of Vitiligo. Although several theories have been proposed as to the cause of Vitiligo, the precise mechanism causing the condition remains unknown.

According to researchers the exact triggers of the condition vary widely patient by patient, thus making it difficult to conclusively define the primary cause. However, given that autoimmune diseases typically involve interactions between genetic risk factors and environmental triggering factors, the autoimmune theory seems to be the most plausible.

After the genetic component (approx 20 -30% of sufferers have at least one affected first-degree relative) is taken into consideration the main triggering factors are considered to be

  • Environmental i.e. poor nutrition
  • Emotional stress
  • Trauma (Koebner Phenomenon)
  • Drugs and exposure to chemicals
  • Infections
  • Toxins and sepsis
  • Exposure to the sun

At the Psoriasis Eczema, we help patients achieve remission of their skin condition by helping them to identify their triggers.

Phillip Bayer (Practitioner at Psoriasis Eczema Clinic)

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Understanding the Triggers in Eczema

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There are many types of eczema. The condition can occur on any part of the body and results in inflammation of the skin with itching. Sometimes dryness and scaling, weeping, blistering and thickening of the skin may be seen.

The most common type of eczema is atopic dermatitis. This is a genetic skin condition often seen in association with asthma and/or hay fever in the patient or their family.  There are many triggers in eczema. They vary by person and by type of eczema.

Below are some of the more common triggers known to be involved in eczema:

  • Allergies – these can be divided into food and inhalant allergies. Inhalant allergies include pollens, grasses, animal hair, and dust. There may be a seasonal component to these allergies, for example, certain types of pollens during spring.
  • Dietary triggers – certain foods may exacerbate eczema by means of their histamine content or histamine-inducing action, or their dehydrating effect on the body. Some foods contain super antigens which make eczema worse. Inversely, certain foods may help eczema improve.
  • Heat and Cold – Both of these triggers are common in eczema, not only does the climate play a role but also air conditioning, which may dry out and exacerbate eczema
  • Stress – A very common triggers in people over the age of 13, emotional stress is often the single biggest trigger in many types of eczema.
  • Chemicals – Any chemical may cause a flare of eczema, but the better-known ones are strong soaps, swimming pool chlorine, and washing detergents.
  • Teething in children – another very common trigger of atopic eczema in children, teething may cause significant flares of otherwise well-controlled eczema in infants and toddlers.
  • Infections, diseases, and fevers – eczema flares are often preceded by infections in children and adults, for example, ear infections and tonsillitis.
  • Hormonal triggers – in women, some patients report their eczema flaring certain times of the month or during the menopause.

For eczema to be managed effectively, it is vital that a person understands their specific triggers and take action to control them. If done well, this can help to keep the condition dormant, or very mild.

At the Psoriasis Eczema, we help patients achieve remission of their skin condition by helping them to identify their triggers.

Phillip Bayer (Practitioner at Psoriasis Eczema Clinic)

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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

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

Atopic Dermatitis (Eczema) and BACTERIAL CUTANEOUS (SKIN) INFECTIONS

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Atopic_3

Atopic dermatitis (AD), also known as atopic eczema, is a chronic inflammatory disorder that causes significant morbidity and has a wide range of allergic and non-allergic comorbid disorders.

Comorbidity is a concurrence of multiple diseases or disorders in association with a given disease. The patient with AD has an increased risk of developing one or more of a number of other diseases/conditions that share many immunological features with AD.

   Cutaneous (skin) infections including:-

   Bacterial – Staphylococcal   / Impetigo contagiosum 

    1, 2, 3, 4, 5, 6, 7

Patients with AD are highly susceptible to certain bacterial, fungal and viral infections.

