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Oriental Kimura’s Disease and its Relation to
Angiolymphoid Hyperplasia with Eosinophilia (ALHE)
Tie-Jun LI 1) and Motoo KITANO 1)

Abstract

Kimura’s disease, a chronic inflammatory condition of unknown cause, is endemic in Orientals. The clinicalfeatures of this disease include young and middle aged male predominance, predilection for the head and neckregions and a long duration. The disease may present as single or multiple lesions, mainly involving subcutaneous
tissues, major salivary glands and lymph nodes in isolation or in combination. Histopathologically, the lesion ischaracterized by hyperplasia of lymphoid tissue with well-developed lymphoid follicles, marked infiltration ofeosinophils, proliferation of thin-walled capillary venules and varying degrees of fibrosis. This paper reviewed thecurrent understanding of this disease and discussed its distinctions to angiolymphoid hyperplasia with eosinophilia(ALHE).
Key words: Kimura’s disease, Angiolymphoid hyperplasia with eosinophilia, Eosinophilic lymphogranuloma,
Lymphadenopathy, Salivary gland, Eosinophils, Eosinophilia

Introduction
Kimura’s disease, a chronic inflammatory condition, often produces subcutaneous tumorlike nodules with a predilection for the head and neck regions. The condition is apparently
more prevalent among Orientals (Kimura et al., 1948; Kawada et al., 1966; Jin & Shi,
1937; Jin et al., 1957; Chang & Chen, 1962; Li, 1988) and often associated with major
salivary glands involvement and regional lymphadenopathy (Leong et al., 1971; Tham etal., 1981; Kung et al., 1984; Urabe et al., 1987; Kuo et al., 1988; Chan et al., 1989; Hui etal., 1989). The majority of the cases had been reported in China and Japan. Similar cases
were also reported from Hong Kong (Tham et al., 1981; Kung et al., 1984; Chan et al.,
1989; Hui et al., 1989), Taiwan (Kuo et al., 1988), Malaysia (Ng et al., 1991) andSingapore (Leong et al., 1971). Angiolymphoid hyperplasia with eosinophilia (ALHE),
however, was first reported in English literature in 1969 as a lesion similar to Kimura’s
disease (Wells & Whimster, 1969). Many authors since then have regarded these two
conditions either as the same entity or as different stages of one disease (Mehregan &Shapiro, 1971; Reed & Terazakis, 1972; Castro & Winkelmann, 1974; Buchner et al., 1980;
1) Department of Oral Pathology, Kagoshima University Dental School, Kagoshima 890, Japan.

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Olsen & Helwig, 1985; Iguchi et al., 1986). ALHE superficially resembles Kimura’s disease because of the similar predilection for the head and neck regions, the frequent recurrence, and the pathologic findings of a vascular lesion accompanied by infiltration of lymphoid cells and eosinophils. However, it has been recently suggested that Kimura’s diseasecan be distinguished from ALHE by clinical, histological and immunohistochemical criteria
and constitutes its own clinical identity (Rosai et al., 1979; Kung et al., 1984; Urabe etal., 1987; Googe et al., 1987; Chan et al., 1989).
In the light of our recent report of 54 cases of Kimura’s disease occurred in mainland
Chinese patients (Li et al., 1996), we intended to have a comprehensive review of theclinical and pathological background of this Asian disease and to discuss its distinctions to
the mainly Western-reported ALHE.

