SPC Kimuras disease as presentation of head and neck tumor.
Two cases report. 2002/1/15 SPC Case1 ** 40 y/o, male DM(-), HTN(-) , Betel nut(+), smoking(+),
Alcohol Drinking(+) Occupation: Family history: non-contributory SPC Chief complain: Bilateral multiple infra-auricular movable, elastic, non-tender progressive enlargement mass noted more than 5 years. SPC Present illness: This 40 y/o male patient is a case of multiple neck mass over bilateral infra-auricular area noted for 5 years. The tumor grew larger slowly. He first visited our OPD at Aspiration and neck CT were done at OPD. Reactive hyperplasia of lymph node was noted. And patient lost of follow up after that. SPC He visited our OPD again at Bilateral multiple infra-auricular mass noted. He was admitted on and received right superficial parotidectomy with deep lobe tumor enucleation. Pathology revealed Kimuras disease. Left infra-auricular mass grew larger progressively. So he received left superficial parotidectomy on And regular follow up at our OPD. SPC Physical Examination:
Left infra-auricular tumor 1*1-2 cm in size three movable, elastic, non-tender tumor. SPC 90-4-3 Arranged Neck CT with contrast. SPC 90-4-2 OP procedure and OP finding
Right superficial parotidectomy and deep lobe tumor enucleation. One infra-auricular tumor over parotid gland was hardly dissected from peripheral tissue. Deep lobe tumor was removed piece by piece. OP procedure and OP finding Left superficial parotidectomy Two infra-auricular tumor over parotid gland, ill-defined margin, hard to dissected from peripheral tissue. SPC Lab data 90.4.2: Hct Hgb MCH MCHC MCV PLT RBC 41.4 14.7 30.3 35.5
85 21.7 485 WBC Eosin Lym Mono Seg 6600 11 38 4 47 BUN Cr GOT GPT Na K Cl 18 0.8 17 13 140 4.7 112 SPC 90-10-21 Hct Hgb MCH MCHC MCV PLT RBC 42.7 14.3 29 33.5 87 24.6
493 WBC Eosin Lym Mono Seg 7700 11 37 8 44 BUN Cr GOT GPT Na K Cl 13 0.8 15 139 4.1 112 SPC Post OP OPD follow up:
Two recurrent tumor 1*1 cm in size, movable, elastic, non-tender neck mass over right infra-auricular area, and two 1*1 cm movable, elastic, non-tender mass over left infra-auricular area. Post-OP treatment: Low dose steroid therapy begun at Dec. Preson 5 mg3# bid*1 week, 2#bid*14 days 1#bid*14 days. SPC Post OP lab. Data follow up 90-12-14 Hct Hgb MCH MCHC MCV PLT RBC
42.0 14.5 29.0 34.5 84 25.3 500 WBC Eosin Lym Mono Seg 6000 18 37 7 IgE 3640 SPC Case 2 ** 52 y/o male DM(-) HTN(-), betel nut(+) ,smoking(+), Alchol drinking(+) Occupation: Family history: non-contributory. SPC Chief complain: Snoring, sleep apnea symptoms noted for years. SPC Present illness: This 52 y/o male patient suffered from snoring, sleep apnea symptoms for years. He received LAUP at hospital 4 years ago. But the symptoms relapse in recent 1 year.So he visited our OPD. SPC Physical examination:
A 5*4*3 cm firm, bulging, non-tender tumor mass over soft palate was noted. Mullers maneuver: Soft palate level: 4+ Tongue base:4+ Hypopharyngeal wall:2+ SPC admission. CT with contrast and MRI with contrast were done at and Polysomnography was arranged on night. Aspiration cytology was done on 11/14 Cytology: suspicious malignancy. Sleep data: RDI:64.4/h Sever OSAS. Sleep fragmentation SPC 90-11-14 Hct Hgb MCH MCHC MCV PLT RBC 43.4 14.7 31 33.9 92 24.5
474 WBC Eosin Lym Mono Seg 8100 42 19 6 32 BUN Cr GOT GPT Na K Cl 16 1.1 13 142 4.3 105 SPC 90-11-16 OP procedure and OP finding
Intra-operative soft palate tumor incisional biopsy. Pathology: Lymphoid hyperplasia Soft palate tumor total excision with blunt dissection, tumor hardly dissected from peripheral tissue. UPPP was done after tumor excision. SPC Post OP OPD follow up:
