Indomethacin-Responsive Hypercalcemia in a Patient with Renal-Cell Adenocarcinoma

Hd, Brereton; Pv, Halushka; Rw, Alexander; Dm, Mason; Hr, Keiser; Vt, DeVita

doi:10.1056/nejm197407112910207

Cited by 143 publications

(10 citation statements)

References 8 publications

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“…Bringhurst et al [15] reported that a cancer cell line derived from a transitional cell carcinoma produced a factor stimulating PGE2 release from bone, which in turn induced bone resorption. The effect of this factor was blocked by indomethacin and calcitonin [15,16,48,49]. In the present study, hypercalcemia, associated with high levels of plasma PGE2, occurred in seven patients.…”

Section: Discussionsupporting

confidence: 50%

Hypercalcemia in breast cancer

et al. 1993

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Hypercalcemia is relatively frequent in malignancy with or without osteolytic bone metastases. It is thought that neoplastic cells may secrete substances which not only stimulate osteoclastic activity but are also capable of modifying the absorption, excretion, and resorption of calcium and phosphate ions. Since 1987, we have studied 24 breast cancer patients with hypercalcemia (22 with bone metastases and two without). The group of 22 patients with bone metastases were divided into two subgroups. The first consisted of 10 patients with high serum levels of humoral factors, such as parathyroid hormone-related protein (PTHrP), and/or prostaglandin E2 (PGE2) and/or interleukin 1 (IL-1), and high levels of bone markers, such as alkaline phosphatase, bone Gla protein and urinary hydroxyproline. The second subgroup consisted of 12 patients with high levels of bone markers alone. Bone histologic analysis showed an osteoclastic activation surrounding metastatic tumor tissue in six out of 10 patients of the first subgroup, while an evident osteolysis caused by the tumor cells was noted in seven out of 12 patients of the second subgroup. The two patients without bone metastases showed normal biochemistry and bone histologic examination. The authors, having tried to explain the pathogenesis of hypercalcemia, emphasize the importance of humoral factors secreted by tumor cells as a direct or indirect cause of hypercalcemia. The origin of hypercalcemia remains unclear in two patients without bone metastases.

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Section: Discussionsupporting

confidence: 50%

Hypercalcemia in breast cancer

et al. 1993

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“…Hypercalcemia is attributed to the production by the tumor of a humoral substance that induces resorption of calcium from bone [33, 34,441. Rapid decline of serum calcium levels following tumor removal and the recurrence of hypercalcemia with tumor regrowth in man [3,41,43], in mice with fibrosarcoma [48], and in rabbits with VX2 carcinoma [49]. Osteoclast-activating factor has been identified in the medium from cultured myeloma and lymphosarcoma cells obtained from people with hypercalcemia [30].…”

Section: Discussionmentioning

confidence: 99%

Hypercalcemia Associated with an Adenocarcinoma Derived from the Apocrine Glands of the Anal Sac

et al. 1981

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Abstract. Clinical, gross. and light microscopic findings are described for 36 dogs, 33 females and three males. with adenocarcinomas arising from the apocrine glands of the anal sac. All tumors had light microscopic features of malignancy and 22 of 23 metastasized to iliac and lumbar lymph nodes. Nine dogs had disseminated metastases, but bone metastases were found in only one dog. Differentiated neoplasms formed secretory acini and tubules lined by tall columnar or cuboidal epithelium. Most neoplasms were histologically bimorphic. with glandular areas and solid nests. Parathyroid glands were atrophic. Hypercalcemia (mean = 16.1 mg/dl) was present in 20 of 22 dogs (90%) and hypophosphatemia (mean = 3.2 mg/dl) in 12 of 17 (7 1%). Remission of hypercalcemia by tumor ablation and recurrence of hypercalcemia with tumor regrowth suggested that the tumor produced a substance that caused hypercalcemia. This unique clinicopathologic syndrome is characterized by hypercalcemia in old. predominantly female, dogs with an adenocarcinoma arising from the apocrine glands of the anal sac.Neoplasms occur frequently in the perineum of the dog, with adenomas derived from the circumanal gland the most common [13,32,50]. Other glands in the perineum that may undergo neoplastic transformation include dermal sebaceous and apocrine glands, merocrine anal glands. and the apocrine glands of the anal sac [ 1,8,12,24,25, 27, 281. We describe a tumor that originated from the apocrine glands of the anal sac. In the most complete description of this unique syndrome, only females were reported to have developed this neoplasm, the tumors were malignant, and all dogs had hypercalcemia [40].A syndrome of hypercalcemia associated with malignancy has been seen in dogs [23, 34,401, mice [48], rabbits [49], rats [39]. and infrequently in the horse [26] and cat [6]. Lymphosarcoma [34] is the tumor most frequently associated with hypercalcemia in dogs, although there are isolated reports implicating other neoplasms [ 18, 23, 3 I, 541. Malignant neoplasms with metastasis to bone are the most common cause of hypercalcemia in hospitalized people [29, 531. Many hypercalcemic people, however, have neoplasms without evidence of osteolysis due to bone metastases 454

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“…39,40 In these cases, nonsteroidal inflammatory drugs may be effective in reducing calcium by inhibiting prostaglandin production by the tumor. 41,42 Our patient was on chronic steroids for treatment of polymyalgia rheumatica, therefore prostaglandin-mediated hypercalcemia is unlikely in this case.…”

Section: Discussionmentioning

confidence: 87%

Renal Cell Carcinoma Presenting with Paraneoplastic Hypercalcemic Coma: A Case Report and Review of the Literature

et al. 2007

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We report a case of a 62-year-old woman with renal cell carcinoma (RCC) presenting with a hypercalcemiainduced coma. A laboratory evaluation indicated nonparathyroid-mediated hypercalcemia with an initial serum calcium level of 18.6 mg/dL. Our patient's parathyroid hormone (PTH)-related peptide level was undetectable. Initial imaging was negative, but PET scan identified a mass in the upper pole of the left kidney. Our patient underwent partial nephrectomy, and the mass was identified as RCC on final pathology. After surgery, her hypercalcemia resolved and PTH returned to normal limits. This case report describes a patient with RCC with the unusual presentation of hypercalcemic coma. We review the differential diagnosis of malignant hypercalcemia and the evaluation of hypercalcemia occurring with RCC. This case illustrates the need to carefully review and interpret all available data, especially when conventional testing in the work-up of hypercalcemia is unrevealing.

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Indomethacin-Responsive Hypercalcemia in a Patient with Renal-Cell Adenocarcinoma

Cited by 143 publications

References 8 publications

Hypercalcemia in breast cancer

Hypercalcemia in breast cancer

Hypercalcemia Associated with an Adenocarcinoma Derived from the Apocrine Glands of the Anal Sac

Renal Cell Carcinoma Presenting with Paraneoplastic Hypercalcemic Coma: A Case Report and Review of the Literature

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