Clinical features of Kimura’s disease
Kimura’s disease usually presents as subcutaneous masses, lymph node enlargement andor swelling of the parotid or submandibular glands, with predilection of head and neckregions in young and middle aged men (Chan et al., 1989; Li et al., 1996). A previous
review (Kawada, 1976) of 194 cases in Japanese literature revealed a male and female ratioof 7:1. A little over one-third of the cases arose in the second decade. The lesion was mostoften solitary but may be multiple. Of the 194 cases, 163 had facial involvement. Other sites
of involvement were the neck (43 cases), axilla (23 cases), groin (35 cases), popliteal
region (40 cases) and forearm (2 cases). Similarly, in a review of 158 cases reported in
Chinese literature since 1937 (Li, 1988), 149 were male and 9 were female. The age of 94
recorded cases ranged from 2 to 59 years with a peak group in the third decade (34 cases).
The disease also showed a predilection for the head and neck regions (86.5％) with occasional occurrences in forearm and inguinal areas. In our recent reported series (Li et al.,1996), the age varied from 1 66 years but peaked at the third and fourth decades (Fig. 1).
There was a male predominance with a male to female ratio of 3.5:1. Multiple lesions weredetected in 23 cases, among those three patients showed bilateral involvement of parotid
glands and one presented with bilateral submandibular glands involvement and inguinal
lymphadnopathy. Kimura’s disease usually presents as a painless subcutaneous swelling.
Skin itchiness, pigmentation only occur in some patients with most cases showing no significant changes of the overlying skin (Li et al., 1996). Deeply seated lesions usually show
no distinct borders, but more superficial lesion or enlarged lymph nodes are welldemarcated. The course of the disease is relatively long and benign, but recurrences arecommon after surgical excision of the lesion. Eosinophilia is almost always present, although there is no systemic visceral involvement. There have been no reported fatalities. In
about 12％ of patients, there may be associated with renal disease, usually presenting asTie-Jun LI and Motoo KITANO : Oriental Kimura’s Disease and its Relation to Angiolymphoid Hyperplasia with Eosinophilia ( ALHE)

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Fig. 1 Age and sex distribution of 47 patients with Kimura’s disease (data taken fromreference Li et al, 1996).

proteinuria and occuring almost exclusively in male patients (Yamada et al., 1982).

Multiple tissue involvement by Kimura’s disease
The disease involves subcutanous tissues, major salivary glands, and lymph nodes inisolation or in combination, chiefly in the head and neck region. Table 1 summarizes thedetailed tissue involvement by Kimura’s disease in our recently reported series (Li et al.,1996). In the soft tissue, the subcutis is the predominant site of involvement, but the contiguous lower and mid dermis, fascia and skeletal muscle could also be involved. Most
lesions have infiltrative borders. However, rare ones are circumscribed, simulating lymph
nodes on low magnification but differing in the absence of sinusoids (Chan et al., 1989).
Involvement of the salivary glands by the disease has been frequently reported (Miyamoto

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Table 1. Clinical features of Kimura’s disease1Sex
42 male, 12 female
Age of diagnosis (47 cases recorded)
1 66 years (mean 33.1 years, peak age at the third decade)Tissue involvement 2
Subcutaneous tissue
Lymph node
Parotid gland
Submandibular gland
Lacrimal gland
Number of lesions
SingleMultiple
Location of lesions
Head and neck (major salivary glands, face, neck,
perauricular and eyelid)
Inguinal3
Axilla3
Forearm3
Duration (51 cases recorded)
One month 13 years (mean 3 years)＜ One year
1 ＜ 5 years
5 10 years＞ 10 years
Size (43 cases recorded)＜ 2 cm in diameter2 5 cm＞ 5 cm1
2
3

29 cases
17 cases
18 cases
3 cases
1 case31 cases
23 cases

54 cases
3 cases
3 cases
1 case15 cases
24 cases
7 cases
5 cases
17 cases
15 cases
11 caese

data adopted from reference (Li et al, 1996)
tissue involvement either in isolation or in combinationfrom cases with multiple lesions& Tani, 1977; Urabe et al., 1987; Li, 1988; Kuo et al., 1988; Chan et al., 1989; Li et al.,1996). In our 54 cases, involvement of salivary glands occurred in 21 patients (39％) and
one patient also showed involvement of lacrimal gland (Li et al., 1996). Clinically andpathologically, the affected glands resemble benign lymphoepithelial lesion of salivary
glands to a certain extent but the latter lesion contains myoepithelial islands andeosinophilic infiltration is absent. Bilateral salivary glands swellings, which had been occasionally reported (Tham et al., 1981; Iguchi et al., 1986; Li, 1988), were found in 4 casesof our present series (Li et al., 1996). Lymphadnopathy in Kimura’s disease has beenreported to range from 42％ to 100％ (Chang & Chen, 1962; Kung et al., 1984; Kuo etal., 1988). Our series revealed a slightly lower incidence of 31.5％ (Li et al., 1996).

