levering trimox antibiotic

online billig trimoxi

”Jag har lärt mig massor som jag kan använda med mina patienter. Dessutom har jag utvecklats personligen genom utbildningen!”
Tandhygienist

”Hypnos är ett fantastiskt sätt att arbeta med människor och ni som lärare är kunniga och inspirerande.” Psykoterapeut

CHP har även en fortsättningsutbildning i hypnospsykoterapi med traumabearbetning, ego-statesarbete mm, för dig med CHP-grund eller motsvarande + minst steg 1 psykoterapi.
Kursstart: Uppdateras inom kort

Nu har Inger Lundmark släppt sin app Hypnos & Hälsa där du kan hitta en rad olika sköna hypnosinspelningar.

Appen är gratis, inne i hypnosbiblioteket kan du sedan klicka och provlyssna eller göra ett köp så laddas den ner.

CD används inte så mycket längre men om du ändå vill ha en CD, mejla kontakt@ingerlundmark.nu. Om du vill kan du även beställa en specialgjord CD för just dig.

070-593 24 76

Arbetar med individuell psykoterapi, parterapi familjeterapi med eller utan klinisk hypnos. Även ego-stateterapi, traumaterapi, handledning.

Leg. Psykoterapeut, Familjeterapeut, Handledare
Aukt. Dramapedagog (RAD)
Gestalterapi 1
Cert. Hypnosterapeut (ASCH)
Lärare i klinisk hypnos

076-240 34 59

Arbetar med individuell psykoterapi och parterapi med eller utan klinisk hypnos. Även ego-stateterapi, traumaterapi, EMDR samt handledning.

Leg. Psykolog
Leg. Psykoterapeut, Handledare

070-433 70 71

Arbetar med individuell psykoterapi med eller utan klinisk hypnos. Även KBT, schematerapi, traumaterapi, stresshantering.

Socionom
Ek. Mag MBA
Leg. Psykoterapeut

070-830 11 81

Arbetar med individuell psykoterapi, parterapi och familjeterapi med eller utan klinisk hypnos. Även KBT och EMDR. Anitas specialitet är terapi med barn och ungdomar.

Pedagog
Leg. Psykoterapeut
Familjeterapeut
Cert. Hypnosterapeut

070-721 52 89

Arbetar med individuell psykoterapi med eller utan klinisk hypnos. Även Traumafokuserad terapi, KBT, schematerapi, anger management.

Beteendevetare
Leg. Psykoterapeut

Är det något du undrar över går det bra att fråga vårdgivaren här.

Snitt 5, baserat på 8 omdömen

18:13 - 12 feb, 2018
S skrev:
Marianne är jättebra och har hjälp mig mycket att komma vidare efter trauma med emdr. Rekommenderar.

17:00 - 16 nov, 2017
Hanna skrev:
Anita är en helt fantastisk terapeut! Klok, inlyssnande, varm och väldigt mänsklig. Jag har fått hjälp med att bearbeta många jobbiga tankar och känslor, och kommer ut på andra sidan med minskad oro och ångest, ökad självkänsla och ett lättare sinne. Alla mina varmaste rekommendationer!

15:42 - 23 apr, 2017
Lotta skrev:
Jag kände direkt tillit till Inger och gick hos henne under knappt ett år. Under det året blev jag hjälpt med mitt grundtrauma som påverkat hela mitt liv och är idag en mycket gladare människa ed stärkt självförtroende och självkänsla som inte längre är rädd för att bli deprimerad. Jag slutade terapin för cirka ett halvår sedan men känner fortfarande hur terapin hjälper mig dagligen, den mognar och växer och utvecklas hela tiden. Dessutom lyssnar jag på inspelningar med Ingers hypnosterapi dagligen då de stärker mig i min fortsatta utveckling.

13:20 - 10 maj, 2016
Helene skrev:
Jag har varit storrökare i över 30 år, efter två möten med Inger så slutade jag tvärt. Helt fantastiskt, nu har det gått 5 veckor och jag tänker inte ens på att röka! Äntligen slipper jag att stinka rök, tack Inger!

