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Case Reports in Oncological Medicine

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Case Reports in Oncological Medicine / 2013 / Article

Case Report | Open Access

Volume 2013 |Article ID 420565 | https://doi.org/10.1155/2013/420565

Nasir Hussain, Moona Khan, Aparna Natarajan, Mubeenkhan Mohammedabdul, Usman Mustafa, Kalpana Yedulla, Aibek E. Mirrakhimov, "A Case of Multiple Myeloma Coexisting with Primary Hyperparathyroidism and Review of the Literature", Case Reports in Oncological Medicine, vol. 2013, Article ID 420565, 8 pages, 2013. https://doi.org/10.1155/2013/420565

A Case of Multiple Myeloma Coexisting with Primary Hyperparathyroidism and Review of the Literature

Nasir Hussain,1 Moona Khan,1 Aparna Natarajan,1 Mubeenkhan Mohammedabdul,1 Usman Mustafa,1 Kalpana Yedulla,1 and Aibek E. Mirrakhimov 1

1Saint Joseph Hospital, Resurrection Health Care, Department of Internal Medicine, 2900 North Lake Shore Drive, Chicago, IL 60657, USA

Academic Editor: F. A. Mauri
Received05 Jan 2013
Accepted30 Jan 2013
Published26 Feb 2013

Abstract

Hypercalcemia is a common medical problem with an estimated prevalence of 15% among hospitalized patients. Multiple myeloma (MM) and primary hyperparathyroidism (PHPT) are among the most common causes of hypercalcemia but coexistence of both pathologic processes in a patient is an extremely rare phenomenon. In this paper we have discussed a patient presenting with this rare phenomenon. We have also provided a comprehensive review of the scientific literature published on codiagnosis of MM and PHPT.

1. Introduction

Hypercalcemia is a common clinical problem with an estimated prevalence of 15% among hospitalized patients [31]. The etiology of hypercalcemia is complex with many factors playing a pathogenic role. From a clinical standpoint, it may present with changes in mental status, generalized weakness, polyuria, and constipation. Multiple myeloma (MM) and primary hyperparathyroidism (PHPT) are among the most common causes of hypercalcemia but coexistence of the two pathologic processes in one patient is an extremely rare phenomenon. In this paper, we have discussed a patient presenting with this rare phenomenon and have reviewed the relevant scientific literature.

2. Case Presentation

A 92-year-old Caucasian female with a past medical history of Alzheimer’s dementia, seizure disorder, osteoporosis, and osteoarthritis was admitted to the hospital for an evaluation of a new onset confusion and constipation. Review of symptoms during admission was significant for anorexia, weight loss, constipation for the last three weeks, and history of a fall one month prior to the presentation. Family history was significant for MM in a sister. At the time of presentation, the patient was using donepezil, memantine, vitamin D with calcium, calcium carbonate (calcium containing antacid), and levetiracetam. Vitals at the time of admission were blood pressure 140/58, pulse 68, respiratory rate 18, oxygen saturation 98% on room air, and temperature 97.4. On physical examination, the patient was alert and oriented in place and person but not in time. Other significant findings were diastolic murmur in right second intercostal space, petechiae over lower extremities, and back tenderness, which the patient attributed to a recent fall. Lumbar spine X-ray was done three weeks prior to the presentation that showed degenerative changes with no evidence of fracture. Basic blood workup including complete blood count and comprehensive metabolic panel was done, which revealed anemia, leucopenia, and hypercalcemia. Home medications were held for concerns of hypercalcemia and confusion.

Endocrinology and neurology services were consulted. MRI of the brain was done, which showed lytic lesions as shown in Figure 1. MM was suspected; serum protein electrophoresis (SPEP), urine protein electrophoresis (UPAP) and bone marrow biopsy were done which confirmed the diagnosis of MM (IgG kappa) (International Staging System stage II). Bone marrow biopsy showed mildly hypercellular bone marrow with plasmacytosis (30%) as shown in Figure 2. Skeletal survey showed diffuse lytic lesions throughout long bones, pelvis, and skull (Figure 3). Surprisingly, intact PTH came back high suggesting primary hyperparathyroidism (PHPT). The data on laboratory tests are presented in Table 1.

