Psoriasis.Care & specialists in Bangladesh

Classic plaque psoriasis appears as well-demarcated, raised red patches covered with thick silvery-white scale, typically symmetric on the elbows, knees, scalp, and lower back. The patches are usually round or oval, can range from coin-sized to large continuous plaques, and may itch, burn, or crack. Nail pitting and scalp scaling beyond the hairline are common.

No. Psoriasis is an immune-mediated genetic disease, not an infection. You cannot pass it to others through skin contact, sharing clothes, or any other means. Genetic susceptibility is responsible for clustering in families.

Eczema causes intensely itchy, ill-defined patches that favor flexural areas (insides of elbows and knees) and usually starts in childhood. Psoriasis causes sharply demarcated plaques with thick silvery scale that favor extensor surfaces and most often starts in adolescence or adulthood. The scale is thicker and more silvery in psoriasis; itch dominates eczema.

There is no permanent cure for psoriasis, but it can be controlled extremely well. Modern biologic therapies achieve 90-100% skin clearance (PASI 90 or PASI 100) in 60-85% of moderate-to-severe patients within 16 weeks, and continuous therapy maintains near-clearance for many years.

Common triggers include streptococcal throat infections, stress, skin trauma (the Koebner phenomenon), cold dry weather, smoking, alcohol, certain medications (beta-blockers, lithium, antimalarials, NSAIDs), and abrupt withdrawal of systemic steroids. Each patient often identifies a personal set of triggers over time.

Yes. About 30% of psoriasis patients develop psoriatic arthritis, usually 5-10 years after skin onset but sometimes before. It causes morning stiffness lasting more than 30 minutes, swollen sausage-shaped fingers (dactylitis), tenderness where tendons attach to bone (enthesitis), and asymmetric joint pain. Early rheumatology referral helps prevent permanent joint damage.

Biologics are injectable proteins that block specific immune signals driving psoriasis. The most effective newer classes target IL-17 (secukinumab, ixekizumab, brodalumab, bimekizumab) or IL-23 (guselkumab, risankizumab, tildrakizumab). They achieve PASI 90 in 60-85% of moderate-to-severe patients at week 16, far higher than older systemic agents.

Yes, substantially. Heritability is roughly 60-70%, and the strongest risk allele is HLA-Cw0602. If one parent has psoriasis the child has about a 16% lifetime risk; if both parents are affected the risk approaches 50%. Environmental triggers determine when and how severely it manifests.

Diet is not a primary cause, but obesity worsens severity and reduces response to treatment. Weight loss of 5-10% measurably improves skin disease in overweight patients. Mediterranean-style eating patterns and limiting heavy alcohol intake are associated with better disease control.

Scalp psoriasis carries thicker scale than skin elsewhere because the scalp grows hair-related keratinocytes more rapidly, and the scale traps inflammatory mediators close to nerve endings. Medicated shampoos containing salicylic acid, coal tar, or ketoconazole reduce scale, and topical clobetasol or calcipotriene solutions or foams reduce itch and inflammation.

Yes. Roughly one-third of psoriasis cases begin before age 20, with a peak between ages 15-20. Guttate psoriasis after streptococcal pharyngitis is particularly common in children and adolescents. Pediatric dermatology has dedicated topical, phototherapy, and biologic options.

Yes. Severe psoriasis raises cardiovascular event risk by roughly 50-70% versus the general population, driven by shared inflammatory pathways and a higher prevalence of metabolic syndrome. Aggressive treatment of skin disease and cardiometabolic risk factors narrows the gap.

Yes. The National Psoriasis Foundation and dermatology societies recommend COVID-19 and other routine vaccinations for psoriasis patients on or off biologics. Live vaccines should be avoided while on most biologics; inactivated and mRNA vaccines are safe and effective.

Controlled UV exposure helps many psoriasis patients, which is why narrowband UVB phototherapy is a mainstay of treatment. Brief regular sun exposure during summer can improve plaques, but sunburn worsens disease through the Koebner phenomenon. Use mineral sunscreen and avoid burning.

PASI stands for Psoriasis Area and Severity Index, a 0-72 score that quantifies erythema, induration, scale, and area across four body regions. Treatment responses are reported as PASI 75, PASI 90, or PASI 100 — meaning a 75%, 90%, or 100% reduction from baseline. PASI 90 is the current standard of care benchmark.

Heavy alcohol intake worsens psoriasis severity and reduces treatment response. Moderate intake (up to one drink per day for women, two for men) is acceptable for most patients. Patients on methotrexate should minimize alcohol because of liver-injury risk.

IL-23 and IL-17 inhibitors have a favorable long-term safety profile in five-year and longer follow-up. Main concerns are infection (particularly upper-respiratory and oral candida with IL-17), reactivation of latent tuberculosis (screen and treat first), and rare paradoxical reactions. Routine monitoring with periodic CBC, LFTs, and clinical assessment is standard.

The Koebner phenomenon is the appearance of new psoriasis plaques at sites of skin trauma — scratches, sunburn, surgical incisions, or tattoos — typically 7-14 days after the injury. Around 25-30% of psoriasis patients show it. Avoiding skin trauma during a flare reduces new lesion formation.

Yes. Acute stressful life events precede flares in 40-80% of patients, and chronic stress reduces response to treatment. Cognitive behavioral therapy, mindfulness-based stress reduction, and integrated mental-health support measurably improve disease control.

Nail changes in psoriasis can be reversed with effective treatment, but improvement is slow because fingernails grow only 3 mm per month. Biologics targeting IL-17 or IL-23 are highly effective for nail psoriasis, with substantial improvement typically visible by 6 months. Long-standing severe nail disease may leave residual changes.

Psoriasis is classified as an immune-mediated inflammatory disease rather than a classic autoimmune disease, because no clearly defined self-antigen has been confirmed. The dominant mechanism is dysregulation of the IL-23/Th17 immune axis. The distinction does not change how psoriasis is treated.