Post traumatic Sternal Mass leading to Multiple Myeloma: Is There a Link?

Naima Ait mouddene*, Wiaam Elkhattabi, Salma Msika, Hajar Bamha, Nabil Bougteb, Hajar Arfaoui, Hicham Afif

Department of Pulmonology and Respiratory Disease, 20 Aout 1953 Hospital, University Hospital Center of Casablanca-Morocco

*Corresponding author

Naima Ait mouddene, Department of Pulmonology and Respiratory Disease, 20 Aout 1953 Hospital, University Hospital Center of CasablancaMorocco

Abstract

Background: Multiple myeloma is an incurable malignant hematologic disorder characterized by abnormal monoclonal plasma cell proliferation in the bone marrow. While its etiology remains unclear, no direct correlation has been established between prior trauma and the development of plasma cell dyscrasia at the same site. However, some cases have suggested a possible association.

Case Presentation: We report the case of a 47-years-old male with a history of anterior thoracic trauma one year prior to the development of a progressively enlarging sternal mass. The patient presented with chest pain, dyspnea, mild hemoptysis, oliguria, and significant weight loss. Radiological or biological investigations revealed a sternal osteolytic mass, a monoclonal gamma peak on serum protein electrophoresis, and bone marrow infiltration by dystrophic plasma cells. A diagnosis of kappa light chain multiple myeloma was established. The patient was treated with a regimen of bortezomib, thalidomide, and dexamethasone (VTD), alongside supportive care. After four months and six chemotherapy cycles, his clinical and biological condition significantly improved.

Conclusion: While the causal relationship between trauma and multiple myeloma remains unproven, our case adds to the limited reports suggesting a potential link. Further research is needed to elucidate whether trauma may act as a predisposing factor or a coincidental finding in plasma cell dyscrasia development.

Introduction

Multiple myeloma is an incurable malignant hematologic disorder with an unknown etiology, characterized by plasma cell dyscrasia, resulting in an abnormal monoclonal plasma cell proliferation in the bone marrow exceeding 10%, compared to a normal population of 2-3% (1-2). This plasma cell proliferation leads to the secretion of non-functional monoclonal immunoglobulins, which accumulate and interact with other bone marrow cells, causing various complications, including anemia, bone pain and pathological fractures, recurrent infections, hypercalcemia, renal failure, fatigue, and pain (3-4). This disease affects men more than women, with a median age at diagnosis of 65 years, and less than 3% of patients present before the age of 40. No direct correlation has been established between a history of trauma and the development of plasma cell dyscrasia at the trauma site. Furthermore, the association between a prior trauma site and the subsequent development of multiple myeloma at the same location has been rarely reported in the literature (2). We report a case of a patient with a history of sternal trauma who, 1 year later, developed multiple myeloma at the same site.

Case Report

Patient Data : A 47-years-old male, a farmer, a chronic smoker (non-weaned) and former chronic alcoholic (weaned for 4 years), was treated for tuberculous pleurisy 8 years ago. One year prior, he suffered an anterior thoracic trauma from an accidental fall onto a pitchfork, impacting the sternum and causing an open wound that was sutured, leaving a visible scar (Figure 1).

Figure 1: Sternal and parasternal mass at the site of an scar (8cm).

Figure 2: Lateral chest X-ray showing a well-defined, rounded radiolucent formation projected over the manubrio-sternal region, surrounded by a thin opaque rim with cortical thinning

Figure 3: Frontal chest X-ray showing a hyperlucent, slightly overdistended lung with blunting of the right cardiophrenic angle.

Figure 4: Skull X-ray showing punched-out osteolytic lesions.

Figure 5: X-ray of the thoracolumbar spine showing osteolytic lesions with some vertebral compressions

Figure 6: Thoracic CT scan showing an osteolytic mass at the sternum extending into the anterior mediastinum

Figure 7: Multiple myeloma cells observed on a histological section (Ref. Firth J. Haematology: multiple myeloma. Clin Med. Jan 2019;19(1):58 60)..

Figure 8: Regression of the sternal mass after chemotherapy, reduced by 3 cm

Figure 9: Chest CT scan showing the regression of the parietal mass and the anterior mediastinal mass after chemotherapy.

