Mesenchymal Neoplasms of the Female Genital Tract
Case 5 -
Disseminated Peritoneal Leiomyomatosis
Teri Longacre, Esther Oliva and Robert Soslow
Disseminated peritoneal leiomyomatosis (DPL) is a rare condition characterized by widespread nodules
of histologically benign smooth muscle in the omentum and peritoneum, often numbering in the tens to
hundreds. The nodules are usually small, firm, gray-to-white, and cover the peritoneal surface of the
uterus, uterine ligaments, ovaries, fallopian tubes, small and large intestine, cul de sac, mesentery,
and retroperitoneum, clinically simulating a disseminated malignancy. DPL typically occurs during the
reproductive years and many patients are pregnant at the time of diagnosis. Most cases are discovered
incidentally at laparotomy. The intraoperative appearance of DPL, first described by Willson and Peale
and subsequently recognized as a distinct entity in 1965 by Taubert and colleagues, is so alarming that
an intraoperative pathological examination with frozen section is often requested to exclude abdominal
Despite the alarming appearance, DPL is usually associated with an
indolent clinical course and can be treated conservatively with long-term follow-up. The condition is
rare; less than 150 cases have been reported in the literature.
DPL is most common in women of reproductive age (mean, 37 years), who are pregnant or have a long-term
history of oral contraceptive use or endogenous increased estrogen production. In fact, the initial
description of this condition was in a woman with an estrogen-secreting granulosa cell tumor.
 Rarely, DPL has been reported in postmenopausal women and in
Familial clustering of DPL in association with Raynaud's syndrome and prurigo nodularis affecting male
and female family members has also been reported. 
Most patients have uterine leiomyomas at the time of diagnosis. Ascites may be present. Most
patients are asymptomatic or develop symptoms resembling adenomyosis or endometriosis; an association
with this latter condition has been reported.  The most common presenting symptom is vague
pelvic pressure, although by report, one patient presented with an acute abdomen due to bowel
The development of DPL has been attributed to elevated hormonal stimulation and/or an enhanced
responsiveness to steroid hormones and the nodules in DPL appear to either regress or show no growth once
the hormonal stimulus is removed (cessation of pregnancy, removal of estrogen-secreting ovarian tumors,
etc.). Extensive surgery is not usually recommended, except for symptomatic relief or patients who have
completed childbearing. Despite these recommendations, many patients have been treated with surgical
debulking and total hysterectomy with bilateral oophorectomy. Because of the strong association with
increased hormonal production in some cases, treatment with gonadotropin-releasing hormone agonists
(GnRH) has been advocated. 
Rarely , DPL is associated with a more aggressive clinical course.  Two young
women, both nulligravid and with no history of oral contraceptive use, developed rapidly progressive
abdominal disease and died within a two year period after an initial diagnosis of DPL. One of the cases
was associated with a large unresectable mass at presentation, which exhibited high-grade leiomyosarcoma
on subsequent histologic examination, while the other was interpreted as a histologically low-grade
sarcoma at the time of recurrence.
Eight other patients with sarcomatous transformation
of conditions resembling DPL have also been reported, three of which occurred in men.
In most of these cases, there was no history of exposure to estrogen and only one was
pregnant at the time of diagnosis. None have had associated uterine leiomyomas. In all cases, a large
smooth muscle tumor, 6 to 40 cm in size, exhibiting features of leiomyosarcoma (= cellularity, nuclear
atypia, tumor cell necrosis, increased mitotic index and infiltrative growth) was identified, either at
the initial presentation or within 12 months of initial presentation of DPL.
The mean age of patients with these aggressive forms does not differ significantly from the more
typical DPL (range, 20 to 48 years) although one occurred in a 70-year-old man and another in a
55-year-old postmenopausal woman.
Most die within two years of initial presentation.
Whether these cases represent true sarcomatous transformation of DPL, inadequate sampling and/or
histologically non-informative sarcomatous tumor nodules, or a coincidental occurrence of two independent
smooth muscle processes is not known, but the short interval between diagnosis of DPL and development of
diagnosable sarcoma indicates that the two may represent related, but distinct entities. 