Result nameResultsReference range
WBC2.9 K/mm cu4.2–11.0
Platelet 156 K/mm cu140–400
Hemoglobin Hb9.0 g/dL12.0–15.0
Hematocrit27.1%36.0–47.0
Reticulocyte0.7%0.5–2.8
Blood urea nitrogen22 mg/dL5–20
Creatinine1.11 mg/dL0.0–1.00
Sodium143 mmol/L135–145
Potassium4.0 mmol/L3.4–5.1
Chloride104 mmol/L98–109
Bicarbonate33 mmol/L23–31
Calcium13.3 mg/dL8.4–10.5
Total protein7.0 g/dL6.4–8.3
Albumin4.0 g/dL3.4–5.2
Aspartate amino transferase20 IU/L0–32
Alanine amino transferase 10 IU/L0–40
Alkaline phosphatase 67 IU/L35–104
Bilirubin total0.2 mg/dL0–10.0
Haptoglobin157 mg/dL36–195
Vitamin B12532 pg/mL211–946
TSH1.160 uIU/mL0.400–5.400
Vitamin D25 OH 47.0 ng/mL30.0–100.0
25 Hydroxy D326 pg/mL  
25 hydroxy D2<8 
Vitamin D 1,25(OH)22618–72
Folate>20.0 ng/mL3.1–17.5
Ferritin64 ng/mL13–150
Phosphorous 2.8 mg/dL2.0–4.0
Lactate dehydrogenase 137 IU/L135–214
Total iron30 ug/dL30–160
Unsaturated IBC234.0 ug/dL110.0–370.0
Total IBC 264.0228.0–428.0
Percentage of iron saturation11%20–55
PTH intact on day of presentation70.5 pg/mL 15.0–65.0
PTH 7 months later540.0 pg/mL  
PTH-related protein18 pg/mL14–27
Beta-2 microglobulin3.3 mg/L (5.8 mg/L four months later)0.8–2.2
Serum viscosity1.5 relative to H2O1.5–1.9
PT/INR10.6/1.0 sec9.211.8/0.9–1.1
APTT29 sec24–33
Immunoglobulins  
 IGA 29 mg/dL50–400
 IGG692 mg/dL (1200, 5 months later)600–1500
 IGM6 mg/dL50–300
 Free kappa light chains15103.3–19.4 mg/L
 Free lambda light chains2.45.7–26.3
 Free Kappa/lambda629.170.26–1.65
Urine protein electrophoresis   
 Urine volume 24 hours1150 mL/24 hour 
 Urine-protein electrophoresis (UPE)253 mg/24 hour 0–165
 Albumin UPE30.6% 
 Alpha116.1% 
 Alpha2 14.1% 
 Beta 17.1% 
 Gamma 22.1% 
 Immunofixation Free kappa light chains  
 24-hour-urine protein310.5 mg/24 hour0–150
 24-hours-urine creatinine 0.7 g/24 hour 0.74–1.57
 24-hour-urine volume1150 cc 
 24-hour-urine creatinine0.5 g/24 hour 0.74–1.57
 24-hour-urine volume 900 mL (repeat test) 
 24-hour-urine calcium239 mg/24 hour 100–300
Serum protein electrophoresis   
 Albumin3.3 g/dL3.1–5.0
 Alpha 1 0.3 g/dL0.2–0.5
 Alpha20.7 g/dL0.5–1.1
 Beta0.6 g/dL0.6–1.1
 Gamma1.5 g/dL0.7–1.7
 Albumin/globulin 1.0 
 M spike 1.09 g/dL  
 Total protein6.5 g/dL6.4–8.3
 Immunofixation Monoclonal paraprotein of class IgG kappa
 CD56 NK cells63%3–35
 CD 138 marker 26% 
 Lambda B-cell marker1%1–7
 Kappa B-cell marker73%2–14%
 CD45 LCA98%92–100
 CD38 Marker26%1–17
Pathology. Normal female bone marrow karyotype. No clonal, structural, or numerical chromosome abnormalities identified. FISH analysis indicates normal hybridization signals with MM probe panel. This excludes majority of chromosome rearrangements known to be associated with MM.
Surgical Pathology. Mildly hyper cellular bone marrow with plasmacytosis consistent with MM.
Leukemia/lymphoma panel. Bone marrow aspirate shows 30–40% plasma cells with kappa light chain restrictions. (plasma cell dyscrasia).
Peripheral Smear. Lymphocytes with foamy cytoplasm, no rouleaux formation, adequate polys with occasional platelet clumps.
Table 1 

Figure 1 
MRI demonstrating lytic lesions.

Figure 2 
Mildly hypercellular bone marrow with plasmacytosis (30%), consistent with multiple myeloma.

Figure 3 
Skeletal survey showing lytic lesions in long bones and skulls.