They have also been noted to have an increased incidence of warts caused by the human papillomavirus (HPV), and fungal infections caused by Trichophyton rubrum and also have a higher incidence of the fungal infections:- tinea pedis, tinea unguium, tinea manuum, tinea cruris, and tinea corporis, as well tinea barbae.7

AD Patients are also susceptible to severe infections caused by herpes simplex type 1 virus (eczema herpeticum or Kaposi’s varicelliform), vaccinia virus (eczema vaccinatum) coxsackie A virus and molluscum contagiosum virus. These viral infections can cause serious complications in AD patient and if not treated promptly have the potential to be life threatening.7

Signs of Secondary Infection include:

  • Sudden flaring (worsening) of eczema all over the body.
  • Weeping crusted areas – crusts are often a golden colour
  • Clusters of pustules (yellow/white pimples).
  • Fever, Shivering and extremely painful skin.
  • Chicken pox-like blisters and sores – this can be caused by the cold sore virus and may require urgent medical attention (Kaposi’s varicelliform)

BACTERIA and ATOPIC DERMATITIS (AD)

The skin is colonized by various different species of bacteria, fungi, and viruses that together are known as the skin microbiome, mainly Corynebacterium spp., Propionibacterium acnes and Staphylococcus epidermidis.

Each person will carry a different combination of these depending upon health and environment. The colonization of bacteria on specific regions on the body depends upon the local skin environment including moisture levels, pH, and keratinocyte cell surface adhesion proteins (Skin Barrier). For instance, Staphylococcus and Corynebacterium species thrive in specific environments on the skin such as the sole of the foot and the back of the knee. Dry environments such as the inside forearm and palm of hand are more prone to harbour a mixed population of bacteria including Propionibacterium acnes. 7

Babies are born microbe free until exposure to the external environment allows for immediate colonization of their skin, this first colonization usually starts as they pass through the vagina. As the child grows and they are exposed to different environments and in physical contact with different people their microbiome will change.7

Environmental factors such as diet, age, and gender also play a role in the makeup of the skin microbial flora.7

Staphylococcus aureus (S. aureus) and Staphylococcus epidermidis (S. epidermidis) are the two most common clinical isolates of the microbiota that is normally found in the nasal passages and on the skin of healthy people. They are Gram-positive cocci found in clusters. S. epidermidis comprises greater than 90% of the aerobic resident flora found on the skin and is considered a normal inhabitant of the skin surface. Some strains of S. epidermidis produce bacteriocins that are toxic to other bacterial species such as Staphylococcus aureus. S. epidermidis can also target S. aureus can prevent S. aureus biofilm formation and growth thus promoting a stronger skin barrier and immune response.7

In AD patients, when the patient suffers skin barrier breakdown and lowered immunity both S. aureus readily colonizes the affected skin lesions. Studies have shown that between 80% and 100% of patients with AD present nasal and skin colonization by with S. Aureus, as opposed to the prevalence of only between 5 to 30% in individuals without AD. To further break down the colonization statistics S. aureus has been isolated from 55–75% of unaffected AD skin, 85–91% of chronic lichenified (thickened/ scratched) lesions and 80–100% of acute exudative (weepy) skin lesions.7, 8

Impetigo contagiosum (contagiosa)

Impetigo is a skin infection caused by Staphylococcus aureus and Streptococcus pyogenes. In Europe and colder climate regions, Staphylococcus aureus is the most common cause. Impetigo can affect any one but is more common in children aged 2yrs. – 6 yrs. of age. It is highly contagious and is spread by direct contact. Children and those affected need to be kept home from day care, kindergarten, school and work.9

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Impetigo is commonly found in people who have skin conditions that cause impaired skin barrier e.g. eczema, scabies, fungal infections or via skin trauma e.g. insect bites. It is also common in crowded environments e.g. schools, day care centres etc. It can be spread through contact sports e.g. wrestling. Impetigo caused by Streptococcus pyogenes is common in hot humid regions.

There are two types of impetigo. The most common is called crusted or non-bullous impetigo. It starts as small blisters, which quickly burst and crust over. The other type, called bullous impetigo, causes large blisters that break easily. It is less common, and mainly affects babies.