In most cases, the nodules in DPL measure 2 to 3 mm in size, but nodules measuring 3 to 4 cm may occur
and nodules as large as 10 cm have been reported. The cut surface of the nodules is typically that of a
benign smooth muscle neoplasm - and consists of a whorled pattern with no necrosis, hemorrhage or soft,
fleshy foci. Sections typically show histologically benign appearing smooth muscle (= spindle-shaped
cells with elongated blunt-ended nuclei arranged in intertwining bundles); occasionally, foci of
endometriosis or sex cordlike elements are also present.
A case report of
"disseminated adenomyomas" probably represents an extreme example of DPL with endometrial tissue.
 Foci of decidualization in pregnant patients and/or hyalinization may be present. Nuclear
pleomorphism and hypercellularity are absent. Mitotic figures are inconspicuous and if present, number
< 3 MF/10 HPF. The nodules are situated immediately beneath the peritonealized surfaces and
unattached to blood vessels. A single case of possible DPL that was centered on medium-sized blood
vessels has been reported in a postmenopausal woman, but this is not a typical feature of the disease.
Lymph node involvement has been reported. 
DPL expresses desmin, smooth muscle actin and CD10.  In addition, most express ER and PR,
often at higher levels than the corresponding myometrium.
Aggressive variants typically
do not express hormone receptors.
The etiology of DPL is unknown. A metaplastic transformation of the subperitoneal mesenchyme has been
proposed, based on the contribution of this tissue to the formation of the uterine myometrium during
embryogenesis. Cases that also feature endometrium have been compared to miniature uteri. 
The presence of fibroblastic and myofibroblastic tissue and the disposition of the nodules amidst the
decidua in pregnant patients led to the interpretation by Parmley and colleagues that DPL may be a
reparative, fibrosing response rather than a neoplastic smooth muscle process. 
Experimental studies in guinea pigs have demonstrated smooth muscle proliferations similar to DPL in
response to high dose estrogen and progesterone. These proliferations regress following removal of the
hormonal stimulus. 
Clonality has been demonstrated based on non-random X chromosome inactivation patterns. 
Clonality in this setting may reflect metastatic spread from a unicentric disease, or an underlying
predisposition to a specific clonal abnormality, as is seen in some uterine leiomyomas. Cytogenetic
abnormalities involving chromosomes 7, 12, and 18 have also been reported.
Since many cases appear to regress without treatment, complete excision of all nodules is not
indicated as long as the diagnosis has been confirmed, usually by intra-operative frozen section.
Adequate sampling of all large nodules should be performed to exclude potentially more clinically
malignant smooth muscle neoplasms (see Differential Diagnosis), especially in those patients with unusual
clinical features (e.g. older age, absence of exogenous or endogenous hormone exposure, nodules > 2
cm). Despite the apparent hormonal responsiveness of the tumors in DPL, oophorectomy is not indicated.
A variety of other smooth muscle proliferations simulate DPL by virtue of their distribution of
disease. These include leiomyosarcoma, intravenous leiomyomatosis, benign metastasizing leiomyoma,
lymphangioleiomyomatosis, parasitic leiomyoma, and malignant gastrointestinal stromal tumor (GIST). In
most instances, malignant variants are easily excluded and the remaining entities are distinguished on
the basis of a variety of clinical and locational attributes.
Gastrointestinal Stromal Tumor vs DPL
Gastrointestinal stromal tumors (GIST) may on occasion present as multiple nodules dispersed
throughout the abdomen, but they are typically not as diffuse or as widespread as in DPL. 
GIST is usually centered on the bowel wall as opposed to the subperitoneum, but approximately 10% of GIST
are extra-intestinal and present in the omentum, mesentery, retroperitoneum or pelvis. Spindle and/or
epithelioid histology may be present. Since the mitotic index and nuclear atypia are often minimal in
GIST, smooth muscle tumors form the primary differential diagnostic consideration in most cases. DPL is
excluded on the basis of distinctive clinical presentation and absence of CKIT (CD117), whereas 85 to 90%
of GIST express this marker. GIST may contain areas of necrosis, a feature that is conspicuously absent
Benign Metastasizing Leiomyoma vs DPL
Benign metastasizing leiomyoma (BML) is a condition consisting of histologically benign smooth muscle
tumors in the lungs, lymph nodes or abdomen that appear to originate from a benign uterine leiomyoma,
which typically is removed many years prior to the development of extra-uterine disease. 