Hypercalcemia was managed with intravenous hydration, calcitonin, bisphosphonates, and furosemide. The patient was started on melphalan and prednisone, which were later switched to lenalidomide with a high dose of dexamethasone due to a poor treatment response. After one and a half year, the patient is still following in our outpatient oncology center being on a low dose of lenalidomide with a stable M protein.

3. Discussion

Hypercalcemia is common in patients with MM and occurs in 28% of myeloma cases [32]. MM may cause hypercalcemia through multiple mechanisms. First, plasma cells produce various cytokines, including TNF-β and IL-6, that activate osteoclasts and lead to calcium washout from bones to the bloodstream [33]. Second, some studies suggest that MM cells may secrete parathyroid hormone-related peptide similarly to other malignancies, such as squamous cell lung carcinoma [34, 35]. Third, serum calcium may be falsely elevated because of a binding to immunoglobulin [36, 37].

Clubb et al. [38] described first-case linking PHPT and paraproteinemia in 1964. Drezner and Lebovitz were the first who described a case of concomitant MM and PHPT in 1979 [30]. Some researchers speculate that the association between MM and PHTP may not be coincidental [39, 40], although mechanisms explaining codiagnosis are not known. Arnulf et al. showed that the prevalence of monoclonal gammopathy is higher in patients with PHTP as compared to general population [40]. Pest et al. hypothesized that elevated PTH may mediate the induction of MM through the downstream biological effects of IL-6 [1]. This hypothesis was supported by the study performed by Pirih et al., who showed that PTH decreases apoptotic cell death of the hematopoietic stem cells via the IL-6 [41].

PHPT leads to hypercalcemia via direct bone resorption [42] mediated by osteoclasts. Another important mechanism is through an increased calcium absorption in the duodenum and greater reabsorption in the kidneys.

The above-mentioned pathogenic mechanism gives an insight to how PHPT and MM may be linked. Some studies have suggested that calcium may act as a mitogenic factor [43], whereas others suggest that myelomatous proteins may interfere with polypeptide hormone synthesis bind their circulating fractions, and/or block their peripheral effects that may secondarily stimulate parathyroid gland [29]. However, both of these diseases are common among elderly and may share similar risk factors, such as ionizing radiation [44, 45], and a simple coincidence may be the case.

Summary of published cases [1–28] is presented in Table 2. Codiagnosis of PHPT and MM should be suspected in cases of difficult-to-control hypercalcemia. Most of the cases of coexistent MM and PHPT have been observed in females (23 out of 29 reported cases). The youngest patient with codiagnosis was a 45-year-old female and the oldest patient was a 92-year-old female. PHPT is more common in females, whereas the opposite is true for MM. Differences in incidence of the two diseases may explain female preponderance (MM less frequent than PHPT). Initial diagnosis was highly variable, eleven cases had primary diagnosis of hyperparathyroidism, ten had primary diagnosis of MM and seven had both diagnosis made at presentation. The type of immunoglobulin chains of MM observed in all the cases was variable as six patients had light chain MM, remaining patients had a combination of heavy and light chain MM, one patient had nonsecretory type of MM. All the patients had calcium ≥11 mg/dL at the time of presentation. Majority of patients had parathyroid adenoma as a cause of PHPT, few had chief cell hyperplasia, and none had parathyroid cancer. Parathyroidectomy, combination of radiotherapy, and chemotherapy had been used for treatment of this coexistent condition with variable success. Rao et al. [2] suggested that parathyroidectomy in patients with coexistent PHPT and MM serves three folds; first, it removes confusion about etiology of hypercalcemia; second, it alters prognosis of myeloma; third, calcium can be used as a tumor marker in cases if there is a recurrence of tumor. Considering age, our patient was not a candidate for surgery, in such patient population medical alternative to parathyroidectomy is needed. Ten out of 29-patients died within 5 years after codiagnosis, and out of those ten, eight died within one year.

