Replacement of the first metatarsophalangeal joint with a Swanson implant accompanied by open-wedge osteotomy of the first metatarsal bone for hallux valgus in rheumatoid arthritis

Hallux valgus is very common in rheumatoid arthritis (RA) and mostly accompanied by varus deformity of the first metatarsal bone, which is often corrected in surgeries for hallux valgus in nonarthritic condition, but rarely in RA. We performed the replacement of the first metatarsophalangeal (MTP) joint with a Swanson hinge toe implant accompanied with open-wedge osteotomy of the first metatarsal bone, aiming at reconstruction of a functioning first MTP joint without recurrence of hallux valgus. Fifteen feet of 11 patients with RA were studied with a mean follow-up period of 45.1 months. The American Orthopaedic Foot and Ankle Society (AOFAS) scale improved significantly from 39 points preoperatively to 81.7 at the last follow-up. The hallux valgus angle (HVA), angle between the first and second metatarsal bones (M1/2), and that between the first and fifth (M1/5), measured on standing anteroposterior radiographs, decreased significantly from 49.8°, 16.7°, and 34.4° preoperatively to 10.9°, 8.7°, and 22.2° at the last follow-up, respectively. Union of the corrected first metatarsal bone was recognized in all cases and no such problems as infection, dislocation, or implant fracture were observed. These data suggest that replacement of the first MTP joint with a Swanson implant accompanied with open-wedge osteotomy of the first metatarsal bone can be a useful option for hallux valgus in RA.     

Thioredoxin-1 protects against hyperoxia-induced apoptosis in cells of the alveolar walls

BACKGROUND: The mechanisms of hyperoxia-induced lung injury remain poorly defined. Thioredoxin-1 (TRX-1) is a small ubiquitous protein that acts as an important radical scavenger. We investigated the effect of TRX-1 on apoptosis in hyperoxia-induced lung injury. METHODS: Mice were exposed to 98% O(2) to produce a model of hyperoxia-induced lung injury. Using transgenic mice overexpressing human TRX-1 (hTRX-1), we assessed lung structure (n=4 per group), immunohistochemical staining for 8-hydroxy-deoxyguanosine (n=4 per group), TUNEL staining (n=5 per group), cytokine (n=5 per group) of IL-1beta and IL-6, and protein (n=6 per group) and m-RNA levels (n=4 per group) (or both) of cytochrome c, Bcl-2, Bax, p21, and p53 in the lungs. RESULTS: After exposure to hyperoxia, hTRX-1 transgenic mice had significantly decreased alveolar damage. The apoptotic index was significantly lower in hTRX-1 transgenic mice than in wild-type (WT) mice after exposure to hyperoxia. Protein expression of cytochrome c in the lung was significantly lower in hTRX-1 transgenic mice than in WT mice after exposure to hyperoxia. Protein expression and m-RNA levels of Bcl-2 in the lung were significantly higher in hTRX-1 transgenic mice than in WT mice after exposure to hyperoxia. TRX-1 had no effect on the protein and m-RNA levels of Bax and p21. The protein and m-RNA levels of p53 was unaffected by hyperoxia in hTRX-1 transgenic mice. The cytokine level of IL-6 was significantly higher in hTRX-1 transgenic mice than in WT mice after exposure to hyperoxia. TRX-1 had no effect on cytokine level of IL-1beta. CONCLUSIONS: These findings suggest that overexpression of hTRX-1 protects against hyperoxia-induced apoptosis in cells of the alveolar walls. The up-regulating Bcl-2 protein is considered to be one of antiapoptotic effects of TRX-1 in hyperoxia-induced lung injury.     

Plasmapheresis Affects T Helper Type‐1/T Helper Type‐2 Balance of Circulating Peripheral Lymphocytes

Abstract: Plasmapheresis not only removes humoral factors, but may also modulate cellular immunity. We investigated whether plasmapheresis influenced T helper type‐1/T helper type‐2 (Th1/Th2) cytokine‐producing‐cell balance in 3 patients with neuroimmunological disease. The production of interferon‐γ (IFN‐γ), interleukin‐2 (IL‐2), and IL‐4 in the culture supernatant of peripheral blood mononuclear cells stimulated by anti‐CD3 and anti‐CD28 was assayed. In 2 of 3 patients, plasmapheresis (immunoadsorption or plasma exchange) reduced Th1/Th2 cytokine ratio. The results may suggest that plasmapheresis induces a shift of Th1/Th2 balance in peripheral blood.     

