MINISTRY OF HEALTH OF UKRAINE

IVANO – FRANKIVSK NATIONAL MEDICAL

UNIVERSITY
Dermatology and Venerology Department

CASE HISTORY
PSORIASIS VULGARIS

Student’s name :- Abhishek Kumar

Faculty :- Medicine
Course:- IV Group:- 59H+
Teacher’s name :- Miner Halyna Yevhenivna

☆☆☆ IFNMU 2022 ☆☆☆

I. PASSPORT DATA
1. Name and surname of the patient:- Vivek Daruwala
2. Age :- 35
3. Sex :- Male
4. Education :- Graduate
5. Address :- Bellevue Square, Ghatkopar, Mumbai
6. Work place, occupation :- G. B. Road, Hotel Manager
7. Date of hospitalization :- 22/02/2022
8. Diagnosis:
8.1Diagnosis during hospitalization :- Psoriasis Vulgaris

8.2 Final diagnosis :- Psoriasis Vulgaris

II. PATIENT’S COMPLAINTS

The patient is referred from outpatient clinic to a hospital dermatology
department with well dermacated erythematous scaly annular plaques,
scattered on his trunk, face and scalp, often covered with silver-colored
scales.
 These plaques are itchy and painful, and they sometimes crack and bleed. In
some cases, the plaques grow and merge, covering large areas.
Disorders of the fingernails and toenails, including discoloration and pitting
of the nails. The nails also crumble or detach from the nail bed.

III. ANAMNESIS OF THE DISEASE

The patient had suffered from psoriasis for the past 6 years. During this
time he was under the care of a general practitioner who treated his
psoriasis with oral and topical steriods- without any improvement.
Following these 10 years of treatment without relief the patient was referred
to specialist care. At the Dermatology outpatient department of a tertiary
hospital the patient was started on different topical therapies which included
Dovonex ointment, a synthetic Vitamin D3 derivative, and UV
phototherapy. However, despite months of follow ups and treatment
adjustments he still remained poorly controlled. Now at his 12 month visit
he has been admitted to hospital due to a severe flare up of psoriasis. He has
been initiated on topical Anthralin (dithranol) in addition to his current
treatment while continuing UV phototherapy.

IV. ANAMNESIS OF LIFE

Past Medical History - No history of joint pain or stiffness.

Past Surgical History - Nil

Family History -

Father- hypertension on treatment

Mother- well

No family history of psoriasis or arthritis

Allergies - None known

Medication - Dithranol, Salicylic acid, Dovonex and UV phototherapy

Social History - Non smoker, No alcohol or illicit drug use

V. GENERAL OBJECTIVE CONDITION OF THE PATIENT
Appearance: Ambulatory male, awake, alert and co- operative
Vitals: Temperature: afebrile
Blood pressure: 132/76
Heart rate: 75
Respiratory rate: 16
No palpable lymph nodes, jaundice, pallor or oedema
Chest : Chest clear
Cardiovascular : Normotensive, No murmurs, no added heart sounds
Abdomen : No distension or tenderness. Bowel sounds present.
Neurological : Normal level of consciousness, alert and co-operative.
Gait, power, tone, sensation and reflexes intact and
functioning within normal limits.
Musculoskeletal : No swellings, no effusions, no tenderness
No joint deformities. Normal range of motion in all joint

V. DESCRIPTION OF LOCUS MORBI

Scattered erythematous medium-large plaques on chest, upper back, lower

limbs, thighs, scalp and face, with silvery scaling.
 Flexural involvement.
Positive Auspitz sign (capillary bleeding occurring after overlying scale
removed)
PASI score (psoriasis area severity index) was E3 S3I3, indicating that
erythema, scale and induration were all severe, with BSA (body surface
area of >25%). The PASI is a measure of overall psoriasis severity and
coverage that assesses body surface area, erythema and scaling.
Scalp lesions extended to the face.
Several lesions on the upper back were tumour-like

VI. PRELIMINARY DIAGNOSIS

Skin sections show a heavy neutrophilic crust with both hyperkeratosis and
parakeratosis overlying a spongiotic and acanthotic epidermis. There is
chronic inflammatory infiltrate of lymphocytes and scattered neutrophils in
the superficial dermis, but no lichenoid infiltrate noted. These histologic
features are in keeping with Psoriasis.