The distinctions between BML and DPL involve a constellation of clinicopathologic and definitional
features. BML usually presents as one or more pulmonary nodules; when it occurs within the pelvis and
abdomen, there are usually only one or two nodules, the nodules are larger, and they tend to be
distributed near the region of the round ligament or iliac veins. Additional sites of involvement have
included bone, skull base and spine, and heart. A history of previously resected leiomyoma or less
commonly, a concomitant uterine leiomyoma is present in the case of BML.
DPL is usually
discovered incidental to some other procedure, often during pregnancy and is also typically associated
with uterine leiomyoma. In most cases, the differential diagnosis can be resolved by attention to the
clinical and distributional features. However, caution should be exercised during intraoperative
consultation in problematic cases. Some surgeons may not proceed further with a frozen section biopsy
diagnosis of DPL since progression is rare and many cases appear to regress without treatment. On the
other hand, BML, which is persistent, is usually resected.
Metastatic Leiomyosarcoma vs DPL
Because of the extensive disease within the peritoneum, the unwary pathologist may confuse DPL with
metastatic leiomyosarcoma. However, the typical gross appearance of metastatic leiomyosarcoma is that of
large, fleshy and necrotic tumor masses and there is significant cytologic atypia and mitotic activity on
microscopic examination. In addition, in most cases of metastatic leiomyosarcoma there will be a history
of a previously resected leiomyosarcoma or a concomitant, large uterine mass. Metastatic leiomyosarcoma
is often concentrated in the pelvis with distribution in the vicinity of the round ligament and iliac
veins, whereas DPL is scattered throughout the abdomen.  In some instances, the metastatic
nodules may not exhibit characteristic features of malignancy and additional sampling of other nodules,
particularly the larger lesions is required. At least some of the reports of DPL with malignant change
may represent leiomyosarcoma with these histologically non-informative metastases.
Intravenous Leiomyomatosis vs DPL
Intravenous leiomyomatosis (IVL) is another rare and unusual smooth muscle condition that tends to
occur in premenopausal, often parous women.  Characterized by intravenous intrusion of
histologically benign smooth muscle, IVL is notorious for its ability to grow into the right heart,
causing cardiopulmonary insufficiency. When confined to the pelvis, the condition is recognized as
worm-like protrusions of smooth muscle from veins at the parametrial margin of hysterectomy specimens.
The smooth muscle in IVL resembles smooth muscle tumors in the uterus in every respect and may feature
epithelioid, myxoid, and sex cord features.  Patients may be asymptomatic, but more
commonly present with a pelvic mass clinically indistinguishable from a typical uterine leiomyoma. IVL
is treated by complete extirpation of the involved veins. Recurrence is uncommon.
Although IVL has been reported to occur in association with BML, there is no clear association with
Extension into the smaller pelvic veins may simulate the peritoneal distribution of
DPL on initial inspection, but DPL only involves subperitoneal surfaces and invasion or involvement of
the lumens of blood vessels does not occur. As in DPL, uniclonality has been demonstrated.
Rearrangements of the HMGA2 gene have also been reported. 
Retroperitoneal Leiomyosarcoma vs DPL
Malignant smooth muscle tumors of the retroperitoneum may feature less cellularity and cytologic
atypia than those arising in the uterus. Conventional criteria for uterine smooth muscle tumors do not
apply to these neoplasms and recent criteria for malignancy includes mitotic index > 3 MF/50 HPF.
Small, nodular metastases of these tumors may not always demonstrate classic histologic
features of malignancy. A key distinguishing feature is the presence of a large dominant mass in
association with the smaller metastatic nodules in retroperitoneal leiomyosarcoma. Many of these tumors
arise in association with blood vessels, although a vascular origin may be difficult to identify on
histologic examination. Retroperitoneal leiomyosarcoma is more common in older age groups. Hormone
receptor expression is often present in retroperitoneal leiomyomas, but is only variably present in the
Parasitic Leiomyoma vs DPL
Pedunculated leiomyomas have been reported to detach from their subserosal point of uterine attachment
due to torsion and necrosis of the pedicle. Reattachment to other sites in the pelvis or omentum then
generates a secondary parasitic vascular supply. This phenomenon, if it occurs at all, is uncommon and
is not associated with the presence of multiple smooth muscle nodules scattered throughout the abdomen.