Quantification of red blood cell fragmentation by automated haematology analyser XE‐2100

The extent of red blood cell fragmentation in peripheral blood is useful for diagnosis and follow‐up in many diseases, e.g. haemolytic uremic syndrome, transplantation‐associated thrombotic microangiopathy (BMT‐TMA). However, this quantification still relies on manual counting of fragmented red cells on blood smears. We have developed a quantification system by gating a fixed area of fragmented red blood cells (Gate 1) on an automated haematology analyser (XE‐2100, Sysmex Co., Kobe, Japan). The fragmented red cell percentage (FRC%) calculated with this system, from 100 samples, was highly correlated with the manual count (r=0.902, P < 0.0001). Because microcytic anaemia specimens usually occupy a lower position on the XE‐2100 scattergram, with microcytic cells overlapping Gate 1 and causing a spuriously high FRC% calculation, a supplementary gate (Gate 2) was added. Using the particle number in this gate as well as in Gate 1, a revised method for such samples was developed and its validity confirmed (revised FRC% correlated with a manual count for 10 subjects (P < 0.001). Because this gating system can be programmed on any XE‐2100, it is likely to prove useful for accurate quantification of red blood cell fragmentation and for the monitoring of the development of BMT‐TMA.     

Extent of pathologic invasion of the inferior vena cava in resected liver cancer compared with possible caval invasion diagnosed by preoperative images

The extent of cancerous invasion of the inferior vena cava (IVC) determined from resected liver cancer was examined pathologically. Ten patients presenting with liver cancer (metastatic liver cancer, five patients; hepatocellular carcinoma, three; and cholangiocellular carcinoma, two) were diagnosed with positive IVC invasion using preoperative imaging techniques of extracorporeal ultrasonography, computed tomography, magnetic resonance imaging, and vena cavography. The diagnostic criterion for positive IVC invasion by preoperative imaging was longitudinal IVC compression measuring over 50 mm, or transverse IVC compression extending to more than half the circumference of the IVC, or the presence of lesions protruding into the IVC lumen, or the presence of developed collateral veins. All patients underwent combined resection of the IVC. However, pathology results revealed that four of the ten patients had no cancerous invasion of the IVC, and that the extent of invasion along both the longitudinal and transverse axes of the IVC was much smaller than the compression shown by imaging results. We believe that detailed preoperative assessment, using a more precise imaging technique, as well as further intraoperative examination, is required to predict the full pathological extent of cancerous invasion of the IVC.     

Femoral Vein Stasis During Laparoscopic Cholecystectomy Effect of an Intermittent Sequential Pneumatic Compression Device

Background: During laparoscopic cholecystectomy (LC), venous stasis of the legs may occur which cannot be prevented by a graded compression bandage used for a standard laparotomy. In this study, we investigated whether femoral vein stasis during LC could be prevented using an intermittent sequential pneumatic compression device (IPC). Methods: The effects of an IPC on blood flow in the legs prior to pneumoperitoneum (baseline), at pneumoperitoneum, at postural change and at deflation were examined by color Doppler ultrasonography on each of two groups, namely the patients without an IPC on the lower extremities (group 1, n = 20) and the patients with an IPC (group 2, n = 20). Results: The peak femoral vein velocity in group 1 at a pneumoperitoneum pressure of 10 mmHg in the reverse Trendelenburg's position was significantly decreased to 29.3 ± 3.4% of the baseline value (P < 0.05). However, in group 2, the velocity was maintained and there was no significant decrease. The blood flow velocity when the IPC was used significantly differed from that when the IPC was not used (P < 0.01). The area of the femoral vein in group 1 at a pneumoperitoneum pressure of 10 mmHg in the reverse Trendelenburg's position significantly increased to 379.5 ± 16.3% of the baseline value (P < 0.05). In group 2, it significantly increased to 387.0 ± 19.1% (P < 0.05). However, the area of the femoral vein when the IPC was used did not significantly differ from that when the IPC was not used. Conclusion: The use of an IPC maintained the peak femoral vein velocity even under pneumoperitoneum and in the reverse Trendelenburg's position.     