14:10 - 24 nov, 2014
Cecilia skrev:
Efter 26 års beroende av snus så bestämde jag mig för att prova hypnos för att bli snusfri. Jag träffade Inger vid två tillfällen i mars 2014 och nu åtta månader efteråt är det fortfarande nästan lite overkligt att det fungerade så bra! Inger är en fantastisk person som inger förtroende och utstrålar värme, det är ingen tvekan om att hon har lång erfarenhet och vet vad hon håller på med. Jag är oändligt tacksam för hjälpen och njuter av varje snusfri dag!!

10:34 - 22 okt, 2014
Tacksam skrev:
Jag har gått hos Inger Lundmark i omgångar vid olika skeden av mitt liv och mitt mående. Inger har alltid varit inkännande och har alltid mött mig där jag för tillfället befunnit mig i min utveckling. Med respekt, värme och genom att vara flexibel inför mina behov, har hon hjälpt mig att komma vidare och uppåt i livet. Jag lever, vilket jag inte är säker på att jag hade gjort utan Ingers trygghet och hennes varma bemötande. Nu lever jag inte bara, utan nu vill jag dessutom verkligen leva. Jag känner en djup tacksamhet inför det medmänskliga, varma omhändertagandet som Inger har givit mig när jag som mest behövt det. Tack Inger!

15:01 - 05 okt, 2013
Helén skrev:
Jag har känt mig mycket trygg och haft stor tillit till min terapeut under några år av hypnosterapi på Grinden. Jag har fått redskap att ta hand om mig själv och mina starka känslor. Jag har lättare att förhålla mig till det som händer i mitt liv och har mer avspända relationer både yrkesmässigt och privat. Idag har jag mer kontakt med min sårbarhet, min styrka och mitt mod att vara den jag är. Jag är mer öppen och vågar kommunicera mina känslor och tankar i mycket större utsträckning och känner mig mer äkta och hemma mig. Jag känner tacksamhet för att jag gav mig själv chansen att gå i hypnosterapi.

14:25 - 03 okt, 2013
Felicia Hume skrev:
Jag hade gått i sex år i psykodynamisk terapi och stod nu inför att ta mig ut ur både depression och lossa gamla barndomstyngder. Med hjälp av Inger Lundmark och hennes hypnosterapi kunde jag gå till djupet med mina barndomsupplevelser, få hjälp att förhålla mig till dem och lära mig skilja på mig själv som barn och som vuxen. Jag fick också verktyg för att upprätta inre gränser och och även bryta mig loss från destruktiva sammanhang, beteenden och mönster. Jag fick i henne en trygg följeslagare i mina egna tillbakablickar. Det hjälpte mig att hitta fram till den jag vill vara och är. Jag skrev om mina upplevelser och det blev den slutgiltiga pusselbiten till att bli en helare och vuxen människa. Hypnosterapin blev ett konkret och ett direkt livsavgörande steg på den vägen. Jag har rekommenderat Inger Lundmark till många av mina vänner och kommer fortsätta att göra det!

Vi arbetar även med handledning, för psykoterapeuter och inom organisationer.

Vi erbjuder kort- och långtidsbehandlingar vid trauma, relationsproblem, stress, sömnstörningar, ångest, fobier, vid sviktande självförtroende/självkänsla, depression, mm.

Psykoterapeuten rådgör med dig och anpassar behandlingsmetod utifrån just dina behov, önskemål och förutsättningar.

Att arbeta med hypnos är att bjuda in upplevelsedelar av hjärnan, att i ett avslappnat tillstånd nå och använda inre bilder, sinnesintryck mm, vilket ofta är ett mycket verksamt sätt att åstadkomma förändring av olika slag. All terapi är ett arbete, men med hypnos blir det ofta mer lustfyllt, kreativt, och går ofta fortare än vid enbart samtal.

køb generisk trimox

The thick keratin of the nail blocks absorption of topical agents.