AuthorAge/ GenderType of MMCa (mg/dL)Therapy for MM and PHPTParathyroid histologyOutcome Initial diagnosis
1 Pest et al. [1]76 FIgA-?13.2Hydration, bisphosphonates, Lasix, melphalan, cyclophosphamide, and steroidsAdenomaSurvived PHPT
2 Rao et al. [2] 54 MIgG-lambda11.2Adriamycin, melphalan, prednisone, cyclophosphamide, and parathyroidectomyAdenomaDied after 12 yearsBoth
3 Jackson and Orland [3]45 FIgG-lambda17.1Hydration, Lasix, prednisone, and melphalanAdenoma—MM
4 Chisholm et al. [4] 80 MKappa13.1Parathyroidectomy, radiotherapy, melphalan, prednisone, vincristine, carmustine, cyclophosphamide, hydration, and LasixAdenoma (c-cells)Died 2 years laterPHPT
5 Francis et al. [5] 70FLambda11.6Norethisterone, vincristine, melphalan, and prednisoneAdenomaDied 3 weeks laterPHPT
6 Mundis and kyle [6]76 FIgG-kappa11.0Melphalan, prednisone, and parathyroidectomyAdenoma (c-cells)survivedMM
7 Stone et al. [7]47 FIgA-kappa13.7Melphalan, prednisone, radiotherapy, parathyroidectomy, hydration, and mithramycinAdenomaDied MM
8 Hoelzer and Silverberg [8]51 FIgA-lambda11.9Parathyroidectomy?Adenoma (c-cells)—PHPT
9 Schneider and Thomas [9]74 FIgG-kappa12.0Melphalan, prednisone, and parathyroidectomyAdenomaSurvived MM
10 Toussirot et al. [10]82 MKappa15.2Melphalan, prednisone, and parathyroidectomyHyperplasia DiedPHPT
11 Goto et al. [11]73 FKappa13.2Parathyroidectomy, melphalanAdenoma Died 1 year later PHPT
12 Otsuka et al. [12] 77 FIgG-lambda Melphalan, prednisone, bisphosphonates, calcitonin, and parathyroidectomy c-cells hyperplasiaSurvived —
13 Fery-Blanco et al. [13]68 FIgG-kappa11.28? chemotherapy and surgery refusedAdenomaDied Both
14 Sarfati et al. [14]62 FIgA-kappa16.4Mithramycin, lasix, plasmaphoresis, Adriamycin, vincristine, prednisone, and parathyroidectomy AdenomaSurvivedMM
15 Rosen et al. [15] 81 MIgG-kappa13.4Hydration, bisphosphonates, melphalan, prednisone, radiotherapy, needle aspiration of parathyroid gland, and refused surgery Adenoma SurvivedMM
16 Tomon et al. [16]60 FIGA-kappa————MM
17 Fanari et al. [17] 59 Flambda12.7Hydration, bisphosphonates, cinacalcet, bortezomib and dexamethasonePossible AdenomaDied 4 months laterBoth
18 Bogas et al. [18]72 FIgG-kappa13.66Melphalan, prednisone, and Interferon?Adenoma Died 4 years laterBoth
19 Katayama et al. [19]50 F     PHPT
20 Romagnoli et al. [20] 70 F——Parathyroidectomy, steroids and chemotherapyAdenoma—PHPT (MEN-1)
21 Toh and Winocour et al. [21]71 M 12.0Melphalan, prednisone, and bisphosphonates Died 6 weeks later MM
22 Sope a et al. [22]77 FKappa (ns)12.9Bisphosphonates, refused surgery, or chemotherapy Died 1 year laterBoth
23 Khandwala and Boctor [23]72 F—11.7/ 16.6*Parathyroidectomy, bisphosphonates, calcitonin, melphalan, and prednisoneAdenoma—PHPT
24 Patel et al. [24]73 FIgG- kappa13.5Bisphosphonates, steroids, thalidomide, plicamycin, and parathyroidectomy Adenoma—MM
25 Avcioglu et al. [25]52 FIgG-kappa12.6Parathyroidectomy and steroids Adenoma —Both
26 Chowdhury and Scarsbrook et al. [26]87 F—————PHPT
27 Dalgleish and Gatenby [27] 59 FIgG-lambda 11.68Hydration, lasix, prednisone, mithramycin, cyclophosphamide, and parathyroidectomy Adenoma Survived MM
28 Peters et al. [28]73 MIgA-lambda 16Parathyroidectomy, chemotherapy, and radiotherapy Hyperplasia Died 1 week laterPHPT
29Our case 92 FIgG-kappa13 .3Bisphosphonates, Lasix, hydration, calcitonin, melphalan, prednisone, lenalidomide, and dexamethasone—Survived Both
30 Johansson and Werner [29] mentioned 3 cases of MM and PHPT (no detail of the cases is given), one other such as has been described by Drezner and Lebovitz [30] without much detail.
Calcium at time of diagnosis of MM.
Table 2 

4. Conclusions

A search for concomitant cause of hypercalcemia should be pursued in cases of difficult-to-control hypercalcemia and in elderly individuals, in whom the incidence of PTHP and MM is common.

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