Tuberculosis osteomyelitis in an old fused hip; activated by prednisolone, salazosulfapyridine, and low-dose methotrexate therapy in a patient with rheumatoid arthritis.

Osteoarticular tuberculosis can occur in patients with rheumatoid arthritis (RA) receiving immunosuppressive therapy. Here, we describe a case of tubercular osteomyelitis in an old fused hip of a patient with RA who received prednisolone, salazosulfapyridine (SASP), and low-dose methotrexate (MTX). A 77-year-old man with a 4-year history of RA was admitted with a complaint of general fatigue. His symptoms of RA had been well controlled with a combination of prednisolone, SASP, and low-dose MTX. Because the laboratory data showed an increase in serum C-reactive protein levels, we suspected pneumonia. There was expansion of a pre-existing consolidation in the right lower lobe of his lung on chest computed tomography, and the sputum culture was positive for Klebsiella oxytoca. His family physician prescribed empiric antibiotics for pneumonia. Although the QuantiFERON® test result was positive, the acid-fast bacillus staining result was negative in the sputum. He started complaining of pain in his left hip, where arthrodesis was performed for an unknown reason at the age of 20 years. Sonographic examination of his left thigh revealed fluid collection. The aspiration culture of the fluid was positive for Mycobacterium tuberculosis. He was initiated on rifampicin, isoniazid, pyrazinamide, and ethambutol. Surgical debridement of the fused left hip was performed twice along with a removal of previously implanted materials. Although infrequent, osteoarticular tuberculosis can occur during immunosuppressive therapy, especially in elderly patients. Physicians should be aware of a history of possible tuberculosis infection, such as hip arthrodesis, when prescribing MTX along with SASP and corticosteroid in the elderly.

Tendon stump type on magnetic resonance imaging is a predictive factor for retear after arthroscopic rotator cuff repair.

BACKGROUND: Fatty infiltration of the rotator cuff musculature increases in larger tears and is a factor in retearing. However, tearing may recur even in patients with small original tears and little fatty infiltration of the rotator cuff musculature. We devised a system to classify the rotator cuff tendon stump by magnetic resonance imaging (MRI) signal intensity and investigated prognosis-related factors associated with retear based on other MRI findings. METHODS: We analyzed and compared the signal intensity of the rotator cuff tendon stump and deltoid on preoperative T2-weighted fat-suppressed MRI in 305 patients who underwent primary arthroscopic rotator cuff repair. We also investigated the tear size, Goutallier stage, and global fatty degeneration index. RESULTS: In a type 1 stump, the tendon stump had a lower (darker) signal intensity than the deltoid. In type 2, the signal intensities of the tendon stump and deltoid were equivalent. In type 3, the signal intensity of the tendon stump was higher (whiter) than that of the deltoid. Multiple regression analysis of the association between retear and other parameters identified stump type (odds ratio [OR], 4.28), global fatty degeneration index (OR, 2.99), and anteroposterior tear size (OR, 1.06) as significant factors. The retear rates were 3.4% for type 1 stumps, 4.9% for type 2, and 17.7% for type 3. CONCLUSIONS: Type 3 stumps had a significantly higher retear rate, suggesting that stump signal intensity may be an important indicator for assessing the stump's condition. Our stump classification may be useful in choosing suture techniques and postoperative therapies.

Cluster differentiation-36 deficiency type 1 and acute coronary syndrome without major cardiovascular risk factors: case report.

A 45-year-old man without major coronary risk factors, including hypertension, diabetes mellitus, smoking, hypercholesterolemia, hyperuricemia, or a family history of early cardiovascular disease, presented with acute coronary syndrome. Angiography showed thrombus formation in segment 7 of the left anterior descending coronary artery, and percutaneous coronary intervention was successful after implantation of a bare metal stent. Scintigraphy showed the absence of 123I-beta-methyl-iodophenyl pentadecanoic acid accumulation in the myocardium. Flow cytometric analysis of platelets and monocytes showed the absence of cluster differentiation (CD)-36 expression. These findings are consistent with a diagnosis of CD36 deficiency type 1, which might be associated with cardiovascular disease. The patient had no apparent major coronary risk factors except for insulin resistance and an abnormal lipoprotein profile. The findings suggest that in this case the CD36 deficiency type 1 was the pathogenic mechanism of acute coronary syndrome relative to insulin resistance and modification of the lipid profile.