RJ, a 26 year old housewife married since 4 years presented to our out patient gynaecological department with complaints of vulval ulcer with foul smelling discharge since one month.

The patient complained of small break in the upper vagina above the urethral opening one-month back with discharge, which progressively increased in size to around 4 x 4 cm. and expanded towards lower abdomen.
She had a foul smelling discharge and pain at the vulval ulcer site. She had no history of multiple sexual partners, blood transfusion. She was unsure of her husband’s sexual history. She had no history of local vulval trauma, local application of chemicals, and no history of growth initially over the site. She had regular present and past menstrual cycles. She was Gravida 1, Para 1, Living 1; with one FTND, female child of 2 years alive and well. No other significant past history.

On examination, general condition was fair.

Local examination of vulva revealed a vulval ulcer involving the clitoris of 4 x 4 cm size triangular shaped with base, extending upto and involving the mons pubis. The depth of the ulcer was 1 to 1.5 cm only. There was irregular shaggy discharge on the floor of the ulcer and base was firm, indurated and extremely tender.

Pap smear, Per speculum and Per vaginum examination was not possible in view of extreme local tenderness.

She was referred to the skin OPD in view of provisional diagnosis of chanchroid.

The dermatologist gave a clinical diagnosis of phagodenic chanchroid. The Gram stain smear was negative; there was absence of Tzanck cells on smear. She was treated with T. Ciprofloxacin 500 mg. b.d. On follow up 14 days later, the ulcer had not healed but had further extended onto the mons pubis and the lower abdomen. There was presence of friable shaggy necrotic tissue in the floor of the ulcer towards the clitoris. The upper part of the vulva involving the mons pubis and lower abdomen had profuse purulent discharge and edges everted. Inguinal lymph nodes were not palpable. ELISA test for HIV infection was positive (pre- and post-est counselling done); VDRL tests negative for both husband and wife.

The patient was referred back to us for admission and management of non-healing vulval ulcer (Fig. 1). Culture swab report of the vulval discharge showed Pseudomonas aeruginosa (Gram negative bacilli) sensitive to Ciprofloxacin and Amikacin. Patient was started on Injection Amikacin 500 mg. i.v. o.d. and local dressing twice a day. After the control of local infection, surgical debridement of the wound was done and biopsy obtained from the edges of the ulcer, send for histopathological examination. The wound infection was controlled and then secondary suturing of the wound was done.

Fig. 1 : Non-healing vulval ulcer involving the mons pubis with shaggy necrotic slough seen in the floor of the ulcer.	Fig. 2 : Histopathological picture of Squamous cell Ca. of Vulva. The arrow points towards the pearl body which is not completely pink.

The histopathological report could not be obtained on scheduled time before secondary suturing due to technical difficulties. The histopathological report revealed Invasive vulval squamous cell carcinoma (Fig. 2).

On follow up, the ulcer had healed completely on suture removal done on day 12. Patient was referred to Tata Memorial Hospital for further management, where she failed to follow up for further treatment due to social reasons and HIV positivity.

Young age at presentation, HIV positivity, vulval ulcer extending onto the mons pubis and lower abdominal wall causing infective necrosis of tissue over mons pubis are important determinants in this case.

Carcinoma of the vulva is usually an uncommon disease commonly seen in elderly postmenopausal women in the sixties and rarely observed in women younger than 30 years of age.3

Association of HIV infection and predisposition of HIV infected women (immunocompromised state) to malignancies makes an important link predisposing these very young women to vulval cancer.

The cause of vulval cancer is unknown but it is reasonable to suppose that any long standing irritative agent, chemical, infective or mechanical, especially if combined with poor hygiene, can be an aetiological factor.4

Spread of vulvar carcinoma by continuity occurs to the vagina, urethra, and rectum. Spread to the skin over mons pubis has not been reported. In our case, spread to mons pubis was seen.5

Clitoral lymphatic drainage occurs partly through lymphatic channels over the symphysis pubis to external iliac nodes, or along the dorsal vein of clitoris to the obturator lymph nodes. However, implantation of malignant cells along the course of lymphatics carrying them does not occur in vulvar carcinoma, unlike melanoma. Thus it could not have been the mechanism of involvement of the skin over the mons pubis.5

Primary carcinoma of the vulva is characteristically a disease of the seventh and eighth decades of life but the average age of patients in whom it is preceded by granulomatous disease is about 40 years.6

Our patient’s immunocompromised state predisposed her to vulval cancer though she was young and not having advanced HIV infection. We did not have CD4 levels due to financial constraints and patient did not have any opportunistic infections.

Women who are immunosuppressed because of HIV infection have a high prevalence of multicentric lower genital tract intraepithelial neoplasia and HPV infection and respond poorly to conventional treatment.6 Giaquinto et al has reported carcinoma of the vulva in a 12 year old girl with vertically acquired Human Immunodeficiency Virus Infection.7

A unique feature about our case is its early onset and it healed completely with dressing and secondary suturing although Ca vulva should not have healed. It is likely to grow again. This is first reported case of Ca vulva, which has healed completely in Medline search of world English literature.