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However, it is worth mentioning that there may be cases with early lymphadenopathy which
are free from clinically detectable lymph nodes (Kung et al., 1984). Histopathologicalconfirmation of that can be difficult because in most cases only the clinically positive nodes
are usually available for examination. The frequent involvement of salivary glands andregional lymph nodes in patients with Kimura’s disease quite often leads to an incorrect
clinical impression, such as salivary gland tumors, Mikulicz’s disease and even lymphomas.

Histological features of Kimura’s disease
The basic histologic features are similar in the different tissues and predominantly thoseof hyperplastic lymphoid tissue containing well-developed lymphoid follicles, infiltration ofeosinophils, vascular (capillary) proliferation and varying degrees of fibrosis (Kimura etal., 1948; Kawada et al., 1966; Jin & Shi, 1937; Jin et al., 1957; Chang & Chen, 1962; Li,
1988; Leong et al., 1971; Miyamoto & Tani, 1977; Tham et al., 1981; Kung et al., 1984;
Urabe et al., 1987; Kuo et al., 1988; Chan et al., 1989; Hui et al., 1989; Li et al., 1996).
Lymphoid cells. There is a moderate to massive lymphoid infiltration associated with few
to numerous lymphoid follicles. The lymphoid follicles are round or oval, and possessed
well delineated mantles and prominent germinal centres (Fig. 2a). An interstitial homogeneous eosinophilic material between the germinal centre cells is often present (Fig. 2b).
When infiltrated by eosinophils, some germinal centres appear to undergo progressive
folliculolysis (Fig. 2c), and some show features of the so called "vascularization of thegerminal centres", in which capillary venules grew into the germinal centres (Fig. 2d).
Between the follicles, there are many small lymphocytes, plasma cells and eosinophils,
some immunoblasts, histiocytes and mast cells.
Eosinophils. Moderate to massive infiltration of eosinophils is a consistent feature in
Kimura’s disease, usually showing a diffused pattern in the interfollicular areas or becoming
denser in perivascular areas. Eosinophilic microabscesses are occasionally seen (Fig. 3).
There is also a tendency for eosinophils to infiltrate the germinal centres resulting in necrosis of the centre structures. This phenomenon has been termed as eosinophilic folliculolysis(Fig. 2c; Kuo et al., 1988 ).
Blood vessels. Various degrees of vascular proliferative changes are frequently observed in
the majority of the lesions. However, the blood vessels are usually thin-walled, high endothelial venules. The venules have slit-like lumina, and are lined by either flattened or low
cuboidal endothelium with pale staining oval nuclei. The cytoplasm is scanty and lightstaining, and is never vacuolated (Fig. 4a). Furthermore, perivenular sclerosis in the formof concentric rings of collagen is frequently seen, with the affected venules showing endothelial atrophy (Fig. 4b).

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Fig. 2 Various appearances of lymphoid hyperplasia in Kimura’s disease. The lymphoidtissue usually contains numerous lymphoid follicles with well-formed germinal centers(a, Hematoxylin-eosin stain; x40); In some cases, the germinal centers may contain aninterstitial homogenous eosinophilic material between the germinal center cells (b,Hematoxylin-eosin stain; x50); Some may undergo folliculolysis (c, Hematoxylineosin stain; x60) or ’vascularization’. The latter shows capillary venules growing into
the germinal centre (d, Hematoxylin-eosin stain; x40).

Fibrous tissue. Fibrosis is always present, most prominently in subcutaneous and salivary
gland lesions. The fibrous tissue is poorly cellular, and is either homogeneous or in the form

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Fig. 3 Massive infiltration of eosinophils in the lesion leads to formation of a eosinophilic
microabscess (Hematoxylin-eosin stain; x60).

Fig. 4 a, Proliferated vessels are thin-walled capillaries lined by either flattened or low
cuboidal endothelium. Many eosinophils and plasma cells are present (Hematoxylineosin stain; x120). b, A blood vessel shows concentric fibrosis accompanied withatrophy of endothelial cells (Hematoxylin-eosin stain; 100).
of thick keloid-like bundles with scattered infiltration of plasma cells and eosinophils (Fig.
5). There are frequent fibrous septa partitioning the lesion into irregular nodules. Sclerotic
zones devoid of inflammatory cells are prominent in lesions of long duration. It appears that

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Fig. 5 In advanced lesions, the stroma shows dense collagenous fibrosis with scatteredinfiltration of plasma cells and eosinophils (Hematoxylin-eosin stain; x100).

