A 53-year-old male patient with a history of hypertension and benign prostatic hyperplasia.
The patient presented a clinical picture of 8 weeks of evolution characterized by intermittent thermal elevations up to 39°C and important nocturnal diaphoresis.
She had no history of travel abroad or contact with animals.
Five days prior to admission, polyuria, low back pain and bad odor urine were associated, which was interpreted as urinary tract infection.
She received outpatient antibiotic treatment without improvement of fever, so she was hospitalized in our center.
Upon admission she was febrile (38.2°C), normotensive with 95% environmental oxygen.
Segmental physical examination did not reveal any significant alteration.
Initial laboratory tests showed: CRP 12.1 (normal value up to 1.0), total leukocytes urinary tract infection 40.6%, leukocytes 8,600, normal leukocyte count, platelets 230,000, erythrocyte sedimentation rate 206.4 mg/dl, alkaline phosphatase
Samples were obtained for two hemocultives, urocultive and antibiotic treatment was initiated empirically (ceftriaxone), since the initial suspicion was a probable urinary tract infection.
However, the hemocultive and urocultive were negative.
Antibiotic treatment was continued thinking of negativization of urine sediment and cultures for previous use of antibiotics.
On the seventh day of treatment fever persisted and inflammatory parameters increased (PCR 24 and ESR 107).
The patient was admitted with computed axial tomography (CAT) of thorax, abdomen and pelvis, without evidence of febrile syndrome.
For this reason, the infectious study was expanded sequentially, highlighting: urine sediment composed of leukocytes (-), dry erythrocytes (-), bacteria (-), cylinders (-) and respiratory tract infection index (HCV), urinary tract
Subsequently, a transesophageal echocardiogram was performed, which was normal.
In view of the above, we requested antinuclear antibodies, antineutrophil cytoplasmic antibodies (ANCA), rheumatoid factor, complementemia and thyroid tests, without finding pathological findings.
Subsequently, the patient presented mild asymptomatic hypercal-cemia (11.2 mg/dL), with normal lactate levels and normal alkaline parathyroid hormone (6.0 pg/ml).
At 48 h calcemia increased to 14.9 mg/dL requiring management in a Critical Care Unit with parenteral hydration, corticosteroids and bisphosphonates.
Given the presence of severe hypercalcemia in the absence of findings suggestive of solid or lymphoproliferative neoplasms, in addition to the search for significant proteinuria in the compound urine sediment, we decided to investigate the presence of a normal monoclonal gammopathy.
Myelogras revealed severe myelomatosis with tapered cells and fibroblasts in 65% of the sample.
With these elements, the diagnosis of kappa light chain secretory MM was finally made and therapy with thalidomide and dexamethasone was initiated, yielding fever and improving its general state after 48 h of treatment.
