Vasculopathy is rarely reported in neurofibromatosis type 1, but when it occurs it primarily involves the aorta and its main branches. Among vasculopathies, aneurysmal dilatation is the most common form. Although several case reports concerning aneurysms or pseudoaneurysms of visceral arteries in neurofibromatosis type 1 patients have been reported, there are no reports describing gastroduodenal artery aneurysms associated with neurofibromatosis type 1. We experienced a case of life-threatening duodenal ulcer bleeding from a ruptured gastroduodenal artery aneurysm associated with neurofibromatosis type 1. We treated our patient by transarterial embolization after initial endoscopic hemostasis. To our knowledge, this is the first reported case of its type. High levels of suspicion and prompt diagnosis are required to select appropriate treatment options for patients with neurofibromatosis type 1 experiencing upper gastrointestinal bleeding. Embolization of the involved arteries should be considered an essential treatment over endoscopic hemostasis alone to achieve complete hemostasis and to prevent rebleeding.
Nonseptic inflammation of the olecranon bursa is frequent because of its superficial location.1 This olecranon bursitis can be due to variable causes such as trauma, overuse, inflammatory arthropathy, chronic degenerative osteoarthritis, rheumatoid arthritis (RA), and gout.2–4 A cyst (or geode) is a subarticular cystic lesion, and this is often seen in osteoarthritis and RA.5 Other forms of arthritis, such as hemophilia, calcium pyrophosphate deposition disease, and gout, can show cysts.5–7 These cysts are usually small but can enlarge and reach 5 or 6 cm in diameter.8 Although cysts are common in RA, cysts occurring in the olecranon have been rarely reported,9–12 and most of them were related to spontaneous fractures through olecranon cysts.9–11 To our knowledge, a report of communication between olecranon bursitis and an olecranon cyst has not been reported in the English literature. We present a case of olecranon bursitis in a 23-year-old rheumatoid patient in which communication with an olecranon cyst was confirmed on sonography and at surgery. On color scale sonography, compression with the ultrasound transducer on the bursa was useful for confirming the communication between the olecranon bursa and the cyst by observation of the color flow signal. A 23-year-old woman had pain, swelling, and a soft, palpable, masslike lesion in the left elbow. She had known RA with polyarthralgia, especially in both wrists and the left elbow, for 3 years. Radiographs of the left elbow joint (Figure 1) showed a large cystic lesion in the olecranon of the ulna and elbow changes consistent with RA. In the olecranon, a relatively well-defined osteolytic lesion with a narrow transitional zone, a thin sclerotic rim, and inner bony ridges or septations was shown. There was no matrix calcification or periosteal reaction. In addition, anterior joint capsular distension and posterior soft tissue bulging were noted. The changes suggested an olecranon cyst as the underlying abnormality, but a differential diagnosis such as a giant cell tumor or other bone tumor had to be included. Radiograph (lateral view) of the left elbow shows a relatively well-defined osteolytic lesion in the olecranon. Soft tissue swelling (white arrows) is shown in the posterior aspect of elbow, and anterior joint capsular bulging (black arrows) is suggested. On sonography (Figure 2), olecranon bursitis was noted, with inner marked synovial hypertrophies, an echogenic fluid collection, and septations. In addition, a communication between the olecranon bursitis and the intramedullary portion of the olecranon was shown through a posterior cortical defect of the olecranon. To-and-fro flow movements were noted through this cortical defect on compression with the ultrasound transducer, and this finding was noted as movement of echogenic material on gray scale sonography and a color flow signal on color scale sonography. In addition, irregular cortical margins, subchondral erosions, a hypertrophied, echogenic synovium with hypervascularity, and joint effusion were shown in the elbow joint. These findings suggested prominent and chronic synovitis such as RA. Magnetic resonance imaging (MRI) was then performed. A, Transverse sonogram shows the olecranon bursa (B) with inner echogenic material. A posterior cortical defect (arrow) of the olecranon (O) is also shown. B, Longitudinal sonogram shows echogenic material and posterior enhancement (arrows) from the bursa (B) in the intraosseous portion of the olecranon (O). C, Transverse color scale sonogram shows a color flow signal (F) from to-and-fro movements of inner fluid and debris through the cortical defect (communication between the bursa and geode) on compression with the transducer. On MRI (Figure 3), it was possible to easily see that the osteolytic lesion in the olecranon was a cyst. Magnetic resonance imaging also showed the presence of communications between the bursitis and the cyst and between the cyst and the articular joint space of the elbow. The patient underwent open synovectomy, removal of the bursa, and careful curettage of the cyst with autogenous iliac bone grafts to relieve the elbow arthritis with bursitis and to prevent a pathologic fracture. During