RESUMEN
Lymphangioleiomyomatosis (LAM) is an abnormal proliferation of smooth muscle-like cells and may occur sporadically or in association with tuberous sclerosis complex. Patients are typically female, nonsmoking and may have cystic lung disease with pneumothorax. Diagnosis can be made by compatible imaging findings with a history of tuberous sclerosis complex, or in conjunction with vascular endothelial growth factor-D 800 pg/ml or greater, a highly specific finding. Sirolimus is first line treatment for LAM.
RESUMEN
Sarcoidosis is a multisystem disease most commonly affecting the lungs but also can rarely manifest as pleural effusions. Sarcoidosis associated pleural effusion occurs in around 1% of patients with sarcoidosis. Pleural fluid is typically exudative, lymphocyte predominant, with high pleural protein levels and normal or mildly elevated lactate dehydrogenase. Diagnosis involves excluding other etiologies of this pleural effusion and can be made clinically or definitively with pleural biopsy showing noncaseating granulomas. Treatment involves corticosteroids to which patients typically have an excellent response with resolution of the pleural effusion.
RESUMEN
Lymphomatoid granulomatosis (LG) is an extremely rare disease and is an unusual cause of central airway obstruction (CAO) with no standard of treatment in these conditions. LG is characterized by angioinvasion and angioinfiltration along with lymphohistiocytic cells. We present a 21-year-old female with LG who developed endobronchial lesions causing malignant CAO and acute hypoxic respiratory failure. She was treated with argon plasma coagulation, as well as a self-expandable metallic stent in the left main bronchus. Her stent was removed 4 months later after chemotherapy. Endobronchial stenting may be a useful bridge in patients who are undergoing more definitive treatment.
RESUMEN
Disseminated intravascular coagulation (DIC) can be caused by cancer. However, it is rare to be the presenting sign of malignancy. The manifestations of bleeding or thrombosis in DIC depend on the balance of the fibrinolytic system. This case centers on a 52-year-old male who presented with DIC and spontaneous bruising, and no obvious cause for DIC. He was found to have metastatic prostate adenocarcinoma. DIC related to solid tumors typically have an indolent course and is only apparent on laboratory analysis. Further, DIC with excessive fibrinolysis in prostate cancer is associated with lower median survival. Treatment involves treating prostate cancer, and supportive treatment with blood products. Epsilon-aminocaproic acid may have a role in life-threatening bleeds, while prophylactic heparin treatment can be given for DIC associated with thrombosis.
RESUMEN
While ionizing radiation is a major form of cancer therapy, radioresistance remains a therapeutic obstacle. We have previously shown that the mandated housing temperature for laboratory mice (â¼22°C) induces mild, but chronic, cold stress resulting in increased circulating norepinephrine, which binds to, and triggers activation of, beta-adrenergic receptors (ß-AR) on tumor and immune cells. This adrenergic signaling increases tumor cell intrinsic resistance to chemotherapy and suppression of the anti-tumor immune response. These findings led us to hypothesize that adrenergic stress signaling increases radioresistance in tumor cells in addition to suppressing T-cell-mediated anti-tumor immunity, thus suppressing the overall sensitivity of tumors to radiation. We used three strategies to test the effect of adrenergic signaling on responsiveness to radiation. For one strategy, mice implanted with CT26 murine colon adenocarcinoma were housed at either 22°C or at thermoneutrality (30°C), which reduces physiological adrenergic stress. For a second strategy, we used a ß-AR antagonist ("beta blocker") to block adrenergic signaling in mice housed at 22°C. In either case, tumors were then irradiated with a single 6 Gy dose and the response was compared to mice whose adrenergic stress signaling was not reduced. For the third strategy, we used an in vitro approach in which several different tumor cell lines were treated with a ß-AR agonist and irradiated, and cell survival was then assessed by clonogenic assay. Overall, we found that adrenergic stress significantly impaired the anti-tumor efficacy of radiation by inducing tumor cell resistance to radiation-induced cell killing and by suppression of anti-tumor immunity. Treatment using beta blockers is a promising strategy for increasing the anti-tumor efficacy of radiotherapy.
