A Case of Pseudo-Pseudo Meigs' Syndrome Despite Optimized Immunosuppressive Therapy for Systemic Lupus Erythematosus.

Pseudo-pseudo Meigs' syndrome (PPMS), also known as Tjalma syndrome, is a rare complication of systemic lupus erythematosus (SLE), characterized by a triad of ascites, pleural effusion, and elevated CA-125 levels. We report a case involving a 74-year-old female with a prior history of SLE who presented with recurrent bilateral pleural effusions, elevated CA-125 levels, and mild ascites. Imaging showed no evidence of any mass or malignancy. In this case, the patient's presentation aligned with the diagnostic criteria for PPMS. Additionally, all other potential causes were investigated, and no alternative pathologies better explained the patient's presentation. PPMS should be considered in the differential diagnosis when evaluating patients with this triad of symptoms and laboratory and imaging findings. Early and more accurate diagnosis can guide research into treatment modalities.

Evaluating the Impact of Early Career Academic Medicine Workshops on Medical Students' Interest.

Introduction Academic medicine is an important field that has had a notable decline in physician interest. The aim of this study was to introduce academic medicine to medical students early in their careers with a workshop in the medical school setting, beyond conferences, to promote even greater interest in the field. Methods This workshop consisted of (1) an informational didactic session using a Microsoft PowerPoint presentation, (2) small-group breakout discussion sessions to review case scenarios, and (3) a faculty panel to provide personal anecdotes and advice to students. The authors administered online pre- and post-workshop surveys to the students. One workshop was presented to first-year medical students and another to second-year medical students at California University of Science and Medicine. Data were analyzed using the IBM SPSS Statistics 27.0 for Windows. Pre- and post-workshop survey question means were compared using a paired t-test. Results There were 104 pre-clerkship student attendees, 83 of whom were in their first year and 21 in their second. Within each class year, there was a statistical significance in pre- and post-workshop survey responses for questions one through four (p < 0.001, p < 0.001, p < 0.001, p < 0.001), but question five responses were not statistically significant (p = 0.78). Conclusion Academic medicine workshops held early in medical students' careers are an effective way to foster interest in the field. Implementing academic medicine scholars' programs, in addition to these workshops, can help provide guidance and resources for students who want to pursue a career in academic medicine.

Methamphetamine-induced encephalopathy in the absence of hyperammonemia.

BACKGROUND: Methamphetamine is an addictive drug with various effects on the neurotransmitters in the central nervous system. Methamphetamine-induced encephalopathy in the absence of hyperammonemia presents a unique challenge in a clinical setting. Previously published cases of methamphetamine-induced encephalopathy suggested that methamphetamine-induced hepatotoxicity and subsequent hyperammonemia may be the cause of encephalopathy. However, the literature is limited on methamphetamine-induced encephalopathy without hyperammonemia. CASE: This case presents a disoriented patient with methamphetamine use disorder in acute toxicity, unable to ambulate independently, and poorly responsive to verbal stimuli. The patient was found to have normal ammonia levels. DISCUSSION: This patient's presentation and laboratory findings, namely normal ammonia levels, suggest a different pathophysiological pathway for methamphetamine-induced encephalopathy. One potential pathway is through the direct action of methamphetamine on the central nervous system through acute disruption of neurotransmitter signaling and disruption of the blood-brain barrier. CONCLUSION: Further research should be conducted into the prevalence and pathophysiology of methamphetamine-induced encephalopathy in the absence of hyperammonemia. KEY POINTS: Methamphetamine-induced encephalopathy (MIE) in the absence of hyperammonemia presents a unique challenge in a clinical setting. Previously published cases of MIE suggest that methamphetamine-induced hepatotoxicity and subsequent hyperammonemia may be the cause of encephalopathy. Further research should be conducted into the prevalence and pathophysiology of MIE in the absence of hyperammonemia.