Typically, there is one or only a few such tumor nodules in parasitic leiomyoma and the nodules are often
larger than those usually seen in DPL. 
Lymphangioleiomyomatosis vs DPL
Lymphangioleiomyomatosis (LAM) is a rare condition occurring in women of reproductive age
characterized by a nodular, often widespread proliferation of myoid cells along lymphatic channels with
involvement of lung and lymph nodes. Sites of affected lymph nodes include mediastinum, retroperitoneum,
and pelvis, where enlarged masses forming lymphangiomas and lymphangiomyomas may be seen. 
Occasionally, uterine involvement is also present.
LAM is usually sporadic but patients
with tuberous sclerosis complex are often affected. The constituent cells are spindle and clear with
epithelioid features. Immunoreactivity for desmin and actin, as well as HMB-45 is present. The
predominant involvement of lymph nodes and association with lymphatic channels distinguishes LAM from
DPL, where the nodules are scattered throughout the peritoneum and associated with the subperitoneum.
Additionally, involvement of pulmonary parenchyma is not a feature of DPL.
Reactive Nodular Fibrous Pseudotumor vs DPL
There are several reactive processes that can present with multiple nodular lesions in the peritoneal
cavity, which have been variously designated as "peritoneal fibrous nodules," "calcifying fibrous
pseudotumor," and "reactive nodular fibrous pseudotumor of the gastrointestinal tract and mesentery".
Histologically, these lesions are characterized by fibrocollagenous nodules composed
of sparse spindle cells within a hyalinized, keloid-type collagen, with or without a chronic lymphocytic
or plasmacellular inflammatory infiltrate. These lesions may occur in men as well as women, and may be
associated with endometriosis when presenting in women during the reproductive years. The nodules in
reactive nodular fibrous pseudotumor are often larger than those usually encountered in DPL and do not
typically express desmin, although expression of CKIT (CD117) has been reported. Often, a prior history
of surgery or peritoneal inflammatory disorder is present.
The presence of multiple leiomyomas in the uterus in conjunction with multiple cutaneous leiomyomas
may occur in the setting of familial leiomyomatosis. Mutations in the fumarate hydratase (FH) gene, an
enzyme involved in the mitochondrial tricarboxylic acid cycle, are associated with an autosomal
dominantly inherited susceptibility to multiple cutaneous and uterine leiomyomas.
cutaneous leiomyomas may be diffuse or segmental and may develop before or after the uterine leiomyomas.
Benign smooth muscle tumors also develop in the skin of affected males. Unlike DPL, no intra-abdominal
involvement has been reported. The leiomyomas are histologically and clinically benign, but a subset of
affected patients develops type II renal cell papillary carcinoma (hereditary leiomyomatosis and renal
A Managerial Approach
Efforts to correctly diagnose and classify neoplasms exhibiting standard smooth muscle
differentiation anywhere in the female genital tract should be directed towards two goals: 1)
distinguishing clinically malignant neoplasms (i.e., leiomyosarcoma) from clinically benign neoplasms
that feature one or more of the following: alternative differentiation (e.g., myxoid or epithelioid),
increased cellularity, marked cytological atypia and necrosis; and 2) distinguishing benign or, at most
clinically indolent, smooth muscle proliferations that involve extrauterine sites, and may produce
morbidity, but only rarely lead to patient death.  These latter proliferations, which are
often incidental findings, either present at high stage or recur after initial presentation at low stage,
but usually have an indolent clinical course, even when recurrence occurs. This group of tumors includes
DPL, intravenous leiomyomatosis, benign metastasizing leiomyoma and lymphangioleiomyomatosis.
Since the criteria for the diagnosis of "leiomyosarcoma" vary depending not only on the
differentiated type (standard versus myxoid versus epithelioid), but also on the primary site (e.g.,
vulva versus uterine corpus versus retroperitoneum), localization is important in the initial assessment
of smooth muscle neoplasms. For all tumors that initially present at an extra-uterine site, the
possibility of metastasis should be considered before applying the diagnostic criteria relevant to that
particular site of presentation. Smooth muscle differentiation should be confirmed and mimics should be
excluded (e.g. GIST, other sarcoma types, high grade carcinoma, and melanoma) with appropriate
immunohistologic stains, when relevant. Whether or not grading leiomyosarcoma in the female genital
tract offers useful prognostic information is debatable. A variety of grading schemes have been
described, most of which rely on mitotic index, cellular atypia and necrosis. If a grade is assigned to
a leiomyosarcoma, the grading scheme used should be explicitly stated in the pathology report.
