Case 390 -- A man in his 70's who has monoclonal gammopathy of undetermined significance, or does he?

Contributed by Beth Clark, MD, Bruce Rabin, MD, PhD
Published on line in May, 2004


The patient was a man in his 70s with a history of right lower extremity deep venous thrombosis with multiple pulmonary emboli with right lower lobe pulmonary infarction (most recent hospitalization), asthma, benign prostatic hypertrophy, and intermittent vertigo.

Two days after discharge, the patient developed severe joint and muscle pains in his shoulders, lower back, right ischial tuberosity, and the posterior aspect of his legs. He also complained of parasthesias and dysesthesias in the posterior aspect of his legs, as well as bilateral leg weakness. Neurologic examination revealed wide-based ataxia, decreased lower extremity reflexes (L>R), decreased lower extremity strength (L>R), and altered sensation in the lower extremities. EMG, nerve conduction studies showed evidence of primary demyelinating sensorimotor polyneuropathy, and mild evidence of ongoing axonal degeneration in a distal leg muscle. MRI of the cervical and lumbar spine showed degenerative disk disease.



Based on the patient's symptoms, laboratory studies, and electromyographic studies, a diagnosis of chronic versus subacute inflammatory demyelinating polyneuropathy (CIDP) was made. The patient was treated with intravenous immunoglobulin, narcotics and neurontin for pain control, and physical and occupational therapy, and showed some minor improvement in symptoms and signs.

Once the diagnosis of CIDP was made, serum protein electrophoresis was performed to evaluate for monoclonal gammopathy.

Serum protein electrophoresis (Figure 1): monoclonal gammopathy 0.62 g/dL.

Immunofixation electrophoresis (Figure 2) was performed to further characterize the band.

When immunofixation electrophoresis was performed, a monoclonal band was not detected with the heavy or light-chain antisera. This raised a concern about the identification of the monoclonal protein. Further investigation was undertaken to resolve this discrepancy. The serum sample used to perform the electrophoresis procedures was visually examined, and fine filamentous yellow precipitate was observed in the serum sample.

Based on the position of the band on serum protein electrophoresis and the precipitate in the test tube, what is the most likely explanation for the laboratory findings? How can this be confirmed?


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