Psychosis-Induced Exertional Rhabdomyolysis without Acute Kidney Injury or Myoglobinuria.

BACKGROUND Rhabdomyolysis is a clinical syndrome that results from skeletal muscle breakdown and the release of intracellular enzymes into systemic circulation [1,2]. We present a case of non-traumatic rhabdomyolysis with transaminitis, without myoglobinuria or acute kidney injury. Cases reports of rhabdomyolysis with elevation of serum creatine kinase (hyperCKemia) in the absence of myoglobinuria or renal failure are limited in the literature. CASE REPORT A 21-year-old man presented to the Emergency Department following an acute psychotic episode. One week earlier, his bloodwork had been within normal limits. Biochemical investigations on admission revealed hyperCKemia (590 000 U/L), transaminitis (AST, 628; ALT, 160), and normal creatinine (0.83), without myoglobinuria. Non-traumatic rhabdomyolysis was suspected, and the patient was treated with aggressive intravenous fluid resuscitation and transferred to Inpatient Psychiatry on day 10 of hospitalization. The complete metabolic panel was trended daily, without indication of kidney injury. The creatine kinase (CK) and liver function tests trended downward. CONCLUSIONS This report presents a rare case of exertional rhabdomyolysis with CK levels nearly 3000 times the upper limit of normal, without myoglobinuria or acute kidney injury. Acute kidney injury is a dangerous complication of rhabdomyolysis. Traditionally, clinicians use serum CK levels to predict the likelihood of acute kidney injury and/or renal failure in rhabdomyolysis. Ultimately, this patient was diagnosed with exertional rhabdomyolysis with hyperCKemia and transaminitis without myoglobinuria or acute kidney injury. More research is needed to elucidate the protective patient characteristics against rhabdomyolysis-associated acute kidney injury, associations between CK and myoglobinuria, and diagnostic criteria for psychosis-associated hyperCKemia

Unresectable Primary Tracheal Synovial Sarcoma

Synovial sarcoma (SS) comprises less than 1% of head and neck cancers, and less than five cases of adult primary tracheal SS have been described. This case describes a patient encountered at a community-based academic hospital, and retrospective chart review was performed for data collection. A woman in her forties presented with shortness of breath due to a superior mediastinal mass found to be an unresectable primary tracheal SS. Primary treatment resorted to curative-intent radiation therapy. Subsequent metastasis required systemic chemotherapy with pazopanib. To the best of our knowledge, this is the first reported case of this nature and adds to understanding the presentation, diagnosis, natural history, and treatment outcomes of primary tracheal SS. This case was exempt from review by the institutional review board and complied with privacy policy standards

Impact of adjuvant radiation therapy after definitive surgery in senior adults \u3e80 years old with advanced head and neck squamous cell carcinoma on overall survival.

Background: Adjuvant radiotherapy (RT) following surgical resection confers a survival benefit for adult patients with locally advanced head and neck squamous cell carcinoma (HNSCC). We aim to investigate if adjuvant RT provides a similar survival advantage to patients ages 80+ through a national curated database. Methods: This retrospective cohort study queried the National Cancer Database (NCDB) for all cases of HNSCC between 2004-2016. Patients treated with surgical resection alone were compared to those treated with surgery plus adjuvant RT. Overall survival (OS) was compared within adult (age \u3c80 \u3eyears) and senior adult (age ≥80 years) cohorts using Kaplan-Meier analysis. Hazard ratios (HR) were assessed using Cox proportional hazards to account for differences in patient characteristics, primary site, and HNSCC stage. Results: NCDB identified 16,504 locally advanced HNSCC treated with definitive surgery with 9,129 (55.3%) also receiving adjuvant RT. The mean age was 63.8 years (SD = 12.0) with 88.7% of patients ages11.3% ages ≥80 years. In the adult cohort, adjuvant RT was associated with a significant increase in OS compared to surgery alone at 1 year (88.4% vs. 83.8%, p= Conclusion: The addition of adjuvant RT in senior patients (age ≥80 years) may not provide a similar OS benefit to that observed in younger patients. Further research is needed to best guide shared-decision making in this population

Growth Factor-Independent 1 Is a Tumor Suppressor Gene in Colorectal Cancer

Colorectal cancer is the third most common cancer and the third leading cause of cancer death in the United States. Growth factor-independent 1 (GFI1) is a zinc finger transcriptional repressor responsible for controlling secretory cell differentiation in the small intestine and colon. GFI1 plays a significant role in the development of human malignancies, including leukemia, lung cancer, and prostate cancer. However, the role of GFI1 in colorectal cancer progression is largely unknown. Our results demonstrate that RNA and protein expression of GFI1 are reduced in advanced-stage nonmucinous colorectal cancer. Subcutaneous tumor xenograft models demonstrated that the reexpression of GFI1 in 4 different human colorectal cancer cell lines inhibits tumor growth. To further investigate the role of Gfi1 in colorectal tumorigenesis, we developed transgenic mice harboring a deletion of Gfi1 in the colon driven by CDX2-cre (Gfi1 ; CDX2-cre) and crossed them with Apc mice (Apc ; Gfi1 ; CDX2-cre). Loss of Gfi1 significantly increased the total number of colorectal adenomas compared with littermate controls with an APC mutation alone. Furthermore, we found that compound (Apc ; Gfi1 ; CDX2-cre) mice develop larger adenomas, invasive carcinoma, as well as hyperplastic lesions expressing the neuroendocrine marker chromogranin A, a feature that has not been previously described in APC-mutant tumors in mice. Collectively, these results demonstrate that acts as a tumor suppressor gene in colorectal cancer, where deficiency of Gfi1 promotes malignancy in the colon. IMPLICATIONS: These findings reveal that GFI1 functions as a tumor suppressor gene in colorectal tumorigenesis