Mini-arthrotomy for lateral discoid menisci in children

BACKGROUND: Long-term results after partial, extended, or complete resection of lateral discoid meniscus in children revealed knee arthritis. The purpose of this study was to evaluate whether the operative approach, arthrotomy or arthroscopy, has an impact on the outcome and the development of arthritis. METHODS: A retrospective comparison of 2 well matching groups totaling 40 children with symptomatic lateral discoid meniscus (48 knees, mean age 8.9 years, 13 male and 27 female patients). Meniscus resection was performed via mini-arthrotomy in group 1 (n=17 patients, 20 knees) and arthroscopically in group 2 (n=23 patients, 28 knees). RESULTS: In the follow-up (mean 57 months in group 1, 62 months in group 2), functional results indicated a trend to better results in the International Knee Documentation Committee score (P=0.12) and in the Lysholm score for group 1 (P=0.13) but not in the Ikeuchi score (P=0.48). The comparison of the radiographic arthritis grading in the follow-up showed no significant arthritis in either group (P=0.22). The overall complication rate was similar in both groups (2/20, 10% in group 1; 3/28, 12% in group 2). CONCLUSIONS: Most likely because of the appropriate visualization of the children's joint and the easier instrumentation, the mini-arthrotomy led to slightly superior results compared with those after arthroscopic resection regarding functional outcome and 5 years after surgery. We can recommend the mini-arthrotomy for the resection of lateral discoid meniscus particularly in young children with narrow joint spaces and for surgeons that are not familiar with arthroscopies of small joints. LEVEL OF EVIDENCE: III (therapeutic study, case series with control group).

VHL inactivation is an important pathway for the development of malignant sporadic pancreatic endocrine tumors

A small subset of familial pancreatic endocrine tumors (PET) arises in patients with von Hippel-Lindau syndrome and these tumors may have an adverse outcome compared to other familial PET. Sporadic PET rarely harbors somatic VHL mutations, but the chromosomal location of the VHL gene is frequently deleted in sporadic PET. A subset of sporadic PET shows active hypoxia signals on mRNA and protein level. To identify the frequency of functionally relevant VHL inactivation in sporadic PET and to examine a possible prognostic significance we correlated epigenetic and genetic VHL alterations with hypoxia signals. VHL mutations were absent in all 37 PETs examined. In 2 out of 35 informative PET (6%) methylation of the VHL promoter region was detected and VHL deletion by fluorescence in situ hybridization was found in 14 out of 79 PET (18%). Hypoxia inducible factor 1alpha (HIF1-alpha), carbonic anhydrase 9 (CA-9), and glucose transporter 1 (GLUT-1) protein was expressed in 19, 27, and 30% of the 152 PETs examined. Protein expression of the HIF1-alpha downstream target CA-9 correlated significantly with the expression of CA-9 RNA (P<0.001), VHL RNA (P<0.05), and VHL deletion (P<0.001) as well as with HIF1-alpha (P<0.005) and GLUT-1 immunohistochemistry (P<0.001). These PET with VHL alterations and signs of hypoxia signalling were characterized by a significantly shortened disease-free survival. We conclude that VHL gene impairment by promoter methylation and VHL deletion in nearly 25% of PET leads to the activation of the HIF-pathway. Our data suggest that VHL inactivation and consecutive hypoxia signals may be a mechanism for the development of sporadic PET with an adverse outcome.

[HPV type 16-associated anal intraepithelial neoplasia (AIN)]

A 25-year-old woman had suffered from a perianal ulcer for approximately 1 year. Topical and systemic treatments had been unsuccessful. Employing virologic and histologic techniques, we confirmed the diagnosis of an intraepithelial neoplasia. Anal intraepithelial neoplasia (AIN) is induced by carcinogenic human papillomaviruses. It can occur anywhere in the anogenital area. Because of its frequency, AIN is a crucial differential diagnosis for lesions of the anogenital area region failing to respond to standard therapies.

[Therapy of disorders with central pain sensitization.]

Previous somatic pain experience (priming), psychobiographic imprinting (pain proneness), and stress (action proneness) are key to an enhanced centralised pain response. This centralised pain response clinically manifests itself in pain sensitization and chronification. The therapeutic approach to chronic centralised pain disorders is multimodal. The overarching aim of the various interventions of a multimodal treatment program is to activate anti-nociceptive areas of the cerebral matrix involved in pain processing. The lists of medications targeting neuropathic and somatoform pain disorder show considerable overlap. Psychotherapy helps patients with central pain sensitization to improve pain control, emotional regulation and pain behaviour.