Fig. 6 The involved parotid gland (a) and submadibular gland (b) show marked infiltration of lymphocytes, plasma cells and eosinophils which resulted in atrophy and lossof acini. The lymphoid follicles often wrap around a small duct (a) and concentric
fibrosis of the residue ducts (b) is commonly seen (Hematoxylin-eosin stain; x40).

the earliest form of sclerosis appeared to begin around the venules, either in the form of athin fibrous sheath or concentric rings of collagen (Fig. 4b). Further sclerosis results inTie-Jun LI and Motoo KITANO : Oriental Kimura’s Disease and its Relation to Angiolymphoid Hyperplasia with Eosinophilia ( ALHE)

295

Fig. 7 In the involved lymph nodes, infiltration of eosinophils is mainly present ininterfollicular areas and marginal sinuses (Hematoxylin-eosin stain; x100).
complete obliteration of the affected venules.
Salivary gland. The paroid or submandibular gland is often involved in a patchy fashion.
Related lesions show irregular areas of inflammation and varying degrees of glandular
destruction. In severe cases, the gland lobules are replaced by fibrous tissue and densely
infiltrated by lymphocytes, plasma cells, mast cells and eosinophils, resulting in atrophy andloss of acini. Concentric periductal fibrosis is common (Fig. 6a). The lymphoid follicles
often appears to wrap around of the residule ducts (Fig. 6b). In less affected salivary
lobules, only ductal dilatation and periductal eosinophilic and lymphocytic infiltration are
seen. The main glandular structures, i.e. acini and ducts, are relatively undamaged.
Lymph node. The architecture of the involved lymph nodes is usually preserved (Fig. 7a).
The enlarged lymph nodes show follicular hyperplasia with large germinal centres and focal
eosinophilic infiltration of interfollicular areas and subcapsular sinuses (Fig. 7b). Similar
to subcutaneous lesions, homogeneous material between the germinal centre cells is often
seen and folliculolysis is often associated with apparent eosinophilic infiltration. Although
not pathognomonic, these nodal changes should alert the pathologist to the possibility of
Kimura’s disease, especially in cases where only the lymph node biopsy specimen is available.

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Etiology of Kimura’s disease
The pathogenesis of Kimura’s disease remains obscure. In view of tissue and blood
eosinophilia, allergy and parasitic infestation were suspected but not proved. Tests for
Paragonimus westermani, Dibothoriocephalus latus, Schistosoma japonicum, Gnathostoma
spinigerum, Wuchereria bancrofti, and for ascariasis and ancylostomiasis are all negative(Tham et al., 1981). Evidence of an insect bite is also not identified (Kawada, 1976). The
deposits of IgE in the germinal centres of Kimura’s disease, the elevated serum IgE,
eosinophilia and the appearance of mast cells suggest that the disease is atopic in nature(Googe et al., 1987; Kuo et al., 1988). It has been proposed that Kimura’s disease is probably an immunologically mediated disorder (Iguchi et al., 1986; Googe et al., 1987; Kuo etal., 1988). Occasional reports of its possible association with systemic nephrotic syndrome(Yamada et al., 1982; Kuo et al., 1988; Matsuda et al., 1992) lend further support for theabove hypothesis. On the other hand, the prevalence of Kimura’s disease in Asian population (Li et al., 1996) and its rarity in the West suggest that racial and or cultural factors
may also contribute to the etiology of this disease.

