Resection of brain lesions with a neuroendoscopic ultrasonic aspirator — a systematic literature review

Neurosurgical Review - The development of minimally invasive neuroendoscopy has advanced in recent years. The introduction of the neuroendoscopic ultrasonic aspirator (NUA) increased the treatment...     

Risk factors for postoperative seizures in patients with chronic subdural haematomas

Neurosurgical Review - Postoperative seizures are a frequently occurring yet not well-understood complication in patients undergoing surgical treatment of chronic subdural haematomas (cSDHs)....     

Diagnostik von Raumforderungen in der Nebenniere

Die Chirurgie - Mit der Zunahme abdomineller Schnittbildgebung werden Raumforderungen der Nebennieren immer häufiger detektiert. Je nach klinischem Kontext ergeben sich daraus unterschiedliche...     

Mast Cells Trigger Disturbed Bone Healing in Osteoporotic Mice

Mast cells are important tissue-resident sensor and effector immune cells but also play a major role in osteoporosis development. Mast cells are increased in numbers in the bone marrow of postmenopausal osteoporotic patients, and mast cell–deficient mice are protected from ovariectomy (OVX)-induced bone loss. In this study, we showed that mast cell–deficient Mcpt5-Cre R-DTA mice were protected from OVX-induced disturbed fracture healing, indicating a critical role for mast cells in the pathomechanisms of impaired bone repair under estrogen-deficient conditions. We revealed that mast cells trigger the fracture-induced inflammatory response by releasing inflammatory mediators, including interleukin-6, midkine (Mdk), and C-X-C motif chemokine ligand 10 (CXCL10), and promote neutrophil infiltration into the fracture site in OVX mice. Furthermore, mast cells were responsible for reduced osteoblast and increased osteoclast activities in OVX mice callus, as well as increased receptor activator of NF-κB ligand serum levels in OVX mice. Additional in vitro studies with human cells showed that mast cells stimulate osteoclastogenesis by releasing the osteoclastogenic mediators Mdk and CXCL10 in an estrogen-dependent manner, which was mediated via the estrogen receptor alpha on mast cells. In conclusion, mast cells negatively affect the healing of bone fractures under estrogen-deficient conditions. Hence, targeting mast cells might provide a therapeutic strategy to improve disturbed bone repair in postmenopausal osteoporosis. © 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).     

Bone Microenvironment-Suppressed T Cells Increase Osteoclast Formation and Osteolytic Bone Metastases in Mice

Immunotherapies use components of the immune system, such as T cells, to fight cancer cells, and are changing cancer treatment, causing durable responses in some patients. Bone metastases are a debilitating complication in advanced breast and prostate cancer patients. Approved treatments fail to cure bone metastases or increase patient survival and it remains unclear whether immunotherapy could benefit patients. The bone microenvironment combines various immunosuppressive factors, and combined with T cell products could increase bone resorption fueling the vicious cycle of bone metastases. Using syngeneic mouse models, our study revealed that bone metastases from 4T1 breast cancer contain tumor-infiltrating lymphocyte (TILs) and their development is increased in normal mice compared to immunodeficient and T-cell depleted mice. This effect seemed caused by the TILs specifically in bone, because T-cell depletion increased 4T1 orthotopic tumors and did not affect bone metastases from RM-1 prostate cancer cells, which lack TILs. T cells increased osteoclast formation ex vivo and in vivo contributing to bone metastasis vicious cycle. This pro-osteoclastic effect is specific to unactivated T cells, because activated T cells, secreting interferon γ (IFNγ) and interleukin 4 (IL-4), actually suppressed osteoclastogenesis, which could benefit patients. However, non-activated T cells from bone metastases could not be activated in ex vivo cultures. 4T1 bone metastases were associated with an increase of functional polymorphonuclear and monocytic myeloid-derived suppressor cells (MDSCs), potent T-cell suppressors. Although effective in other models, sildenafil and zoledronic acid did not affect MDSCs in bone metastases. Seeking other therapeutic targets, we found that monocytic MDSCs are more potent suppressors than polymorphonuclear MDSCs, expressing programmed cell death receptor-1 ligand (PD-L1)⁺ in bone, which could trigger T-cell suppression because 70% express its receptor, programmed cell death receptor-1 (PD-1). Collectively, our findings identified a new mechanism by which suppressed T cells increase osteoclastogenesis and bone metastases. Our results also provide a rationale for using immunotherapy because T-cell activation would increase their anti-cancer and their anti-osteoclastic properties. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).     