VII. RESULTS OF LABORATORY OR SPECIAL TESTS :-

Skin Biopsy : Due to the unusual morphology of some of his lesions on the upper
back, being tumour like, a skin biopsy was performed to exclude Mycoses Fungoides
(MF), but the skin biopsy confirmed Psoriasis

VIII. DIFFERENTIAL DIAGNOSIS

VIII. FINAL DIAGNOSIS
On the basis of information from complaints,Anamnesis of life. Anamnesis
of disease & physical examination the diagnosis is Psoriasis Vulgaris

IX. ETIOLOGY AND PATHOGENESIS OF THE DISEASE

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.
Environmental factors
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. 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.
Genetic factors
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. [13]
Immunologic factors
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.
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. 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.
 X. TREATMENT

As patient was not tolerating appropriately administered conventional psoriasis

treatment with topicals and phototherapy, he was switched to systemic treatment
using Triamcinolone acetone and calcitrioli ointments. He was also started on Folic
Acid supplements

XI. PRESCRIPTIONS
i) Rp: Ung. Triamcinolone acetone 0.1%
Da. Signa. Apply a thin film 2-4 times daily
ii) Rp: Calcitrioli 0.0003%

Da. Signa. Apply on affected areas.

XII. PROGNOSIS FOR THE PATIENT

Although psoriasis is usually benign, it is a lifelong illness with remissions
and exacerbations and is sometimes refractory to treatment. It progresses to
arthritis in about 10% of cases. About 17-55% of patients experience
remissions of varying lengths.
Mild psoriasis does not appear to increase risk of death. However, men with
severe psoriasis died 3.5 years earlier compared with men without the
disease. Women with severe psoriasis died 4.4 years earlier compared with
women without the disease.
Psoriasis is associated with smoking, alcohol, metabolic syndrome,
lymphoma, depression, suicide, potentially harmful drug and light therapies,
and possibly melanoma and nonmelanoma skin cancers.
XIII. PREVENTION AND MANAGEMENT
Diet
Ample literature suggests that weight loss can help psoriasis, but other attempts
to show improvement with more specific diets, such as a gluten-free diet, are
less conclusive. Studies of very-low-calorie diets and the “Mediterranean Diet"
have both shown improvement in anecdotal reports and small studies. [53, 54]
Nutritional supplements have shown limited benefit, with the exception of fish
oil. [55] Vitamin D itself has also been reported to be of benefit in small
studies. [56] Much more work needs to be done before enthusiastic support of
any particular supplement or dietary plan may be offered.
 Activity
Any restrictions on activity would relate to concomitant arthritis and how well
it is being controlled. Natural sunlight can help psoriasis and may explain why
it is relatively rare on the face. It has been suggested that a more active lifestyle
can help psoriasis, but whether this is an independent factor or more related to
better weight control is less certain.

Prevention
No specific strategies prevent psoriasis, although healthy lifestyles that avoid
obesity and reduced alcohol use can make control easier and increase the
chances of at least temporary remission. Whenever possible, patients who are
currently being treated for psoriasis or have a history of psoriasis should avoid
over-the-counter and prescription medications known to exacerbate it. This
includes the use of over-the-counter NSAIDs such as ibuprofen and naproxen.
XIV. REFERENCE
- Lectures.
- Stepanenko V.I., Dermatology, venereology. Textbook 2013. Kyiv, 560 p.

Menter A et al. (2008). Guidelines for the care and management of psoriasis
and psoriatic arthritis. J Am Acad Dermatol ; 58: 826-850

Girolomoni G et al. (2012) Psoriasis: rationale for targeting interleukin-17. Br

J Dermatol. Oct;167(4):717-24

Cai Y et al. (2013). Dermal yo-T cells – A new player in the pathogenesis of
psoriasis. Int Immunopharmacol. Mar 13. pii: S1567-5769(13)00060

Johnston A et al. (2013). Keratinocyte overexpression of IL-17C promotes

psoriasiform skin inflammation. J Immunol. Mar 1;190(5):2252-62.

Jordan CT et al. (2012). Rare and common variants in CARD14, encoding an

epidermal regulator of NF-kappaB, in psoriasis. Am J Hum Genet. May
4;90(5):796-808.