A 69-year-old, previously healthy woman was admitted for a 1-year history of weight loss of 15 kg, muscle weakness of the lower limbs, pain with walking and subsequent reduction of the bipedal strength.
Six months before admission she was diagnosed with type 2 diabetes mellitus, starting oral hypoglycemic agents and later insulin therapy.
Three months before admission, hypothyroidism was diagnosed and levothyroxine was started, with mild symptomatic improvement.
At the same time, lower limb symptoms progressed, leading to prostration.
Generalized hyperpigmentation of the skin and lines of the hands and papules red seal on trunk and proximal portion of the extremities developed.
On physical examination at admission, severe malnutrition, spontaneous skin acrocia of hands and the changes already described were observed, without polyadenopathy or organomegaly.
On neurological examination with superior functions, severe paresis of distal predominance of upper and lower extremities, marked decrease of muscular conservatism and generalized areflexia, without pathological reflexes.
Her tests showed a normal blood count and biochemical profile and a negative autoimmunity study (antiproteinase 3 and MPO, ANA and ENA).
The dorsal spine radiography showed an osteolytic lesion in T7, whose biopsy was negative for neoplasia.
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Flow cytometry of the lytic lesion showed a monoclonal gammopathy pattern of uncertain significance.
Intense positive CD38 was found in 0.2% of plasma cells, of which 90% showed evidence of clonality with intense coexpression and restriction of CD20 and CD19 axis in absence of CD20 expression.
Blood protein electrophoresis showed a M component of 0.4 g/dl. Myelocytes were non-myelocyte.
Electromyography described a sensory motor subacute axonal polyneuropathy.
Endocrinological study ruled out adrenal insufficiency and autoimmune chronic thyroiditis.
Biopsy of a cutaneous erythematous papule showed multiple dermal telangiectasias grouped with intraluminal capillary aggregates, compatible with superficial capillary hemangioma with gomeruloid component.
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Fa patient started treatment with melphalan and prednisone in cycles of four days every four weeks, presenting hyperglycemides controlled with insulin.
Outside the hospital discharge, the patient did not return to control, and his subsequent clinical evolution was unknown.