Non Bullous Impetigo normally presents as:

  • Small vesicles that rupture, dries and forms golden- coloured, brown or even brownish black crusts/scabs.
  • Lesions can be up to 2cm in diameter.
  • Usually found on the face – around the mouth and nose, but they can also be found on the limbs.
  • In mild cases there is normally no systemic symptoms, but if it is an extensive eruption, it may be accompanied by fever and swelling.

Bullous Impetigo presents as:

  • Large fluid filled blisters > 2cm, which rupture easily.
  • May be golden in colour, brown or even brownish black.
  • The limbs and torso are more likely to be affected.
  • It is normally accompanied by fever and swelling.

Bullous impetigo is only caused by S aureus.

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Impetigo has been commonly called “school sores”. It is important, due to the contagious nature of the condition, that hands are washed regularly and especially after having touched or scratched the impetigo lesions. Anything that has been in contact with the sores e.g. clothing or anything that has been on the sores can spread the infection to other family members, friends and colleagues. In order to prevent the spread of the condition it is very important that clothes, towels, pillows and bed linen, nail scissors, razors or toothbrushes etc. are not shared. Clothing, towels and bedding etc. should be washed separately using hot water, washing powder and a disinfectant or eucalyptus/tea tree oil added to the wash.

REFERENCES

  • Simpson EL.; Comorbidity in Atopic Dermatitis; Curr Dermatol Rep. 2012 March 1; 1(1): 29–38. doi:10.1007/s13671-011-0003-5
  • Augustin M. et al.; Epidemiology and Comorbidity in Children with Psoriasis and Atopic Eczema; Dermatology 2015;231:35–40 DOI: 10.1159/000381913
  • Deckert S. et al.; Nonallergic comorbidities of atopic eczema: an overview of systematic reviews; Allergy 69 (2014) 37–45 © 2013
  • Ellis CN. et al.; Validation of Expert Opinion in Identifying Comorbidities Associated with Atopic Dermatitis/Eczema; Pharmacoeconomics 2003; 21 (12)
  • Silverberg J.I. and Silverberg N.B.; Atopic Dermatitis: Update on Pathogenesis and Comorbidities
  • Cogen A.L. et al.; Skin microbiota: a source of disease or defence?; Br J Dermatol. 2008 March ; 158(3): 442–455. doi:10.1111/j.1365-2133.2008.08437.x
  • Williams M. R. et al.; The Role of the Skin Microbiome in Atopic Dermatitis; Curr Allergy Asthma Rep (2015) 15: 65 DOI 10.1007/s11882-015-0567-4
  • Baviera G. et al.; Staphylococcus Aureus And Atopic Dermatitis: Which Came First, The Chicken Or The Egg?; EMJ Dermatol. 2015;3[1]:92-97.
  • Petry V. et al.; Bacterial skin colonization and infections in patients with atopic dermatitis; An Bras Dermatol. 2012;87(5):729-34.
  • Leung DYM.; The role of Staphylococcus aureus in atopic eczema; Acta Derm Venereol 2008; Suppl 216: 21–27
  • Baker S.; The role of microorganisms in atopic dermatitis; 2006 British Society for Immunology, Clinical and Experimental Immunology, 144: 1–9

Atopic Dermatitis (Eczema) and Psychological Disorders

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Psychological Disorders: –

Depression

Anxiety

Attention Deficit/Hyperactivity Disorder (ADHD)

Autistic Spectrum Disorder (ASD)

Atopic Dermatitis (AD) is a multifactorial, immune mediated, chronic and relapsing skin disease, with significant emotional distress, sleep disturbance and Quality of Life (QoL) difficulties. 1,2,3

Most cases of AD begin in childhood or adolescence, with more than 80% of pediatric patients having persistent symptoms of itch and dry skin in adulthood. The early age of onset and disease chronicity, plus impaired quality of life weighs heavily on a child’s psychological and behavioural development. This often leads to delayed social development throughout life and very high rates of psychological and behavioural disorders.5, The impairment of quality of life caused by childhood AD has been shown to be greater than or equal to other common childhood diseases such as asthma and diabetes, emphasising the importance of AD as a major chronic childhood disease.1,2,3