For onycholysis, a topical corticosteroid in a solution vehicle may be used under the nail. Systemic therapy may be required to improve severe disease.

The thin skin of the genitalia is highly sensitive to the adverse effects (atrophy) of topical corticosteroids.

A low-potency topical corticosteroid ointment is recommended. Topical calcipotriene, which is not associated with a risk of atrophy, may be used.

The thick stratum corneum of palms and soles is a barrier to penetration of topical agents.

A highest-potency topical corticosteroid is recommended. Methotrexate (Rheumatrex) or acitretin (Soriatane; a systemic retinoic acid analog) may be needed.

Topical corticosteroids are the most commonly prescribed treatment for psoriasis.5 They are available in ointment, cream, lotion and solution forms. Corticosteroids have well-recognized anti-inflammatory and antiproliferative effects, which are thought to be their primary mechanism of action in psoriasis.6 Topical steroids are classified as low-, medium-, high- and super-high potency agents (Table 2). In general, treatment is initiated with a medium-strength agent, and high-potency agents are reserved for the treatment of thick chronic plaques that are refractory to weaker steroids. Low-potency agents are used on the face, on areas where the skin tends to be thinner, and on the groin and axillary areas, where natural occlusion increases the potency of a low-potency agent to the equivalent of a higher potency agent. Use of high-potency agents in these areas increases the risk of side effects and therefore should be avoided.

Potential side effects from corticosteroids include cutaneous atrophy, telangiectasia and striae, acne eruption, glaucoma, hypothalamus-pituitary-adrenal axis suppression and, in children, growth retardation. The true incidence of corticosteroid-induced hypothalamus-pituitary-adrenal suppression is unknown, but it is of concern with prolonged use.7 Often, evidence of hypothalamus-pituitary-adrenal axis suppression is found on the laboratory results, even when clinical symptoms are absent. Careful long-term follow-up of patients receiving topical corticosteroid therapy is highly recommended to detect potential complications.

Although corticosteroids are rapidly effective in the treatment of psoriasis, they are associated with a rapid flare-up of disease after discontinuation, and they have many potential side effects. Consequently, topical corticosteroids are frequently used in conjunction with another agent to maintain control. Topical calcipotriene is often used in combination with topical corticosteroids to speed clearing of the lesions and maintain control after the initial phase of treatment is completed.

Calcipotriene is a vitamin D3 analog available in cream, ointment and solution formulations. It inhibits epidermal cell proliferation and enhances normal keratinization. This agent has a slow onset of action, and patients should be aware that the effects of calcipotriene may not be noticeable for up to six to eight weeks after the initiation of therapy.

Although calcipotriene monotherapy has been shown to be moderately effective in reducing the thickness, scaliness and erythema of psoriatic lesions,8 maximal benefits are achieved when calcipotriene is used in combination with potent topical corticosteroids. A simplified approach for combination therapy is to begin therapy with a “quick-fix” phase, followed by a “transitional phase” and then a “maintenance phase.”9 For example, treatment could be initiated with twice-daily applications of a topical corticosteroid and calcipotriene until the lesions are flat; the maximum duration of this phase is four weeks.

When the lesions have become flat, therapy can then be changed to twice daily use of calcipotriene only, with corticosteroid “pulse” therapy twice daily on weekends only. This second phase helps prevent rebound from abrupt withdrawal of corticosteroids. When the lesions have remained flat and the intensity of their color has declined from bright red to pink, the maintenance phase begins, with use of calcipotriene alone and discontinuation of the weekend use of topical corticosteroids.

After appropriate control of the disease is maintained, topical therapy can be discontinued until a flare-up occurs. Use of emollients should be recommended, to reduce the scaly appearance of the lesions and to potentially reduce the amount of corticosteroid needed.