Distinctions between Kimura’s disease and ALHE
In literature, there is much confusion between Kimura’s disease and angiolymphoid
hyperplasia with eosinophilia (ALHE). The detailed comparisons of the two conditions are
summarized in Table 2.
Since its first description (Wells & Whimster, 1969), ALHE has been widely stated as
the same entity to Kimura’s disease, probably representing the different stages of the disease(Mehregan & Shapiro, 1971; Reed & Terazakis, 1972; Castro & Winkelmann, 1974;
Buchner et al., 1980; Olsen & Helwig, 1985). Clinically, young people are affected by bothlesions and other similarities include predilection for the head and neck regions, a relatively
long course and good prognosis. Furthermore, common histopathological features such as
lymphoid hyperplasia, eosinophilic infiltrates and vascular proliferation suggests these two
diseases are identical. However, several papers have recently argued that theclinicopathologic differences are more than sufficient to justify their separation into two
distinct entities (Rosai et al., 1979; Kung et al., 1984; Urabe et al., 1987; Googe et al.,
1987; Kuo et al., 1988; Chan et al., 1989; Li et al., 1996). There is a male predominancein Kimura’s disease, while patients with ALHE show roughly equal sex distribution (Olsen& Helwig, 1985; Iguchi et al., 1986); The lesions of Kimura’s disease are usually large(about 2 5 cm in diameter) and deeply seated without a distinctive border. Initially, there
is little visible change in the overlying skin. However, the eruptions of ALHE are usuallysmall (about 1 cm in diameter) and superficially located. They form elevated papules orTie-Jun LI and Motoo KITANO : Oriental Kimura’s Disease and its Relation to Angiolymphoid Hyperplasia with Eosinophilia ( ALHE)

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Table 2. Comparison of clinicopathological changes between Kimura’s disease and ALHE
Kimura’s disease
Clinical features
Sex

Male predominance.

ALHE
Overall no sex predilection.

Age

1 80 years (reported mean range 27 40 10.5 80 years (mean 35 years).
years).

Race

Prevalence in Orientals.

Occurs in all races (more frequent in theWest)

Discrete nodules or localized swelling.
Solitary or multiple (bilateral or in multiple regions). Size 1 20 cm, average 3 cm.
Insidious onset, often of long duration(mean range 4 10 years).

Nodules or erythematous papules which
may ulcerate or bleed. Solitary lesion or
multiple lesions clustered in the same region. Size 0.2 1.5 cm, average 1 cm. Of
shorter duration (mean 13 months).

Subcutaneous and deep soft tissue, major
salivary glands, lymph node and sometimes oral cavity. Superficial dermal andvisceral involvement do not occur.
Usually in head and neck region, but caninvolve axilla, groin, limbs and trunk.

Skin, subcutaneous tissue, blood vessel,
and almost any tissue, e.g. muscle, bone,
lymph node, oral cavity, orbit and penis.
Usually in head and neck region.

Regional lymph
node enlargement

Common (over 50％). The lymph nodes
often show histological evidence of involvement.

Uncommon, if enlarged, show reactive
changes only.

Peripheral blood
eosinophilia

Present in majority of cases.

Occurs in about 20％ of cases.

Presentation

Sites

CourseHistological features
OutlineLymphoid
component

Eosinophils

Blood vessels

FibrosisNature of lesion

The course is progressive, often becoming Benign lesion which recurs in about 30％
stationary after years. Recurrence is com- of cases. However, recurrence is rare if
mon (15 40％), but there is no fatality. excision is complete.
Rarely, there may be association with anephrotic syndrome.
Usually non-circumscribed.

Often circumscribed except dermal lesions.

Abundant lymphocytes and plasma cells;
lymphoid follicles are always found, diffusely or patchily distributed throughout
the lesion. Interstitial homogeneous
eosinophilic material between the germinal center cells, vascularization and necrosis of germinal centers are common.

Sparse to heavy infiltrate of lymphocytes
and plasma cells, with or without lymphoid follicles. Vascularization and necrosis of germinal centers are uncommon.

Moderate to abundant; eosinophilic abscesses, some of which occur within germinal centers, are common.
Degree of vascular proliferation (high endothelial venules) does not exceed thatseen in florid lymphoid hyperplasia. No
uncanalized cords. Involvement of wall ofmuscular vessels and intravascular growth
do not occur. Endothelial cells are flat tolow cuboidal and possess oval nuclei withfine chromatin. Cytoplasm scanty andlight-staining
withonvacuoles.
Perivenular sclerosis is common.