The central incision line of soft palate necrosis. A bulging tumor over right soft palate noted at and local injection with 5 ml diprospan was done at OPD. Post-OP treatment: Low dose steroid therapy begun at Nov. Preson 2#bid*1 month. SPC Post OP lab. Data follow up 90-12-14 Hct Hgb MCH MCHC MCV PLT RBC
40.4 13.2 31.7 32.7 97 32.8 417 WBC Eosin Lym Mono Seg 9700 1 11 7 81 IgE 6748 Kimuras disease Introduction:
Kimuras disease (KD) is a rare entity causing subcutaneous swelling of the head and neck. Benign lymph node enlargement with eosinophilic infiltrate were first described in China in In 1948 Kimura describing an unusual granulation and hyperplastic changes of lymphatic tissue and the disease known as Kimuras disease (KD). Kimuras disease The typical presentation is in a young oriental male with nontender subcutaneous swelling in the head and neck region, predominately in the preauricular and submandibular areas. Rare cases report in orbital scalp, skeletal muscle and prostate gland. Lymphadenopathy, peripheral eosinophilia and elevated serum IgEwere noted. The systemic manifestation is renal involvement and nephotic syndrome in up to 60% of patient. Kimuras disease KD differential diagnosis: Angiolymphoid hyperplasia with eosinophilia (ALHE). Kaposis sarcoma, tuberculosis, nodal metastasis (breast and rectal cancer), eosinophilc granuloma, harmatoma, lymphoma, lymphocytoma, epitheliod hemagioma, angiofollicular hyperplasia, low grade angiosarcoma, parotid tumor . Kimuras disease The etiology of Kimuras disease: unknown
Immune reaction, atopic reaction to continuous antigenic stimulus( Candida albicans). C. albicans may be the agent responsible for the peripheral blood eosinophilia and eosinophilic infiltrate into lymph nodes. Kimuras disease C.albican never be isolated in lesion of KD..
The disease may be caused by the absorption of soluble substance rather than the growth of the fungus. Specific IgE antibody to C. albican in patient with KD, and a positive skin reaction to Candida have been identified Kimuras disease The mechanism of renal disease: Elevated serum IgE , lymph proliferation and eosinophilia all account for glomerulopathy. MGN, MCD, DPGN, MPGN have been demonstrated on renal biopsy in patient with proteinuria. IgE deposites along the glomeruli resulting in proteinuria. IgE deposites along the capillary wall and paramesangial area been noted. Marked podocyte detachment and epithelial bleb formation. Elevated IgE and eosinophilia noted in active GN, regression of proteinuria is seen with control of the allergic state. Kimuras disease Treatment:
Surgical excision is the most common diagnostic measure and is often also therapeutic. 2. Systemic steroid therapy, radiotherapy, and observation. The recurrence is common, occurring in upon to 25% of cases treated with surgical excision alone. 3. Recurrent mass may be managed with steroid therapy, starting on high dose of prednisone. Kimuras disease Concern for secondary malignancy limited the use of radiotherapy. However, 80% control with 25 to 30 Gy of local irradiation has been reported. Secondary malignancy in field irradiated for KD has not been reported. Indication of radiotherapy: mass refratory to steroid therapy, tumor relapse after steroid withdrawal. The advantage of radiotherapy is that it offset the need of long term steroid. Renal function regular follow up by nephrologist, bimonthly 24 hours urine protein excretion. Kimuras disease The purpose of reporting this two case and Kimuras disease is to draw attention to this disease, as its presentation could easily cause it to be confused with malignancies.