The treatment for the second group of important, but clinically benign or indolent smooth muscle
tumors differs depending on the diagnosis. The treatment of choice for BML and IVL is complete excision,
while the management of lymphangioleiomyomatosis is directed towards estrogen reduction therapies and
maintenance of pulmonary functioning.  Because of the potentially confusing picture in some
cases of DPL and the partial histologic overlap with morphologically non-informative leiomyosarcoma, the
nodules in DPL must be at least partially excised, with particular attention to the larger nodules.
Extensive sampling of the larger nodules to exclude cellular atypia, necrosis and increased cellularity
should also be performed. Since many cases appear to regress without treatment, it is important to bear
in mind that a frozen section biopsy diagnosis of DPL may not result in complete excision of all nodules.
Despite the apparent hormonal responsiveness of the tumors in DPL, oophorectomy is not indicated.
Women who present with DPL in absence of 1) uterine leiomoymas, 2) exogenous or increased endogenous
estrogen exposure, and 3) hormone receptor expression on immunohistochemical studies should be regarded
as harboring potentially malignant tumors and followed closely. All discrete tumors exceeding 3 to 4 cm
should be excised and extensively sectioned. In addition, any early (= within first year of diagnosis)
recurrence or evidence of progression of disease after estrogen has been decreased should probably be
regarded as a potentially malignant process and such patients should undergo a full evaluation in order
to exclude sarcomatous transformation.  To date, all men with DPL-like presentations have
had a uniformly aggressive clinical course.
Table 1. Differential Diagnosis of Smooth Muscle Proliferations in the Female Genital Tract
| ||DPL ||BML ||IVL ||LAM ||LMS|
|Clinical features ||Pregnancy, steroid hormone exposure ||Prior benign uterine smooth muscle tumor ||Uterine leiomyoma with intravascular protrusion ||Tuberous sclerosis complex may be present ||Uterine or retroperiotenal leiomyosarcoma|
|Site ||Throughout abdomen, subperitoneum ||Uterus, lung, lymph nodes, abdomen ||Uterus, pelvic veins, inferior vena cava, right heart ||Lymphatic channels, lung, lymph nodes of mediastinum, pelvis, retroperitoneum ||Pelvis or retroperitoneum|
|Size ||Usually <2 cm, but larger tumors have been reported ||Variable, but often >2 cm ||Worm-like venous intrusions vary, but may be quite large ||Usually <2 cm, but larger lesions have been reported ||May be large|
|Behavior ||Usually regress ||Recurrence and metastases with prolonged course ||Intravenous extension ||Slowly progressive pulmonary dysfunction ||Recurrences & metastases common with rapid course|
|Mitotic index ||Low ||Low ||Low ||Low ||May be high (<10/10hpf)|
|Cellular atypia ||Absent ||Absent or minimal ||Absent - similar to smooth muscle tumors of uterus ||Spindle and epithelioid (clear) cells ||Usually severe|
|Necrosis ||Absent ||Absent ||Absent ||Absent ||Present|
- Abulafia O, Angel C, Sherer DM, et al. Computed tomography of leiomyomatosis peritonealis disseminata with malignant transformation. Am J Obstet Gynecol 1993;169:52-54.
- Advincula AP, Hernandez JC, Lieberman R. Images in reproductive medicine. Disseminated leiomyomatosis peritonei. Fertil Steril 2005;84:1505-1507.
- Akkersdijk GJ, Flu PK, Giard RW, et al. Malignant leiomyomatosis peritonealis disseminata. Am J Obstet Gynecol 1990;163:591-593.
- Alam NA, Olpin S, Leigh IM. Fumarate hydratase mutations and predisposition to cutaneous leiomyomas, uterine leiomyomas and renal cancer. Br J Dermatol 2005;153:11-17.
- Arif S, Ganesan R, Spooner D. Intravascular leiomyomatosis and benign metastasizing leiomyoma: an unusual case. Int J Gynecol Cancer 2006;16:1448-1450.