The only cutaneous side effect of calcipotriene is local irritation, which occurs in approximately 15 percent of patients.10 Calcipotriene is not recommended for use on the face or with occlusion. Hypercalcemia is a potential side effect of this agent when the dosage exceeds 100 g per week. This effect does not usually occur with weekly use of 100 g or less.11, 12 Most reports of hypercalcemia have been in patients who received prolonged therapy with 200 g or more per week. For localized psoriasis, the recommended dosages do not require monitoring of serum or urinary calcium levels. However, calcipotriene should be used with caution in patients with compromised renal function or a history of renal calculi.

Coal tar is a black viscous fluid that was first described by Goeckerman in 1925, when it was combined with ultraviolet light for the treatment of psoriasis. It is thought to suppress epidermal DNA synthesis.13

Coal tar is available as an ointment, cream, lotion, shampoo, bath oil and soap. Coal tar is most effective when it is used in combination with other agents, especially ultraviolet B light. Like calcipotriene, coal tar is effective when it is combined with topical corticosteroids. Coal tar shampoo can be used in combination with a corticosteroid scalp solution for the treatment of psoriasis on the scalp.

Because coal tar is messy and malodorous and can stain clothing, nighttime application is recommended. Patients should be advised to use old bed linens and and to wear old pajamas when they are using coal tar. Tar products can cause folliculitis, but they otherwise are generally not associated with side effects.

If good control of psoriasis is not achieved with topical corticosteroids, alone or in combination with calcipotriene or coal tar, consideration should be given to the addition of anthralin or tazarotene therapy. Anthralin, also known as dithranol, is an antipsoriatic topical preparation derived from wood tar.4 It has been available since 1916, but it is a second-line agent because of its irritating and staining properties.

Anthralin is available in 0.1 percent to 1 percent ointments, creams and solutions. It is generally used on notably thick, large plaques of psoriasis, and therapy is initiated at low concentrations for short periods. The concentration and duration of contact with each treatment is gradually increased, up to a maximum of 30 minutes per application.4 Anthralin can be combined with ultraviolet phototherapy; this is known as the traditional Ingram regimen.

Patients should be warned that anthralin has a tendency to stain any surface, including the skin, clothing and bathtub. Its use should be limited to well-demarcated plaques, and it should be applied with a cotton-tipped applicator or a gloved hand. Patients should be warned that normal skin surrounding the psoriatic lesion may become irritated if it comes in contact with anthralin.

Topical tazarotene is the first topical receptor-selective retinoid approved for the treatment of psoriasis. It is available only in gel form and exerts its effects through gamma and beta retinoic acid receptors. Tazarotene helps to normalize the proliferation and differentiation of keratinocytes, as well as to decrease cutaneous inflammation.14, 15 Once-daily application of tazarotene gel, 0.05 percent or 0.1 percent concentration, has been shown to be as effective as twice-daily application of 0.05 percent fluocinonide cream.16

As monotherapy, tazarotene has been shown to significantly reduce plaque elevation in mild to moderate psoriasis.17 However, because of its modest efficacy, slow onset of action and high potential for causing irritation, tazarotene should usually be used in combination with corticosteroids. The primary side effect of topical tazarotene is minor skin irritation and increased photosensitivity. Tazarotene is classified as a pregnancy category X drug and its use should be avoided in women of childbearing age.

Sun exposure in addition to topical therapy may be beneficial when multiple areas are affected with psoriasis. Patients should be encouraged to obtain natural sunlight exposure or tanning-bed light exposure for a few minutes a day, and then to slowly increase the duration of exposure as tolerated. Unaffected areas should be covered with a sunscreen, especially the face. Ultraviolet light exposure can be used judiciously to prevent flare-ups during the maintenance phase of therapy.

Psoriatic plaques that fail to respond to topical therapy may be improved by administration of intralesional corticosteroid injections. Triamcinolone (Kenalog) is often used for this purpose. The agent is injected directly into the dermis of a small, persistent plaque. The concentration is generally 3 to 10 mg per mL, depending on the size, thickness and area of the lesion. The dose of triamcinolone is released gradually over three to four weeks; additional injections may be needed every four to six weeks to improve the response. Disadvantages of intralesional injections include pain during the injection and potential side effects of local atrophy and systemic absorption.

