Case Presentation: A 79 year old African American female with non-ischemic cardiomyopathy, EF 35-40%, hypertension, chronic kidney disease, hypothyroidism, mild pulmonary hypertension, obesity, and mixed hyperlipidemia, presented with worsening dizziness and bipedal edema for 2 weeks. Patient reported stopping diuretics and carvedilol due to persistent hypotension for several months. Patient noted unintentional weight loss of 70 pounds, generalized weakness, and early satiety in the past year along with dry mouth from reduced salivation. Patient denied recent fever, chest pain, palpitations, near-syncope or syncope, hematochezia, changes in bowel habits, history of falls or loss of consciousness, tick bite or viral infections.Patient did not have recent mammogram or colonoscopy. In emergency department, patient was afebrile, non-tachycardic, with borderline blood pressure of 90/60 mmHg. Her oxygen saturation was 100% on room air. Physical examination showed no jugular venous dilatation, minimal bibasal crackles, Grade 3 pitting bipedal edema with normal gross muscle strength of extremities. Laboratory findings were WBC 3.72x10E3/ul; hemoglobin 13.8 mg/dL; platelets 107x10E9/L, BUN 23mg/dl, creatinine, 2.23 mg/dl, calcium, 9.8 mg/dl, total protein, 7.7 g/dl, albumin, 3.4 g/dl, pro-BNP, 13,123. Chest X-ray revealed severe cardiomegaly and bilateral pleural fluid. Patient was restarted on low-dose diuretics and beta blocker, but could not tolerate due to persistent hypotension. Orthostatic vital signs were negative. TSH was 0.45mIU/ml with elevated FT4 of 2.21. Levothyroxine was held and patient started midodrine and compression stockings. Lyme antibody was negative. Cortisol level was normal. Repeat echocardiogram was not significantly changed from prior. Renal ultrasound was unremarkable. Upper endoscopy and colonoscopy revealed no obvious malignancy. Computed tomography revealed anasarca but was negative for bone lesions. Extensive rheumatologic workup was negative. However, SPEP showed 1.3 g possible M spike, and urine immunofixation showed IgG lambda M protein with lambda light chains specificity and monoclonal free lambda light chains.

Discussion: Multiple myeloma typically presents with hypercalcemia, renal insufficiency, anemia, and bone lesions due to proliferation of a plasma cell clone and subsequent overabundance of monoclonal paraprotein (M protein) leading to end organ damage. Here we describe a case of multiple myeloma presenting as persistent symptomatic dysautonomia.

Conclusions: Some studies describe paraproteinemic neuropathy as heterogeneous set of neuropathies due to excessive abnormal clonal proliferation of paraproteins and immunoglobulins in the serum affecting motor, sensory, or vasomotor nerve fibers. These excess immunoglobulins could reflect underlying monoclonal antibody-producing conditions. Strong suspicion for patients with dysautonomia along with clinical signs of bone marrow hypoproliferation even in the absence of anemia, high protein gap, multiorgan involvement, and significant weight loss without clear etiology should consider plasma cell neoplasm in the differential diagnosis.