Sparse to abundant; eosinophilic abscessis rare.
Florid angiomatous proliferation of capillary-sized vessels to muscular vessels.
Uncanalized
cords
may
occur.
Fibromyxoid matrix commonly present.
Involvement of endothelium and muscularvessels are common; sometimes lesions
are entirely intravascular. Endothelial
cells are cuboidal to dome-shaped, andpossess nuclei with irregular folding.
Cytoplasm moderate in amount anddeeply eosinophilic; vacuoles can often be
found.

Significant at all stages, particularly
prominent in long-standing lesions.

Not a prominent feature.

Primarily chronic inflammatory lesion inwhich there are high endothelial venules.
An aberrant immune response to an unknown stimulus.

Atypical endothelial proliferation, possibly neoplastic, which is associated with avariable inflammatory component.

Note: All data summarized from the references with a ’＊’ mark in the reference list.

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nodules and bleed easily when irritated (Kuo et al., 1988; Chan et al., 1989); The frequentfeature of regional lymph nodes and salivary glands involvement in Kimura’s disease is lessfrequent in ALHE (Wells & Whimster, 1969; Mehregan & Shapiro, 1971; Reed &Terazakis, 1972; Castro & Winkelmann, 1974; Buchner et al., 1980; Olsen & Helwig, 1985;
Iguchi et al., 1986; Chan et al., 1989). Whilst cases identical to ALHE have also beenreported among Orientals (Urabe et al., 1987; Kuo et al., 1988; Chan et al., 1989), theiroccurrences appear to be less common. According to our experience, only one case identicalto ALHE was encountered during the same period when 54 cases of Kimura’s disease werediagnosed (Li et al., 1996).
The most important histopathological difference is in the blood vessel component of thetwo conditions. Vascular changes of Kimura’s disease reveal mainly capillary proliferationand increased number of the thin-walled blood vessels, which never reach the degree of thevascular change described in ALHE. The latter contains thick-walled blood vessels with theso-called histiocytoid or epithelioid endothelial cells characterized by hypertrophied or
vacuolated endothelial cells protruding into the vascular lumen or even occluding the lumen(Wells & Whimster, 1969; Mehregan & Shapiro, 1971; Reed & Terazakis, 1972; Castro &Winkelmann, 1974; Buchner et al., 1980; Olsen & Helwig, 1985; Iguchi et al., 1986). Thisfeature has led some to classify ALHE under the name of "histiocytoid hemangioma"(Rosai et al., 1979; Chan et al., 1989), representing the benign end within a broad spectrumof epithelioid vascular tumors (Tsang & Chan, 1993). While hyperplastic lymphoid follicles with well-developed germinal centres are consistently present in Kimura’s disease,infiltration of lymphocytes is more variable in ALHE lesions, sometimes, without the presence of lymphoid follicles (Tham et al., 1981; Kung et al., 1984; Chan et al., 1989).
Frequent folliculolysis and vascularization of germinal centers in Kimura’s disease are also
uncommon in ALHE (Chan et al., 1989). Fibrosis is prominent at all stages in Kimura’s
disease, but is often absent or only detectable at the edge of the lesion in ALHE (Wells &Whimster, 1969; Reed & Terazakis, 1972). Based on these substantial clinicopathologicaldifferences between the two conditions, we concur with the view that Oriental Kimura’s
disease is different from ALHE.

Conclusion
Kimura’s disease is an important category of chronic inflammatory condition in the
Oriental population. Its frequent involvement of salivary glands, simultaneous multiple
lymphadenopathy and occasional association with the nephrotic syndrome often pose problems in diagnosis and treatment. Furthermore, the rarity of this disease in the Westerncountries helps to obfuscate its relation to the mostly Western-reported angiolymphoid
hyperplasia with eosinophilia (ALHE). Although the precise nature and etiology of bothTie-Jun LI and Motoo KITANO : Oriental Kimura’s Disease and its Relation to Angiolymphoid Hyperplasia with Eosinophilia ( ALHE)

299

conditions are still unknown, the spectrum of the clinicopathological changes suggests that
Kimura’s disease most likely represents an aberrant immune reaction to an unknown stimulus, whereas ALHE might be a vascular neoplastic disease in nature.

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