The incidence of trochlear dysplasia in anterior cruciate ligament tears

Purpose

The purpose of the present epidemiologic study is to record the radiographic presence of trochlear dysplasia and patella alta in patients who undergo anterior cruciate ligament (ACL) reconstruction as a potential underlying factor for post-operative anterior knee pain (AKP).

Methods

All consecutive cases of skeletally-mature ACL-deficient knees that would undergo ACL reconstruction in three different hospitals were prospectively included during a six-month period. Inclusion criteria were acute and sub-acute ACL injury with no previous ipsilateral knee operation. Patients with chronic ACL tears, prior-to-ACL-injury history of patellar instability or other PF disorders were excluded from the study.

Results

A total of 299 knees were included (mean age 32 ± ten years). Forty-four (14.7 %) knees had a positive ‘crossing sign’ in the lateral X-rays and 255 (85.3 %) had no sign of trochlear dysplasia (p < 0.01). Among the cases with trochlear dysplasia, 41 (93 %) had type A trochlear dysplasia with the presence only of the ‘crossing sign’ and three (7 %) had type C trochlear dysplasia. Patellar height results included a mean Caton-Deschamps index of 1.0 ± 0.14 (0.5–1.4). Twenty (6.6 %) knees had an index of less than 0.8, and two (0.6 %) knees had an index less than 0.6. In contrast, 15 (5.0 %) knees had an abnormal value of more than 1.2, indicating patella alta.

Conclusions

The most important finding of the study is the increased prevalence of trochlear dysplasia and patella alta in patients with ACL injury, when compared to the incidence of trochlear dysplasia and patella alta in the general population in the literature. This finding could sound as an alert of a possible additional risk factor for post-operative anterior knee pain after ACL reconstruction.     

Laparoscopic inguinal hernioplasty after radical prostatectomy: is it safe? Prospective clinical trial

Introduction

Despite inguinal hernia repair being one of the most common elective operations performed in general surgical practice, there are many controversies including indications for repair and selection of the surgical technique. In recent years, laparoscopic repair has gained wider acceptance because it is associated with fewer postoperative complications and less chronic pain when compared with conventional approaches with similar recurrence rate. However, patients with lower abdominal surgery are contraindicated for laparoscopic approach. There are few studies that evaluated whether patients who have been subjected to radical prostatectomy might be subjected to laparoscopic hernia repair with the same benefits as those without previous radical prostatectomy.

Methods

Between March 2010 and March 2013, 20 consecutive patients, who had been subjected to prior radical prostatectomy, underwent laparoscopic transabdominal inguinal repair and were followed prospectively. Surgical procedure was performed using a standard technique.

Results

Mean operative time was 67.5 min. There was only one (5 %) intraoperative minor complication, an injury to the inferior epigastric vessels, which was managed by clipping of the vessels. There were no major postoperative complications. After 24 h and on the seventh postoperative day, 85 and 90 % of patients had no pain or only complained of discomfort, respectively. Nine patients (45 %) did not need any analgesics postoperatively. The mean time to return to leisure activities and to work was 3.1 and 5.6 days, respectively. There was no conversion to open surgery. All patients were discharged within 24 h. After a mean follow-up of 14 months, none of the patients presented recurrence.

Conclusion

TAPP after prostatectomy is safe and effective. It seems that patients undergoing laparoscopic repair after radical prostatic resection have the same benefits as those without prostatectomy.     

Cytokine activation during attacks of the hyperimmunoglobulinemia D and periodic fever syndrome

The hyperimmunoglobulinemia D and periodic fever (hyper-IgD) syndrome is typified by recurrent febrile attacks with abdominal distress, joint involvement (arthralgias/arthritis), headache, skin lesions, and an elevated serum IgD level (> 100 U/mL). This familial disorder has been diagnosed in 59 patients, mainly from Europe. The pathogenesis of this febrile disorder is unknown, but attacks are joined by an acute-phase response. Because this response is considered to be mediated by cytokines, we measured the acute-phase proteins C-reactive protein (CRP) and soluble type-II phospholipase A2 (PLA2) together with circulating concentrations and ex vivo production of the proinflammatory cytokines interleukin-1 alpha (IL-1 alpha), IL-1 beta, IL-6, and tumor necrosis factor alpha (TNF alpha) and the inhibitory compounds IL-1 receptor antagonist (IL-1ra), IL-10, and the soluble TNF receptors p55 (sTNFr p55) and p75 (sTNFr p75) in 22 patients with the hyper-IgD syndrome during attacks and remission. Serum CRP and PLA2 concentrations were elevated during attacks (mean, 213 mg/L and 1,452 ng/mL, respectively) and decreased between attacks. Plasma concentrations of IL-1 alpha, IL-1 beta, or IL-10 were not increased during attacks. TNF alpha concentrations were slightly, but significantly, higher with attacks (104 v 117 pg/mL). Circulating IL-6 values increased with attacks (19.7 v 147.9 pg/mL) and correlated with CRP and PLA2 values during the febrile attacks. The values of the antiinflammatory compounds IL-1ra, sTNFr p55, and sTNFr p75 were significantly higher with attacks than between attacks, and there was a significant positive correlation between each. The ex-vivo production of TNF alpha, IL-1 beta, and IL-1ra was significantly higher with attacks, suggesting that the monocytes/macrophages were already primed in vivo to produce increased amounts of these cytokines. These findings point to an activation of the cytokine network, and this suggests that these inflammatory mediators may contribute to the symptoms of the hyper-IgD syndrome.     

