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1 All authors: Department of Radiology, University of California San Francisco, 505 Parnassus Ave., M372, San Francisco, CA 94143-0628.
Received May 30, 2003;
accepted after revision August 21, 2003.
Address correspondence to B. M. Yeh.
Abstract
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MATERIALS AND METHODS. Seventeen patients with peritoneal calcification were identified through retrospective review of reports from 74,765 abdominopelvic CT examinations performed during a 7-year period. We determined the cause of peritoneal calcification by examining medical and histopathologic records. Calcification morphology was classified as nodular or sheetlike on the basis of the consensus interpretation by two independent radiologists. The radiologists also recorded the presence or absence of associated soft-tissue components or lymph node calcification. The association between the CT findings and the cause of calcification was assessed using chi-square analysis.
RESULTS. Peritoneal calcification was due to peritoneal dialysis (n = 4), prior peritonitis (n = 3), cryptogenic origin (n = 1), or peritoneal spread of ovarian carcinoma (n = 9). Sheet-like calcification was more common in patients with benign calcification (seven of eight patients) than in those with malignant calcification (two of nine patients, p < 0.05). Nodal calcification was seen only in patients with malignant calcification (five of nine patients vs none of eight, p < 0.05).
CONCLUSION. Common causes of peritoneal calcification are dialysis, prior peritonitis, or ovarian cancer; sheetlike calcification indicates a benign cause, whereas associated lymph node calcification strongly suggests malignancy.
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On the basis of this review, 17 patients were considered to have had peritoneal calcification. The final study group consisted of 14 women and three men whose mean age was 54 years (range, 30–83 years). To determine the cause of peritoneal calcification in these patients, two of the authors reviewed all available medical records and recorded pertinent histopathologic and clinical findings, including prior surgery, peritoneal dialysis, peritonitis, or confirmed malignancy (before or after the CT examination). Calcification was considered benign if patients had a history of peritoneal calcification known to have a benign cause and no histopathologic evidence of peritoneal malignancy. Calcification was considered malignant if patients had proven peritoneal carcinomatosis.
CT Technique
CT scans were obtained using helical CT scanners (LightSpeed [n =
8 patients] or HiSpeed [n = 9 patients] General Electric Medical
Systems, Milwaukee, WI). Sixteen patients received 150 mL IV iohexol
(Omnipaque 350, Nycomed Amersham, Princeton, NJ). Sixteen patients received
800 mL oral diatrizoate meglumine (Hypaque, Nycomed Amersham). Two patients
received 250 mL rectal diatrizoate meglumine (Hypaque). Slice collimation was
5 (n = 8), 7 (n = 6), 8 (n = 1), or 10 (n
= 2) mm. All images were contiguous. Indications for CT scanning were
evaluation of abdominal symptoms (n = 7) or of known or suspected
tumor (n = 10). Abdominal symptoms consisted of pain, nausea, or
vomiting.
Image Interpretation and Analysis
Two attending radiologists reviewed all CT scans and made interpretations
by consensus, unaware of clinical or histopathologic findings. The
interpreters classified calcification morphology as nodular (circumscribed and
focal) or sheetlike (flat, curvilinear, and extending along a peritoneal
plane). Both patterns were recorded if simultaneously present in the same
patient. The interpreters also recorded the presence or absence of associated
soft-tissue components and lymph node calcification (Figs.
1A,
1B,
2A,
2B,
3A,
3B). Soft-tissue components
were considered to be present if structures with CT densities of between 20
and 80 H were observed as being contiguous to the calcification without an
intervening fat plane and separate from adjacent organs. The association
between CT findings and cause was assessed using chi-square analysis. A
p value less than 0.05 was considered to be significant.
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Nine patients had malignant peritoneal calcification. In eight of these patients, calcification was due to peritoneal spread of ovarian cancer and in one, it was due to primary papillary serous peritoneal carcinoma. Five of the patients with ovarian cancer had serous cystadenocarcinoma; for three patients, the histopathologic type was unspecified. Lymph node calcification was seen in five (56%) of these nine patients. Eight of the patients had undergone total abdominal hysterectomy, bilateral salpingo-oophorectomy, omentectomy, and lymph node dissection before undergoing CT, and three had received chemotherapy. One patient with malignant peritoneal calcification had previously received radiation therapy, and none of the patients with benign peritoneal calcification had previously received radiation therapy.
Distinction Between Benign and Malignant Peritoneal Calcification
The clinical and CT characteristics of patients with benign and malignant
peritoneal calcification are shown in Table
1. Sheetlike calcification was significantly more common
(p < 0.05) in patients with benign calcification (seven of eight
patients) than in those with malignant calcification (two of nine). Nodal
calcification was seen only in patients with malignant calcification (five of
nine vs none of eight, p < 0.05). Combining findings of sheet-like
calcifications and absence of nodes or other permutations of findings was not
helpful in distinguishing patients with benign calcification from those with
malignant calcification.