History of PresentIllness: The diseasebegan six monthsagowith the progressive appearance of a thoracic mass at the sternal scar site, associatedwithincreasingdyspnea, whichrapidlyprogressed to mMRC stage II. Twomonthslater, the patient developedmildhemoptysis (<50 cc). At that time, healsoreported postprandial vomiting, oliguria, feverish sensations, and rapiddeterioration of generalhealthstatus.

Examination on Admission: The patient wasadmitted in poorgeneral condition (PS = 3), anxious, pale, and underweight (BMI = 15.4 kg/m²) without digital clubbing or lowerlimbedema. He wasafebrile, eupneic (20 breaths/min), had an oxygen saturation of 95% on room air, normal blood pressure (110/88 mmHg), and a heart rate of 90 bpm.

Pleuro-pulmonaryexaminationrevealed an 8 cm x 8 cm anteriorthoracic mass at the manubrio-sternal junction, corresponding to a horizontal scar. The mass was hard at the center, painless, fixed to bothunderlying and overlying planes, and showed no inflammatorysigns. Pulmonary auscultation revealed no audible rales. Osteoarticularexaminationfound no bonetenderness, and the rest of the physicalexaminationwasunremarkable.

Radiological and Biological Workup Imaging Studies: A chest X-ray (frontal and lateralviews) showed a well-demarcated, grosslyroundedlesionprojected over the manubrio-sternal region, with a clear content surrounded by a thin opaque rim and cortical thinning, suggestive of a probable bone mass (Figure 2). Pulmonaryparenchymalanalysisrevealedhyperlucent, slightlyoverdistendedlungswithdiaphragmaticflattening and blunting of the right cardiophrenic angle (Figure 3).

Biological Workup: Blood count showednormochromicnormocyticanemia (Hb = 9 g/dL) withoutleukocytosis or lymphopenia. C-reactiveproteinwaselevated (51.9 mg/L), with an acceleratederythrocytesedimentation rate (ESR = 110 mm/h). Electrolyte panel showedhyponatremia (128 mEq/L) and hypercalcemia (correctedCa²⁺: 133 mg/L). Serumcreatininewaselevated (21.5 mg/L) withlow urine output (350 mL/24h). Serumproteinanalysisshowedhyperproteinemia (139 g/L) withseverelydecreasedalbuminlevels (16 g/L). Giventhesefindings, serumproteinelectrophoresis (SPE) wasperformed, revealing a monoclonal gamma peak, raising suspicion of multiple myeloma or plasmacytoma.

Multiple Myeloma Workup: Skull X-ray revealedpunched-out osteolyticlesions (Figure 4), whilethoracolumbarspine X-ray showedosteolyticlesionswithvertebral compression fractures (Figure 5). However, pelvic and long bone X-rays wereunremarkable. A thoracic CT scan showed an osteolytic sternal mass extendingdeeplyinto the anteriormediastinum, without calcification or evidence of pulmonaryparenchymal invasion (Figure 6). Bronchoscopyrevealed a diffuse  inflammation of the tracheobronchialtree . Bronchial biopsies showed non-specificfibro-inflammatory changes with no malignancy.

Biological Investigations: Immunofixation of serumproteinsconfirmed monoclonal IgG lambda. Bone marrow aspiration revealed 53-55% dystrophic plasma cells and rouleaux formation of redbloodcell, suggestive of multiple myeloma (Figure 7). A 24-hour urine studyshowedoliguria (350 mL) withproteinuria (0.32 g/24h). Urine proteinelectrophoresisdetectedelevated free kappa light chains (22.31 mg/L). Cytogeneticanalysis of bonemarrowcellsshowed a hypodiploid clone (44 chromosomes) withnumerical and structural abnormalities. Beta-2 microglobulinwaselevated (13.95 mg/L) (Table 1).

Table 1: Biological assessment during multiple myeloma

Table 2: Follow-up biological assessment after chemotherapy treatment

Final Diagnosis : Based on clinical, radiological, and biological findings, along with bone marrow results, a diagnosis of kappa light chain multiple myeloma was confirmed, presenting as a sternal mass at the site of prior trauma.

Treatment: The patient received symptomatic treatment, including rehydration, electrolyte correction, and a high-protein diet. Etiologic treatment was initiated in collaboration with hematologists, comprising VTD (bortezomib, thalidomide, and dexamethasone). Additionally, hospitalizationwasused as an opportunity to offer smoking cessation counseling.