The patient with refractory lesions may benefit from more advanced forms of treatment, such as phototherapy (ultraviolet B alone or psoralens plus ultraviolet A), outpatient treatment at a clinic specializing in psoriasis and systemic therapy with oral retinoids, methotrexate (Rheumatrex) or cyclosporine (Sandimmune). Combination therapy has also been shown to be effective, especially phototherapy in combination with topical anthralin, coal tar or calcipotriene (Table 4).

Psoriasis er en kronisk inflammatorisk hudsygdom, karakteriseret ved et aktiveret immunsystem og hyperproliferation af keratinocytterne i epidermis. Sygdommen ses hos 2-3% af befolkningen. Den mest almindelige præsentation er nummulate plaques, som typisk er lokaliseret til knæ, albuer og skalp. De første udbrud af sygdommen kan være i form af et papuløst eksantem (guttat psoriasis). Ved invers psoriasis afficeres hudfolder.

Diagnosen psoriasis stilles sædvanligvis på de kliniske forandringer, dog kan der være behov for histologisk verificering ved atypisk præsentation.

Lokalbehandling vil ofte være tilstrækkelig ved mild til moderat psoriasis, mens fototerapi og systemisk behandling anvendes ved sværere former, herunder psoriasisartritis.

  • Calcipotriol i kombination med gruppe III-kortikosteroidet betamethason har effekt på linje med meget stærkt virkende kortikosteroider (gruppe IV), og kan ved daglig anvendelse i 4 uger inducere hurtig remission. Efter 4 uger aftrappes behandlingen gradvis. Ved relaps kan gentagen behandling med calcipotriol i kombination med betamethasondipropionat initieres efter behov.
  • Kortikosteroider kan være virksomme ved mild til moderat nummulat-plaquepsoriasis. Generelt anvendes stærkere virkende kortikosteroider til hårbund, krop og ekstremiteter, og svagerevirkende kortikosteroider til ansigt, hudfolder og ano-genitalregionen. Stærkt virkende kortikosteroider bør ikke anvendes ved svær udbredt psoriasis på grund af risiko for præcipitering af pustuløs- eller erytrodermisk psoriasis.
    I starten bør salver foretrækkes frem for cremer, idet salvegrundlaget er med til at opløse psoriasisskæl. Ved meget hyperkeratotiske forandringer kan det være en fordel dagligt at fjerne det tykke stearinagtige skællag med madolie eller salicylsalve 5% eller 10% før påsmøring af det aktive stof, dog er det ikke nødvendigt at fjerne skæl før anvendelse af calcipotriol-betamethason gel til psoriasis, herunder skalp psoriasis.
  • Tjæresalve eller -bade, ofte givet under indlæggelse, kan være et alternativ til kortikosteroid- og calcipotriolbehandling. Se endvidere Tjæreholdige midler mod psoriasis.

Systemisk behandling og fototerapi

Ved udbredt psoriasis eller svær psoriasis på hænder og fødder, eller svær ano-genital psoriasis, vil man ofte vælge at behandle med:

  • enten fototerapi UVB eller UVB-TL01 (smalspektret UVB)
  • eller systemisk behandling med fotokemoterapi (PUVA), methotrexat, acitretin, dimethylfumarat, ciclosporin, apremilast eller et biologisk middel.

Systemisk behandling kan med fordel kombineres med lokalbehandling med calcipotriol, idet der opnås additiv effekt.