AD patients have been described with lower self-competence and self-efficacy, when compared with healthy individuals and there is also a clear relationship between the prevalence of a mental health disorder and the reported severity of the skin disease. 1,2,3

Psychological stress and AD symptoms seem to form a vicious cycle. However, the exact mechanism as to how stress affects AD is as yet largely unknown. Evidence suggests that stress stimulates the hypothalamic-pituitary-adrenal (HPA) axis releasing neuropeptides and neurotrophins, which influence the development and course of AD, inducing epidermal barrier dysfunction, and lowering the itch threshold.4

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The current incidence of psychiatric disorders among dermatological patients is estimated at about 30-40% and the association between anxiety and depression, and AD is well documented in scientific and medical journals.1,2,3 AD and clinical depression interact closely, and causal relationships between the two conditions have frequently been observed; e.g. the onset or exacerbation of AD often follows stressful life events such as severe disease in a family member, divorce, or parental separation.5

This may reflect the psychological distress produced by both the stigma associated with visible AD skin lesions and the unpredictability of disease flares, and may be manifested by the high proportion of patients (approx. 60%) who reported being embarrassed by or self-conscious of their skin condition in various studies. The psychological burden can further negatively impact mood and QoL. Thoughts of suicide have been reported in 15% of patients in an AD population in Europe and up to 20% of individuals with severe disease.3

In Dermatology Life Quality Index (DQLI) questionnaires, approximately 46% AD patients report severe pruritus (itch) with almost 15% rating it as unbearable, 86% experience itching every day and approx. 42% state that they itch up to 18 hours per day. Nearly all patients also reported the frequent occurrence of bleeding, oozing, cracking, flaking, or drying of their skin. AD and itching has a significant impact on patient-reported sleep with approx. 68% of patients reporting that itch delayed falling asleep and occasionally or frequently woke them up at night, with up to 36% reporting that their sleep was disturbed every night. Loss of sleep may contribute to daytime sleepiness and fatigue, further reducing functional activities and adversely affecting mood and QoL due to the fact that sleep likely has a reciprocal relationship with mental health.3

Children with AD face a slightly different set of challenges and often have negative self-esteem (subjective perception of self-worth) and poor self-image (subjective perception of abilities, appearance). They experience frustration, fussiness, irritability, unhappiness, loneliness, self-consciousness and emotional sensitivity. Parents have reported that their AD children often cry, and are nervous and insecure. Researchers observed perfectionism, rigid and obsessive thought patterns, anxiety and depression, obsessive and compulsive traits in paediatric AD patients. Children with AD also have difficulties in social interaction and impaired social competence.6

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Sixty percent of children with AD experience sleep disturbance caused by their disease, with 83% reporting sleep disturbance during exacerbations. The sleep of children with eczema was characterized by problems with settling and maintaining sleep while their daytime functioning was characterized by excessive daytime sleepiness and higher ADHD and Oppositional Behaviour scores as well as poor performance in daytime activities, specifically school performance.6 Problematic behavioural patterns that include hyperactivity, impaired attention, scratching to get attention; stubbornness, aggressiveness, disruptive and oppositional behaviour have been documented. A significant association was found between Attention Deficit Hyperactivity Disorder (ADHD) and AD. It is suggested that these behavioural difficulties are possibly mediated by disturbed sleeping patterns, difficulty in coping with the discomfort of AD and its treatment, disfigurement, stigmatisation and disciplinary challenges.7

Various studies have consistently indicated an association between AD and Autism Spectrum Disorder (ASD) and ADHD which is independent of environmental exposures and other comorbidities. Particularly infant AD appears to be associated with later development of ADHD symptoms. Children with previous or prevalent AD have an approximately 43 % increased risk to be diagnosed with ADHD or to display clinical ADHD symptoms.8, 9

