A white female patient aged 66 with a history of gastrointestinal haemorrhage due to peptic ulcer at the age of 42, menopause at the age of 50, osteoporosis, dorsal-lumbar arthrosis, dyslipidaemia, appendectomy. She was usually treated with rabeprazole 10 mg/24 hours, almagate on demand. She consulted for pain and stiffness in proximal areas of the limbs of 1 year of evolution, which in the last 3 months was accompanied by fever, asthenia, anorexia, loss of about 8 kg of weight and a depressive syndrome associated with organic pathology. Physical examination showed a good general condition with a temperature of 37.5ºC, blood pressure was normal, skin pallor and cardio-respiratory auscultation was normal.
Analyses revealed a haemoglobin of 10.8 g/dL, MCV 88.1 fl, ESR 75 mm, CRP 94 mg/dL, and D-dimers 400 ug/l. On biochemical examination GGT 139 U/L, f alkaline 217 U/L, iron 19 ug/dL, ferritin 436 ng/ml, glucose, creatinine, calcium, phosphorus, cholesterol, triglycerides, protein, GOT, GPT, LDH, CPK, sodium and potassium normal. Negative rheumatoid factor. Normal thyrotropin. b2 microglobulin, CEA and CA 19.9 normal. Blood cultures were negative. Urine sediment was normal. Faecal occult blood was negative. Chest X-ray showed a fibrous tract with residual appearance in the right lower lobe. Gastroduodenal transit was normal. Abdominal ultrasound and abdominal CT scan were normal. Gastroscopy was normal. Temporal artery biopsy was performed and showed only signs of arteriosclerosis.
With the diagnosis of polymyalgia rheumatica, treatment was started with deflazacort 30 mg/24 hours, with improvement and normalisation of haemoglobin, CRP and ESR. Deflazacort was progressively reduced and 7 months after starting treatment the patient was asymptomatic and was on a dose of 6 mg deflazacort per day.
When the patient was 69 years old, she was being treated with deflazacort 6 mg/24, paroxetine 20 mg/24, gabapentin 400 mg/12 h, omeprazole 20 mg/24, lormetazepam 1 mg/24. A routine check-up had been performed 6 months earlier, the patient was asymptomatic and haemoglobin, ESR and CRP were normal. She consulted for febrile fever and occasionally fever of 38.5 ºC predominantly in the evening with no apparent source, dry cough, anorexia, and diffuse abdominal pain. Physical examination was normal.
Blood tests showed haemoglobin 10.4 g/dL, Ht 31.9% (normal MCV, MCH and RDW). ESR 109 mm, and CRP 93 mg/dL. Biochemical analysis showed GGT 220 U/L, GPT 45 U/L, GOT 44 U/L, and ALP 153 U/L, iron 20 ug/dL, and ferritin 441.6 ng/ml. CK. Proteinogram normal. Normal thyroid hormones. Normal folate and cobalamin, normal haptoglobin. Negative direct Coombs' test. Urine sediment. Negative blood cultures, stool cultures and urine cultures. Serology of Toxoplasma, Cytomegalovirus, Epstein Barr, Salmonella tiphy and parathiphy, Brucella, Coxiella burnetti, adenovirus, respiratory syncytial virus, influenza A FC, B FC, parainfluenza 1+3 FC negative. HIV, hepatitis B and C virus serology negative. Sputum ZN negative. Mantoux test was negative. CEA and beta-2-microglobulin were normal. Ig G 10.60, IgA 1.76, IgM 2.55. Complement C3 and C4 normal. Rheumatoid factor, ANA, AMA, ANCA and anti LKM negative. Faecal occult blood was negative.
Chest X-ray showed cardiomegaly. The spine X-ray showed an area of sclerosis at L4, which in the lumbar spine CT scan corresponded to a bone infarction at L4. There were no significant findings on abdominal ultrasound. Thoracic-abdominal CT showed only a pericardial effusion. Gastroscopy was normal and colonoscopy showed diverticula and internal haemorrhoids.

The ECG showed sinus rhythm Fc 90 x' q in DIII and AVF and lack of septal vector activation. An echocardiogram showed severe anteroposterior pericardial effusion associated with a pattern of poor ventricular relaxation, without haemodynamic compromise. Pericardiocentesis was performed and approximately 200 cc of yellowish serous-fibrinous fluid was obtained, with a gelatinous character that solidified at rest; pericardial fluid analysis showed red blood cells 680/mm3, leukocytes 30 mm3, glucose 98 mg/dL, proteins 4.46 g/dL, LDH 284 UL, ADA 18 U/L; pericardial fluid culture was sterile, ZN stain negative; cytology was negative for malignant cells, with abundant fibrin, some inflammatory and mesothelial cells without atypia. The cardiac study was completed with myocardial perfusion scintigraphy which showed no perfusion abnormalities suggestive of myocardial ischaemia or necrosis. A temporal artery biopsy showed a transmural inflammatory infiltrate consisting of a mixture of polymorphonuclear, lymphocytes and giant cells; the infiltrate was accompanied by fracture of the internal elastic band. Treatment with deflazacort at 60 mg/day was started, improving the symptoms in a few days, and the pericardial effusion resolved in 3 months.