surgery, marked synovial hypertrophy and rice bodies were visible all over the elbow joint. The bursa was distended with inner fluid and inflammatory granulelike tissue, and the cyst was filled with an extensive granulationlike appearance of the tissue. In addition, there were communications between the olecranon bursitis and the olecranon cyst and between the olecranon cyst and the articular elbow joint space. Histologic examination of the tissue in the bursa and cyst revealed nonspecific chronic inflammation similar to a pannus, with lymphoplasmacytic infiltration and eosinophilic nodular proliferation. There was no bacterial growth on a culture of aspirated fluid. The postoperative course of the patient was uneventful, and she was asymptomatic with no radiologic findings of recurrence at the 5-month follow-up. The olecranon bursa is a subcutaneous space lined with a synovial membrane that secretes fluid to provide smooth and almost frictionless motion between the skin, the subcutaneous tissues, and the olecranon. Nonseptic olecranon bursitis can be due to overuse, repetitive trauma, inflammatory arthropathy, or obesity.1 In addition, diseases that lead to a complicated aspect of affected and noninfected bursae include chronic degenerative arthritis, repetitive trauma, acute trauma, RA, and gout.1 Bursitis can be diagnosed by sonography, computed tomography, and MRI. On these imaging modalities, a fluid collection with lobulation, septation, complexity, wall thickening, adjacent joint effusion, soft tissue edema, and wall enhancement posterior to the olecranon can indicate a diagnosis of olecranon bursitis.1 A. Sagittal proton-weighted fat-suppressed MRI (repetition time, 2200 milliseconds; echo time, 20 milliseconds) shows a large cyst (C) in the olecranon. A communication (arrow) between the cyst and the articular joint space is clearly shown. There are synovial changes and subchondral changes in the elbow joint with joint capsular bulging. B, Enhanced axial T1-weighted fat-suppressed MRI (repetition time, 600 milliseconds; echo time, 20 milliseconds) shows a communication between the olecranon bursa (B) and the olecranon cyst (C) through a posterior cortical defect. Thick peripheral enhancements are shown in the walls of the cyst and bursa. Thick and irregular synovial enhancements (arrows) are visible in the elbow joint space. The term “geode” was originally a geologic term meaning a rounded pocket of gas in a mineral specimen.5,13 Geode (or cyst) is used interchangeably with subchondral cyst and can be subarticular, subchondral, or synovial.7 Cyst formation is most commonly associated with osteoarthritis but is also associated with other forms of arthritis such as RA, hemophilia, calcium pyrophosphate deposition disease, and gout.7 In RA, the commonly affected sites by cysts are the tibial plateau and the femoral neck.13,14 Large cysts may be confused with other destructive lesions that develop close to joints. These include osteomyelitis, septic arthritis, pigmented villonodular hyperplasia, hemophilia, and tumors such as giant cell tumors and metastases.7 Although the mechanism of cyst formation has not been made clear, 2 theories have been suggested.7,13 One is that the pannus, arising from the synovial membrane under inflammatory conditions, causes destruction of articular cartilage and extends to the subchondral bone. At this time, the pannus becomes a cyst, with increased pressure from the joint cavity being transmitted to subchondral space.15 In this theory, communication between the articular cavity and the cyst may be essential. Actually, there were communications between cysts and joint cavities in surgically proven and image-based reports by Maher et al,5 Torikai et al,12 and Lohse et al.16 Another theory involves the development of true intraosseous rheumatoid nodules in the subchondral regions.13,17 In our case, a cortical defect between the nonarticular cortex of the olecranon and the olecranon bursa was present. In addition, there were several cortical defects in the articular side of the olecranon, showing communications with the articular cavity and the cyst. Therefore, we think that first the cyst formation was made from invagination of the intra-articular synovium into the olecranon; the second inflammatory synovium in the cyst eroded the posterior olecranon cortex; and then a communication between the olecranon cyst and the olecranon bursa was formed, rather than secondary cyst formation after direct erosion of the posterior olecranon cortex by the inflammatory olecranon bursa. We think that detection of communications between an olecranon cyst and a bursa/articular joint is important because communications through the cortex are weak areas, and these can be beginnings of cortical fractures. In addition, more careful procedures are needed to prevent intraoperative fractures and recurrence of intraosseous cysts and superficial bursitis in these areas during the curettage and bone grafting. In conclusion, we report unusual findings of communication between the olecranon bursa and an olecranon cyst confirmed by sonography before MRI and surgery. On color scale sonography, compression with the ultrasound transducer on the bursa was useful for confirming the communication between the olecranon bursa and the cyst by observation of the color flow signal.