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Peritoneal calcification is caused by two primary mechanisms. Metastatic calcification may be a result of a systemic mineral imbalance in entities such as uremia or hyperparathyroidism, whereas dystrophic calcification may result from tissue injury, aging, or disease, including malignancy [10]. It is not surprising that malignant disease is more likely to cause lymph node involvement, and hence lymph node calcification, than is renal failure, hyperparathyroidism, or postsurgical changes. However, it is surprising that we found lymph node calcification associated only with malignancy and not with infectious or inflammatory causes such as tuberculosis or fungal infection. This finding may reflect, to some extent, the patient population at our institution or may reflect the rarity of peritoneal calcification in infectious calcified nodal disease. This notion is supported by several large studies of abdominal tuberculosis that have reported CT findings of calcified nodal disease but have not reported any case of peritoneal calcification [11–16]. We are aware of only three case reports of peritoneal calcification associated with tuberculosis, and in each of these case reports, the association with tuberculosis was made by exclusion: no acid-fast bacteria or granulomas were identified at histology in the calcified peritoneal deposits of these patients [5, 17, 18].
We did not identify peritoneal calcification associated with any malignancy apart from ovarian cancer or primary papillary serous peritoneal carcinoma. Although some malignancies, such as squamous cell lung cancer, renal cell carcinoma, and melanoma, are known to induce paraneoplastic hyperparathyroidism and hypercalcemia [19] and could conceivably mimic a benign pattern of peritoneal calcification, we did not observe such an occurrence. Other malignancies may also cause calcified peritoneal carcinomatosis, colon cancer [20], and gastric cancer [21], but we did not find such calcified peritoneal masses in this series. Our institution serves a large oncology population, but less than 20% of the CT examinations ordered by the oncology service are for gynecologic oncology patients, and the lack of malignancies other than ovarian or primary papillary serous peritoneal carcinoma causing peritoneal calcification in our series is not likely to be due to merely a disproportionate number of patients with ovarian carcinoma at our hospital. The proportion of patients in our study with ovarian cancer, peritoneal calcification, and concurrent calcified lymph nodes (5/9 or 56%) was higher than that reported by Mitchell et al. [1], who described calcified lymph nodes in only one of six such patients (17%). The apparent increased prevalence of calcified lymph nodes in our series may reflect improvement in CT technology since 1986. Much like serous ovarian adenocarcinoma, primary papillary serous peritoneal carcinoma is known to cause calcified peritoneal carcinomatosis and lymph node calcification [2].
Meconium peritonitis is the most common cause of peritoneal calcification and can cause microscopic and macroscopic calcified deposits with varied appearances [6, 22–24], but peritoneal calcification associated with numerous other entities has been described in several reports. In one series, two of the three patients with AIDS and extrapulmonary Pneumocystis carinii infections had calcifications of multiple lymph nodes; one of these two patients had concurrent small nodular calcifications of the pleural and peritoneal surfaces [8]. Three case reports of diffuse nodular peritoneal calcified deposits of varying sizes, all attributed to tuberculosis, were found at laparoscopy (n = 2) and autopsy (n = 1) [5, 17, 18]. In one case report of peritoneal mesothelioma, diffuse peritoneal calcification was reported [25], whereas in another case report of benign cystic peritoneal mesothelioma, a large intraperitoneal cystic mass with nodular calcifications was described [26]. A case report of diffuse peritoneal amyloidosis described omental and peritoneal thickening with nodular calcifications as well as retroperitoneal lymph node calcification [27].
Our study has a number of limitations. Characteristics of our study population may not allow our findings to be extrapolated to the general population. Although none of our patients with benign peritoneal calcification had lymph node calcification, none had a history of tuberculosis or P. carinii infection, entities that have been associated with calcification of both lymph nodes and the peritoneum [5, 8]. Other noninfectious benign entities, such as amyloid and systemic sclerosis, have also been associated with calcified lymph nodes [28, 29] and potentially the concurrent presence of such benign disease processes may cause peritoneal calcification to be misinterpreted as being of malignant origin. Our findings most likely reflect the population of patients referred to our institution, an urban tertiary-care North American teaching hospital, and should be extrapolated with caution in populations where infectious causes of calcified lymph nodes are more prevalent. For example, our institution supports a large kidney transplantation and oncology service, which possibly contributed to a disproportionate number of patients with peritoneal dialysis and malignancy found with peritoneal calcification. Another limitation is that our study probably did not include every case of peritoneal calcification seen on CT in our hospital because the interpreting radiologists may not have reported incidental peritoneal calcifications, or if they did, they may not have used words in their report that would have been captured by our character string search. In addition, the sensitivity of CT in the detection of subtle calcifications may be limited because contrast material was used in all CT examinations. A further limitation is that among the patients included in our study, eight of the nine patients with malignant disease had previously undergone intraabdominal surgery, which may have led to the formation of peritoneal calcification with a benign postsurgical cause.
Notwithstanding these limitations, we found the common causes of peritoneal calcification to be dialysis, prior peritonitis, or ovarian cancer. Sheetlike calcification suggests a benign cause, whereas associated lymph node calcification strongly suggests malignancy.
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