Evolution and Prognosis: After four months of treatment and six chemotherapy cycles, the patient's condition significantly improved, with a PS of 0 (vs. 3), a weight gain of 12 kg, resolution of dyspnea, and regression of the sternal mass (3 cm vs. 8 cm) (Figure 8). Biological parameters (Table 2) and CT findings (Figure 9) showed marked improvement. Prognostic assessment using the Durie and Salmon classification placed the patient at Stage III, with an estimated survival of 23 months.

Discussion

No direct link between trauma and multiple myeloma (MM) has been conclusively established, but some case reports suggest a possible association (2). Our case describes a 47-year-old man who developed a sternal mass 18 months after a thoracic trauma. This temporal correlation raises the question of whether trauma could act as a predisposing factor for multiple myeloma. Trauma could trigger chronic inflammation, as a result of that creating a local environment conducive to the proliferation of plasma cells. This could lead to the clonal expansion of abnormal plasma cells, particularly in genetically predisposed individuals. Chronic inflammation and the resulting immune response could stimulate the bone marrow microenvironment, thus promoting malignant transformation (5-6-7-8-9). Previous case reports, such as those by Mongkonsritragoon (9), Suna (10), and Hussein et al. (2), have documented cases of plasma cell dyscrasia developing at the site of a previous trauma, including burns, head trauma, and bone fractures. In these cases, a variable latency period was observed, ranging from a few months to several decades, and the development of multiple myeloma appears to depend on both the nature of the trauma and the individual's genetic predisposition (2-5-10). Our patient's developed a multiple myeloma within six months, which is a shorter latency period than in the reported cases. Furthermore, genetic mutations and chromosomal abnormalities, such as hypodiploidy, are commonly associated with multiple myeloma, as observed in our patient. Whether trauma directly influences these genetic changes remains speculative, but it could act as a trigger in individuals who are already genetically predisposed. Although the causal relationship between trauma and multiple myeloma remains uncertain, our case contributes to the growing body of evidence suggesting a potential link. Further research is needed to explore the mechanisms by which trauma might predispose individuals to multiple myeloma and whether it serves as a trigger for the disease.

References

  1. Tift BD; Prickett JT; Sampson LK (2020). Scalp mass: an atypical presentation of multiple myeloma. J Surg Case Rep. 28 oct. (10):rjaa410.
  2. Hussein MA; George R; Rybicki L; Karam MA (2003). Skeletal trauma preceding the development of plasma cell dyscrasia: eight case reports and review of the literature. Med Oncol Northwood Lond Engl. 220(4):349‑54.
  3. Brigle K; Rogers B (2017). Pathobiology and Diagnosis of Multiple Myeloma. Semin Oncol Nurs. Août. 33(3):225‑36.
  4. Firth J (2019). Haematology: multiple myeloma. Clin Med. janv 2019;19(1):58‑60.
  5. Caligaris-Cappio F; Bergui L; Gregoretti MG; Gaidano G; Gaboli M; et al (1991). ’Role of bone marrow stromal cells in the growth of human multiple myeloma. Blood. 15 juin. 77(12):2688‑93.
  6. Ruiz-Argüelles GJ; Katzmann JA; Greipp PR; Gonchoroff NJ; Garton JP;et al (1984). Multiple myeloma: circulating lymphocytes that express plasma cell antigens. Blood. Août. 64(2):352‑6.
  7. Epstein J; Barlogie B; Katzmann J; Alexanian R (1988). Phenotypic heterogeneity in aneuploid multiple myeloma indicates pre-B cell involvement. Blood. avr. 71(4):861‑5.
  8. Billadeau D; Greipp P; Ahmann G; Witzig T; Van Ness B (1995). Detection of B-Cells Clonally Related to the Tumor Population in Multiple Myeloma and MGUS. In: Potter M, Melchers F, éditeurs. Mechanisms in B-Cell Neoplasia 1994. Berlin, Heidelberg: Springer; 1995. p. 9‑16.
  9. W M; Ra K; Rr S; Pr G (1998). Primary plasmacytoma at the site of exit wounds after electrical injury. Am J Hematol [Internet].58(1).
  10. Suna D; Erdinçler P; Bayindir C; Hepgül K; Ongören S; et al (1997). [Intracerebral solitary plasmacytoma. Apropos of a case possibly induced by head injury]. Neurochirurgie.43(4):255‑9.
TOP