Patientenkontrollierte Analgesie (PCA) bei ambulanten Tumorschmerzpatienten

Introduction

In the home-care setting, cancer pain patients in need of parenteral analgesia have to be switched to patient-controlled analgesia using portable pumps. But there is a paucity on data on the logistic requirements or the success rate of such a cost-intensive therapy performed by specialized home-care services.

Methods

In a retrospective study we analyzed data on care intensity, logistics and outcome of 46 consecutive palliative cancer patients with patient-controlled analgesia (PCA) in a home-care setting.

Results

On days 1, 2, and 3 of PCA the switch to parenteral analgesia resulted in a significant increase of the median daily opioid dose in comparison to the dose just prior to PCA. Concurrently, pain scores were significantly reduced. The median duration of PCA was 25 days (range 2–189 days). On average, each patient was seen by the home-care team every 7.4 days. The median duration of the home visits was 60 min (range, 10–190 min). Of the visits 20% were unscheduled, most of these visits being due to problems regarding analgesia. Most patients died at home. Insufficient analgesia required prefinal hospitalization in only a single case.

Conclusion

If the indications are correct, intravenous PCA for palliative cancer pain patients results in higher opioid consumption and better pain control. Home-care PCA requires a lot of human and financial resources, but pain-related hospitalization can be prevented.     

Molecular diagnosis of kidney transplant failure based on urine

In light of the organ shortage, there is a great responsibility to assess postmortal organs for which procurement has been consented and to increase the life span of transplanted organs. The former responsibility has moved many centers to accept extended criteria organs. The latter responsibility requires an exact diagnosis and, if possible, omission of the harmful influence on the transplant. We report the course of a kidney transplant that showed a steady decline of function over a decade, displaying numerous cysts of different sizes. Clinical workup excluded the most frequent causes of chronic transplant failure. The filed allocation documents mentioned the donor’s disease of oral‐facial‐digital syndrome, a rare ciliopathy, which can also affect the kidney. Molecular diagnosis was performed by culturing donor tubular cells from the recipient´s urine more than 10 years after transplantation. Next‐generation panel sequencing with DNA from tubular urinary cells revealed a novel truncating mutation in OFD1, which sufficiently explains the features of the kidney transplants, also found in the second kidney allograft. Despite this severe donor disease, lifesaving transplantation with good long‐term outcome was enabled for 5 recipients.     

One-stage double free flap arteriovenous loop reconstruction of a massive abdominothoracic defect following necrotizing fasciitis: A case report

We report the case of a 67-year old male with necrotizing fasciitis after injection of the glenohumeral joint. After extensive debridement a massive defect from the left hip joint to the left upper arm, exposing ribs, scapula, axillary vessels and brachial plexus (45 × 40 cm) was present. Reconstruction was performed with a conjoined right myocutaneous tensor fasciae lata/vastus lateralis flap and a left myocutaneous vastus lateralis flap in combination with an arteriovenous loop originating from the axillary vessels using the greater saphenous vein. Revisional surgeries were necessary including ribs resection and flap re-advancements. Due to multiorganic failure invasive ventilation, renal replacement- and extensive transfusion therapy was required. After 241 days the patient was discharged for rehabilitation. At the 12 months follow-up wounds were sufficiently closed without the need for further intervention. This case illustrates that immediate diagnosis followed by an aggressive multidisciplinary treatment approach is crucial for the patient survival.