T cells from patients with Hodgkin's disease have a defective T-cell receptor zeta chain expression that is reversible by T-cell stimulation with CD3 and CD28

To investigate the mechanisms underlying the deficiency of T lymphocytes from patients with Hodgkin's disease, we investigated the expression of the T-cell receptor (TCR) zeta chain in patients with Hodgkin's disease. By flow cytometry using an anti-zeta chain monoclonal antibody, peripheral blood T lymphocytes from patients with untreated Hodgkin's disease were shown to express decreased levels of the TCR zeta chain. After stimulation by combined CD3 and CD28 cross- linking, T cells from Hodgkin's disease patients upregulated zeta chain protein expression to normal values within 48 hours and achieved a cytolytic potential and levels of interleukin (IL)-2 secretion that were not different from T cells obtained from healthy controls. These results show that downregulation of the TCR zeta chain in Hodgkin's T lymphocytes is a reversible event. Costimulation of CD3 and CD28 is a novel approach for overcoming the T-cell deficiency in Hodgkin's disease and might be exploited clinically. As upregulation of the zeta chain can also be achieved using bispecific monoclonal antibodies (BI- MoAbs) with specificity for tumor antigens and CD3 and CD28, respectively, an immunotherapy with CD3/CD30 and CD28/CD30 Bi-MoAbs may overcome and should therefore, not be jeopardized by the inherent T- cell deficiency in patients with Hodgkin's disease.     

High-dose intravenous gammaglobulin in alloimmunized platelet transfusion recipients

High-dose intravenous gammaglobulin (polyvalent immunoglobulin G) has been shown to be of benefit in some patients with immune thrombocytopenic purpura (ITP), possibly by producing reticuloendothelial system blockade. We studied this approach in patients refractory to random donor platelet transfusion using an IV IgG preparation manufactured by the Swiss Red Cross. Eleven adult patients with acute leukemia received either 0.4 g IgG/kg/d intravenously X five days (four patients) or 0.6 g/kg/d X five days (seven patients). All patients had high levels of lymphocytotoxic antibody and poor responses to random donor platelets. Except for mild headaches in two patients, there were no side effects related to the IgG infusions. All patients had significant elevations of serum IgG on the day after completion of treatment. Either random donor or partially HLA-matched platelet transfusions were administered the day after and, in some cases, during the IgG therapy. No patient had an improvement in one hour posttransfusion platelet count increments. Two additional patients received pooled platelet concentrates incubated for 30 minutes at 37 degrees C with IgG at a final concentration of 3 g% prior to transfusions. These results indicate that high-dose IgG, an extremely expensive treatment, cannot be recommended for alloimmunized adults with leukemia.     

High incidence of monoclonal proteins in the serum and urine of chronic lymphocytic leukemia patients

Chronic lymphocytic leukemia (CLL) is generally considered a nonsecretory B cell immunoproliferative disorder. Conventional electrophoretic and immunoelectrophoretic methods have revealed serum monoclonal proteins in less than 10% of these patients. However, there is increasing experimental evidence from in vitro studies demonstrating that CLL cells may secrete immunoglobulins, particularly free light chains. We examined the serum and urine of 36 consecutive CLL patients for monoclonal proteins using sensitive immunochemical methods (high resolution agarose gel electrophoresis combined with immunofixation). The results obtained were correlated with the Rai stage, quantitative immunoglobulin levels, and lymphocyte membrane immunoglobulin phenotype of the leukemic cells. Twenty-three monoclonal proteins were identified in the serum or urine of 22 patients, an incidence of 61%. Six patients had serum monoclonal proteins, seven had only urinary monoclonal proteins, and nine had monoclonal proteins in serum and urine. In every instance the monoclonal protein was the same light chain type as expressed on the leukemic cells. Our findings suggest that the monoclonal proteins observed in the serum or urine of CLL patients are secretory products of the tumor cells and that their discovery is a function of the sensitivity of the method used for their detection.     

Immune responses to major histocompatibility complex homozygous lymphoid cells in murine F1 hybrid recipients: implications for transfusion-associated graft-versus-host disease

Graft-versus-host disease (GVHD) is currently encountered after bone marrow transplantation and transfusion. GVHD associated with transfusion (TA-GVHD) in apparently immunocompetent recipients has been recently reported with increasing frequency. A consistent finding in many of these cases is that the recipient received blood from a donor homozygous for one of the recipient's HLA haplotypes. However, the observed frequency of TA-GVHD is much lower than the estimated probability of this donor/recipient combination. The potential role of recipient immune responses in controlling TA-GVHD was investigated using an analogous murine model in which GVHD is induced by the injection of parental lymphoid cells into unirradiated F1 hybrid recipients. The effect of various immune manipulations of the recipient of GVHD induction was assessed by determining the number of donor lymphoid cells required to induce GVHD responses. Whereas depletion of recipient CD4+ cells increased the number of donor cells needed to induce GVHD, depletion of recipient CD8+ and natural killer cells resulted in fewer donor cells being needed to induce a GVHD response. These studies suggest a central role for functioning recipient CD8 and natural killer cells in the down-regulation of TA-GVHD development in recipients.