Ved i øvrigt behandlingsrefraktær moderat til svær psoriasis eller ved intolerans/kontraindikationer mod anden systemisk behandling kan et biologisk middel eller apremilast anvendes. Det er alment accepteret at man før anvendelse af et af de biologiske midler eller apremilast har forsøgt behandling med mindst en anden systemisk behandling, herunder methotrexat.

trimox piller golfer

Consider obtaining the following baseline laboratory studies in patients being initiated on systemic therapies (eg, immunologic inhibitors):

Medications used in the management of psoriasis include the following:

The American Academy of Dermatology (AAD) guidelines recommend treatment with methotrexate, cyclosporine, and acitretin, with consideration of contraindications and drug interactions. [5]

A 2013 international consensus report on treatment optimization and transitioning for moderate-to-severe plaque psoriasis include the following recommendations [6]:

Management of psoriasis may also involve the following nondrug therapies:

Ocular manifestations such as trichiasis and cicatricial ectropion usually require surgical treatment. Progression of corneal melting, inflammation, and vascularization may require lamellar or penetrating keratoplasty.

See Treatment and Medication for more detail.

Psoriasis is a chronic, noncontagious, multisystem, inflammatory disorder. Patients with psoriasis have a genetic predisposition for the illness, which most commonly manifests itself on the skin of the elbows, knees, scalp, lumbosacral areas, intergluteal clefts, and glans penis. The joints are also affected by psoriasis in up to 30% of patients with the disease. (See Pathophysiology and Etiology.)

Psoriasis has a tendency to wax and wane with flares related to systemic or environmental factors, including life stress events and infection. It impacts quality of life and potentially long-term survival. There should be a higher clinical suspicion for depression in the patient with psoriasis. (See Prognosis.)

Multiple types of psoriasis are identified, with plaque-type psoriasis, also known as discoid psoriasis, being the most common type. Plaque psoriasis usually presents with plaques on the scalp, trunk, and limbs (see the image below). These plaques appear as focal, raised, inflamed, edematous lesions covered with silvery-white “micaceous” scales. (See Clinical Presentation.)

Ocular signs occur in approximately 10% of psoriasis patients, and they are more common in men than in women. Patients with ocular findings almost always have psoriatic skin disease; however, it is rare for the eye to become involved before the skin. [7]

The diagnosis of psoriasis is clinical. (See Workup.) Management of psoriasis may involve topical or systemic medications, light therapy, stress reduction, climatotherapy, and various adjuncts such as sunshine, moisturizers, and salicylic acid. (See Treatment and Management.)

For more information, see the following:

Psoriasis is a complex, multifactorial disease that appears to be influenced by genetic and immune-mediated components. This is supported by the successful treatment of psoriasis with immune-mediating, biologic medications.

The pathogenesis of this disease is not completely understood. Multiple theories exist regarding triggers of the disease process including an infectious episode, traumatic insult, and stressful life event. In many patients, no obvious trigger exists at all. However, once triggered, there appears to be substantial leukocyte recruitment to the dermis and epidermis resulting in the characteristic psoriatic plaques.

Specifically, the epidermis is infiltrated by a large number of activated T cells, which appear to be capable of inducing keratinocyte proliferation. This is supported by histologic examination and immunohistochemical staining of psoriatic plaques revealing large populations of T cells within the psoriasis lesions. One report calculated that a patient with 20% body surface area affected with psoriasis lesions has around 8 billion blood circulating T cells compared with approximately 20 billion T cells located in the dermis and epidermis of psoriasis plaques. [8]

Ultimately, a ramped-up, deregulated inflammatory process ensues with a large production of various cytokines (eg, tumor necrosis factor-α [TNF-α], interferon-gamma, interleukin-12). Many of the clinical features of psoriasis are explained by the large production of such mediators. Interestingly, elevated levels of TNF-α specifically are found to correlate with flares of psoriasis.

One study adds further support that T-cell hyperactivity and the resulting proinflammatory mediators (in this case IL-17/23) play a major role in the pathogenesis of psoriasis. [9]

Key findings in the affected skin of patients with psoriasis include vascular engorgement due to superficial blood vessel dilation and altered epidermal cell cycle. Epidermal hyperplasia leads to an accelerated cell turnover rate (from 23 d to 3-5 d), leading to improper cell maturation.