With an increased use of the press-through package (PTP) tablet, there has also been an increase in mis-swallowing cases, especially in elderly patients. We report a rare case of PTP-induced small bowel perforation and fistula formation with adjacent small bowel in a healthy elderly patient, who experienced persistent abdominal pain of unknown cause. A 62-year-old healthy man was admitted to our hospital with left abdominal pain that started one month ago. Neither abdominal tenderness nor rebound tenderness was present on physical examination. His vital signs and all other test results were within normal limits. However, a 2.5 cm curved radiopaque material within his thickened small intestine was incidentally detected on an abdominal computed tomography. He underwent laparoscopic small bowel resection, which revealed foreign body in the distal small intestine. Edema, perforation, and adhesions with the surrounding tissues were also noticed in the distal small intestine. Foreign body was turned out to be PTP, and this was considered to be responsible for the small bowel perforation and fistula formation. Precautions regarding PTP usage are necessary to prevent inadvertent PTP ingestion and its related complications, such as perforation, especially in the elderly population.
Abstract Background/Aim: Cirrhosis is a long‐term consequence of chronic hepatic injury and no effective therapy is currently available for this disease. Recent reports have shown that the mesenchymal stem cells (MSCs) have the capacity to differentiate into hepatocytes, and umbilical cord blood is a rich source of MSCs. Hence, we investigated the effect of infusing of human umbilical cord blood‐derived MSCs (HMSCs) in carbon tetrachloride (CCl 4 )‐induced cirrhosis in a rat model. Methods: The effect of HMSCs on cirrhosis was evaluated using haematoxylin and eosin and Masson's trichrome staining. To evaluate cirrhosis‐related factors, we measured protein and mRNA expression of transforming growth factor β 1 (TGF‐β 1 ), collagen type I and α‐smooth muscle actin (α‐SMA). Results: Histological findings showed that liver fibrosis in rats was alleviated by HMSCs infusion. Interestingly, CM‐DiI‐labelled HMSCs expressed the hepatocyte‐specific markers, human albumin and α‐fetoprotein. Infusion of HMSCs significantly inhibited TGF‐β 1 , collagen type I and α‐SMA expressions in CCl 4 ‐induced cirrhotic rats. Conclusion: Our results showed that HMSCs infusion could improve liver fibrosis in rats with CCl 4 ‐induced cirrhosis, raising the possibility for clinical use of HMSCs in the treatment of cirrhosis.
A 75-year-old man attended our hospital for replacement of a percutaneous endoscopic gastrostomy (PEG) tube. He had originally undergone PEG tube placement at our hospital 2 years ago, and after insertion the position of the hub had been checked by gastroscopy. However, placement of the most recent PEG tube had been done at another hospital 1 year ago, with no gastroscopic evaluation. When the patient attended our hospital 1 year later for replacement of the PEG tube, we could not find its hub in the stomach on gastroscopy. Instead, a scar was detected at the previous gastrostomy site. A nonenhanced abdominal computed tomography (CT) scan taken to check the location of the PEG tube revealed that it had been inserted into the small intestine ([Fig. 1 a, b]).
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