- Aterman K, Fraser GM, Lea RH. Disseminated peritoneal leiomyomatosis. Virchows Arch A Pathol Anat Histol 1977;374:13-26.
- Badeloe S, van Geel M, van Steensel MA, et al. Diffuse and segmental variants of cutaneous leiomyomatosis: novel mutations in the fumarate hydratase gene and review of the literature. Exp Dermatol 2006;15:735-741.
- Bekkers RL, Willemsen WN, Schijf CP, et al. Leiomyomatosis peritonealis disseminata: does malignant transformation occur? A literature review. Gynecol Oncol 1999;75:158-163.
- Bergen S, Owen J, Snider WR, et al. Disseminated adenomyomas of the abdominal and pelvic cavities: a case report. Am Surg 1981;47:232-235.
- Brumback RA. Intestinal leiomyomatosis: a variant of leiomyomatosis peritonealis disseminata? Arch Pathol Lab Med 1993;117:7-8.
- Clement PB. Reactive tumor-like lesions of the peritoneum. Am J Clin Pathol 1995;103:673-676.
- Clement PB, Young RH, Scully RE. Intravenous leiomyomatosis of the uterus. A clinicopathological analysis of 16 cases with unusual histologic features. Am J Surg Pathol 1988;12:932-945.
- Due W, Pickartz H. Immunohistologic detection of estrogen and progesterone receptors in disseminated peritoneal leiomyomatosis. Int J Gynecol Pathol 1989;8:46-53.
- Fujii S, Nakashima N, Okamura H, et al. Progesterone-induced smooth muscle-like cells in the subperitoneal nodules produced by estrogen. Experimental approach to leiomyomatosis peritonealis disseminata. Am J Obstet Gynecol 1981;139:164-172.
- Gosh K, Dorigo O, Bristow R, et al. A radical debulking of leiomyomatosis peritonealis disseminata from colonic obstruction: a case report and review of the literature. Am Coll Surgeons 2000;191:212-215.
- Goyle KK, Moore DF, Jr., Garrett C, et al. Benign metastasizing leiomyomatosis: case report and review. Am J Clin Oncol 2003;26:473-476.
- Gyure KA, Hart WR, Kennedy AW. Lymphangiomyomatosis of the uterus associated with tuberous sclerosis and malignant neoplasia of the female genital tract: a report of two cases. Int J Gynecol Pathol 1995;14:344-351.
- Halama N, Grauling-Halama SA, Daboul I. Familial clustering of Leiomyomatosis peritonealis disseminata: an unknown genetic syndrome? BMC Gastroenterol 2005;5:33.
- Hales HA, Peterson CM, Jones KP, et al. Leiomyomatosis peritonealis disseminata treated with a gonadotropin-releasing hormone agonist. A case report. Am J Obstet Gynecol 1992;167:515-516.
- Hendrickson MR, Longacre TA, Kempson RL. Problems in uterine corpus pathology. In: Gershenson DM, Gore M, McGuire WP, Thomas G, Quinn MA, eds. Gynecologic Cancer: Controversies in Management. Philadelphia: Elsevier, 2004.
- Hendrickson MR, Longacre TA, Kempson RL. The uterine corpus. Evaluation of endometrial and myometrial specimens. In: Mills SE, ed. Sternberg's Diagnostic Surgical Pathology. New York: Lippincott Williams and Wilkins, 2004.
- Hsu YK, Rosenshein NB, Parmley TH, et al. Leiomyomatosis in pelvic lymph nodes. Obstet Gynecol 1981;57:91S-93S.
- Kitazawa S, Shiraishi N, Maeda S. Leiomyomatosis peritonealis disseminata with adipocytic differentiation. Acta Obstet Gynecol Scand 1992;71:482-484.
- Koh DM, Burn PR, King DM. Benign metastasizing leiomyoma with intracaval leiomyomatosis. Br J Radiol 2000;73:435-437.
- Kokcu A, Alvur Y, Baris YS, et al. Leiomyomatosis peritonealis disseminata. Acta Obstet Gynecol Scand 1994;73:81-83.
- Kuo T, London SN, Dinh TV. Endometriosis occurring in leiomyomatosis peritonealis disseminata: ultrastructural study and histogenetic consideration. Am J Surg Pathol 1980;4:197-204.