It has been speculated that ADHD/ASD symptoms, AD, food hypersensitivity and sleep disruption may be linked by shared pathophysiological factors and that these impairments are characterized by a relevant developmental interplay, especially in early infancy and childhood. Disturbed sleep is a characteristic feature of ASD/ADHD and eczema and may be one mediating factor in the observed associations. However, other mechanisms may also be involved such as genetic or neuro-immunomodulatory mechanisms. It has been suggested that the non-allergic activation of TH1 and TH17 cells, which mediate the inflammatory processes, may be of relevance in the association between AD and ADHD. Also excessive cytokine release may impact on the central nervous system as they are able to pass the blood–brain barrier, thus possibly affecting both neurotransmission and brain circuits which are known to be involved in ADHD and/or affecting the sleep–wake rhythm.8, 9

Recent studies have also linked sleep disturbance to obesity and hypertension (blood pressure PB) in children.  The long-term effect of increased BP are unknown in children, but it is possible that cumulative increases of BP are associated with cardiovascular disease later in life, similar to that observed in psoriasis. The mechanism of association between obesity and AD remains unknown. Previous studies have suggested that adipose (fat) tissue may directly influence the risk of AD. 10  The association between AD and in particular, central obesity – where excessive fat is stored around the stomach and abdomen, in particular, is of major concern. Central obesity has previously been reported to have particularly harmful effects on a variety of medical disorders, including asthma, dyslipidemia, diabetes, coronary artery disease, and myocardial infarction.

 

Also read our BLOGS – Stress, Anxiety, Depression – Atopic Eczema (AE)/Atopic Dermatitis (AD) and associated Itch

Stressed About Your Skin Condition – Identify Your Stressors and Your Stress Responses 

REFERENCES

  • Lewis-Jones S. (2006), Quality of life and childhood atopic dermatitis: the misery of living with childhood eczema. International Journal of Clinical Practice, 60: 984–992. doi:10.1111/j.1742-1241.2006.01047.x
  • Mina, Shaily et al. “Gender Differences in Depression and Anxiety Among Atopic Dermatitis Patients.”Indian Journal of Dermatology 2 (2015): 211.PMC. Web. 20 Oct. 2016.
  • Simpson M.I. et al.; Patient burden of moderate to severe atopic dermatitis (AD): Insights from a phase 2b clinical trial of dupilumab in adults; J AM ACAD DERMATOL MARCH 2016
  • Sang Ho Oh et al.; Association of Stress with Symptoms of Atopic Dermatitis; Acta Derm Venereol 2010 Preview
  • Sewon Kim er al.; The Association between Atopic Dermatitis and Depressive Symptoms in Korean Adults: The Fifth Korea National Health and Nutrition Examination Survey, 2007–2012; Korean J Fam Med 2015;36:261-265
  • Gouws A.; The Impact Of Atopic Dermatitis On The Psycho-Social Wellbeing Of Children And Their Families; Current Allergy & Clinical Immunology, March 2016, Vol 29, No 1
  • Camfferman D et al.; Eczema, Sleep, and Behavior in Children; Journal of Clinical Sleep Medicine, Vol. 6, No. 6, 2010
  • Schmitt J. et. Al.; Association of atopic eczema and attention-deficit/hyperactivity disorder – meta-analysis of epidemiologic studies; Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie (2015), 41, pp. 35-44. DOI: 10.1024/1422-4917/a000208
  • Tzu-Chu Liao et al.; Comorbidity of Atopic Disorders with Autism Spectrum Disorder and Attention Deficit/Hyperactivity Disorder; The Journal of pediatrics · February 2016 DOI: 10.1016/j.jpeds.2015.12.063
  • Silverberg J. I. et al.; Central Obesity and High Blood Pressure in Pediatric Patients With Atopic Dermatitis; JAMA Dermatology February 2015 Volume 151, Number 2

Nail Psoriasis – Part 2

skinconditionsblogcategory

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.

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Subungal                                                       Hyperkeratosis          

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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.

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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.

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   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.

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Mild                                                      Mild                                              

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 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. 

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     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.

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Onychomycosis

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

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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.