Cells that normally lose their nuclei in the stratum granulosum retain their nuclei, a condition known as parakeratosis. In addition to parakeratosis, affected epidermal cells fail to release adequate levels of lipids, which normally cement adhesions of corneocytes. Subsequently, poorly adherent stratum corneum is formed leading to the flaking, scaly presentation of psoriasis lesions, the surface of which often resembles silver scales.

Conjunctival impression cytology demonstrated a higher incidence of squamous metaplasia, neutrophil clumping, and nuclear chromatin changes in patients with psoriasis. [10]

Psoriasis involves hyperproliferation of the keratinocytes in the epidermis, with an increase in the epidermal cell turnover rate. (See Pathophysiology.) The cause of the loss of control of keratinocyte turnover is unknown. However, environmental, genetic, and immunologic factors appear to play a role.

Many factors besides stress have also been observed to trigger exacerbations, including cold, trauma, infections (eg, streptococcal, staphylococcal, human immunodeficiency virus), alcohol, and drugs (eg, iodides, steroid withdrawal, aspirin, lithium, beta-blockers, botulinum A, antimalarials). One study showed an increased incidence of psoriasis in patients with chronic gingivitis. Satisfactory treatment of the gingivitis led to improved control of the psoriasis but did not influence longterm incidence, highlighting the multifactorial and genetic influences of this disease. [11]

Hot weather, sunlight, and pregnancy may be beneficial, although the latter is not universal. Perceived stress can exacerbate psoriasis. Some authors suggest that psoriasis is a stress-related disease and offer findings of increased concentrations of neurotransmitters in psoriatic plaques.

Patients with psoriasis have a genetic predisposition for the disease. The gene locus is determined. The triggering event may be unknown in most cases, but it is likely immunologic. The first lesion commonly appears after an upper respiratory tract infection.

Psoriasis is associated with certain human leukocyte antigen (HLA) alleles, the strongest being human leukocyte antigen Cw6 (HLA-Cw6). In some families, psoriasis is an autosomal dominant trait. Additional HLA antigens that have shown associations with psoriasis and psoriatic subtypes include HLA-B27, HLA-B13, HLA-B17, and HLA-DR7. [12]

A multicenter meta-analysis confirmed that deletion of 2 late cornified envelope (LCE) genes, LCE3C and LCE3B, is a common genetic factor for susceptibility to psoriasis in different populations. [13]

Obesity is another factor associated with psoriasis. Whether it is related to weight alone, genetic predisposition to obesity, or a combination of the 2 is not certain. Onset or worsening of psoriasis with weight gain and/or improvement with weight loss is observed.

Evidence suggests that psoriasis is an autoimmune disease. Studies show high levels of dermal and circulating TNF-α. Treatment with TNF-α inhibitors is often successful. Psoriatic lesions are associated with increased activity of T cells in the underlying skin.

Psoriasis is related to excess T-cell activity. Experimental models can be induced by stimulation with streptococcal superantigen, which cross-reacts with dermal collagen. This small peptide has been shown to cause increased activity among T cells in patients with psoriasis but not in control groups. Some of the newer drugs used to treat severe psoriasis directly modify the function of lymphocytes.

Also of significance is that 2.5% of those with HIV develop worsening psoriasis with decreasing CD4 counts. This is paradoxical, in that the leading hypothesis on the pathogenesis of psoriasis supports T-cell hyperactivity and treatments geared to reduce T-cell counts help reduce psoriasis severity. This finding is possibly explained by a decrease in CD4 T cells, which leads to overactivity of CD8 T cells, which drives the worsening psoriasis. The HIV genome may drive keratinocyte proliferation directly.

HIV associated with opportunistic infections may see increased frequency of superantigen exposure leading to similar cascades as above mentioned.

Guttate psoriasis often appears following certain immunologically active events, such as streptococcal pharyngitis, cessation of steroid therapy, and use of antimalarial drugs.

ampicillin til salg skilte