- Lausen I, Jensen OJ, Andersen E, et al. Disseminated peritoneal leiomyomatosis with malignant change, in a male. Virchows Arch A Pathol Anat Histopathol 1990;417:173-175.
- Longacre TA, Hendrickson MR, Kapp DS, et al. Lymphangioleiomyomatosis of the uterus simulating high-stage endometrial stromal sarcoma. Gynecol Oncol 1996;63:404-410.
- Ma KF, Chow LT. Sex cord-like pattern leiomyomatosis peritonealis disseminata: a hitherto undescribed feature. Histopathology 1992;21:389-391.
- Nam MS, Jeon MJ, Kim YT, et al. Pelvic leiomyomatosis with intracaval and intracardiac extension: a case report and review of the literature. Gynecol Oncol 2003;89:175-180.
- Nguyen GK. Disseminated leiomyomatosis peritonealis: report of a case in a postmenopausal woman. Can J Surg 1993;36:46-48.
- Paal E, Miettinen M. Retroperitoneal leiomyomas: a clinicopathologic and immunohistochemical study of 56 cases with a comparison to retroperitoneal leiomyosarcomas. Am J Surg Pathol 2001;25:1355-1363.
- Parmley TH, Woodruff JD, Winn K, et al. Histogenesis of leiomyomatosis peritonealis disseminata (disseminated fibrosing deciduosis). Obstet Gynecol 1975;46:511-516.
- Quade BJ, Dal Cin P, Neskey DM, et al. Intravenous leiomyomatosis: molecular and cytogenetic analysis of a case. Mod Pathol 2002;15:351-356.
- Quade BJ, McLachlin CM, Soto-Wright V, et al. Disseminated peritoneal leiomyomatosis. Clonality analysis by X chromosome inactivation and cytogenetics of a clinically benign smooth muscle proliferation. Am J Pathol 1997;150:2153-2166.
- Rivera JA, Christopoulos S, Small D, et al. Hormonal manipulation of benign metastasizing leiomyomas: report of two cases and review of the literature. J Clin Endocrinol Metab 2004;89:3183-3188.
- Rubin BP. Gastrointestinal stromal tumours: an update. Histopathology 2006;48:83-96.
- Rubin SC, Wheeler JE, Mikuta JJ. Malignant leiomyomatosis peritonealis disseminata. Obstet Gynecol 1986;68:126-130.
- Saglam EA, Usubutun A, Kart C, et al. Reactive nodular fibrous pseudotumor involving the pelvic and abdominal cavity: a case report and review of literature. Virchows Arch 2005;447:879-882.
- Sharma P, Chaturvedi KU, Gupta R, et al. Leiomyomatosis peritonealis disseminata with malignant change in a post-menopausal woman. Gynecol Oncol 2004;95:742-745.
- Taubert HD, Wissner SE, Haskins AL. Leiomyomatosis Peritonealis Disseminata; an Unusual Complication of Genital Leiomyomata. Obstet Gynecol 1965;25:561-574.
- Tomlinson IP, Alam NA, Rowan AJ, et al. Germline mutations in FH predispose to dominantly inherited uterine fibroids, skin leiomyomata and papillary renal cell cancer. Nat Genet 2002;30:406-410.
- Torres VE, Bjornsson J, King BF, et al. Extrapulmonary lymphangioleiomyomatosis and lymphangiomatous cysts in tuberous sclerosis complex. Mayo Clin Proc 1995;70:641-648.
- Valente PT. Leiomyomatosis peritonealis disseminata. A report of two cases and review of the literature. Arch Pathol Lab Med 1984;108:669-672.
- Weiss SW. Smooth muscle tumors of soft tissue. Adv Anat Pathol 2002;9:351-359.
- Willson JR, Peale AR. Multiple peritoneal leiomyomas associated with a granulosa-cell tumor of the ovary. Am J Obstet Gynecol 1952;64:204-208.
- Yamaguchi T, Imamura Y, Yamamoto T, et al. Leiomyomatosis peritonealis disseminata with malignant change in a man. Pathol Int 2003;53:179-185.
- Yantiss RK, Nielsen GP, Lauwers GY, et al. Reactive nodular fibrous pseudotumor of the gastrointestinal tract and mesentery: a clinicopathologic study of five cases. Am J Surg Pathol 2003;27:532-540.