Endoscopic and histological comparison of nonulcer dyspepsia with and without Helicobacter pylori infection evaluated by the modified Sydney system

OBJECTIVE: Our aim was to identify endoscopic features associated with Helicobacter pylori (H. pylori) infection in patients with nonulcer dyspepsia. METHODS: A total of 50 infected patients with nonulcer dyspepsia who underwent endoscopy with antral and corporal biopsies and 50 patients matched for age and sex but with nonulcer dyspepsia without H. pylori were reviewed retrospectively by three endoscopists blinded to the H. pylori status and the patient's history. The endoscopic findings of gastritis, classified by a modification of the Sydney system as present or absent, were evaluated, and the histological severity was graded by the updated Sydney system. RESULTS: For endoscopic features, the odds ratio was 53.1 (95% confidence interval, 6.8-414.9) for edema, 18.8 (5.8-60.5) for erythema with reddish streaks excluded, 0.0275 (0.0002-0.477) for reddish streaks, 17.4 (0.97-313.7) for friability, 14.2 (5.1-40.0) for exudate, 17.2 (2.2-137.6) for flat erosions, 2.54 (0.81-7.94) for raised erosions, 40.1 (2.3-694.5) for rugal hypertrophy, 19.1 (2.4-151.6) for rugal atrophy, 96.2 (23.4-395.9) for a vascular pattern, 0.125 (0.010-1.06) for bleeding spots, and 21.0 (2.6-166.5) for nodularity. The histological severity of inflammation, neutrophil activity, and atrophy in the antrum and corpus and of metaplasia in the antrum was greater in the infected patients than in the noninfected patients. CONCLUSIONS: Endoscopic features associated with H. pylori were a vascular pattern, edema, rugal hypertrophy, nodularity, rugal atrophy, erythema with reddish streaks excluded, flat erosions, and exudate. These endoscopic features were associated with the histological findings of inflammation, neutrophil activity, atrophy, and metaplasia.     

CASE REPORT: Pure Red Cell Aplasia Associated with Parvovirus B19 Infection in a Patient with Ulcerative Colitis

Anemia is a common problem that results from various causes in patients with ulcerative colitis (UC), but there is little information on the association of UC with pure red cell aplasia (PRCA). We describe the first case of parvovirus-induced PRCA in UC. A 28-year-old woman with chronic UC was admitted to the hospital for treatment of active pancolitis. Three courses of pulse therapy with methylprednisolone provided complete remission. However, the patient developed reticulocytopenia and a subsequent fall in hemoglobin to 6.2 g/dl. Bone marrow examination revealed selective aplasia of red cell precursors and giant pronoromoblasts. Enzyme immunoassay identified specific immunoglobulin M antibody against parvovirus B19 in the serum. Based on these findings, the diagnosis of PRCA caused by the virus was made. The patient was treated with a 3-day course of intravenous immunoglobulin (5 g/day), resulting in brisk reticulocytosis, folowed by normalization of hemoglobin level. In conclusion, Chronic or acute blood loss in UC associated with enhanced red cell turnover might be a risk factor for PRCA when affected patients contract parvovirus B19 infection.     

Expression of apoptosis-associated protein RCAS1 in macrophages of histiocytic necrotizing lymphadenitis

Receptor-binding cancer antigen expressed on SiSo cells (RCAS1), which is recognized by the 22-1-1 monoclonal antibody (MoAb) against human uterine adenocarcinoma cell line SiSo, has been identified on various kinds of cancer cells. RCAS1 appears to be an apoptosis-associated protein that induces apoptosis in activated T-cells and erythroid progenitor cells. We previously demonstrated that monocytes/macrophages express RCAS1. In the present study, we investigated RCAS1 expression by 22-1-1 MoAb in histiocytic necrotizing lymphadenitis (HNL), which is characterized by necrotic lesions consisting of T-cells undergoing apoptosis and macrophages in proliferation. Expression of RCAS1 was analyzed by immunohistochemical staining in 9 cases of HNL and in 9 cases of reactive lymphadenitis used as a control. The ratio of RCAS1+ cells to CD68+ cells (monocytes/macrophages) was significantly higher in the patients with HNL than in the patients with reactive lymphadenitis (P = .0002; paired t test). Our findings suggest that RCAS1 expressed on macrophages may play an important role in the induction of activated T-cell apoptosis in cases of HNL.