Multiple Intracranial Tuberculomas with an Intra-medullary Spinal Cord Tuberculoma in a Pediatric Patient.

Central nervous system (CNS) tuberculosis (TB), caused by Mycobacterium tuberculosis (MT), is a severe form of TB, which presents as meningitis, cerebritis, abscesses, spinal tuberculous arachnoiditis, and rarely tuberculomas. CNS TB is prevalent in the underdeveloped or developing world and is common in malnourished, alcoholics, children, young adults, immunocompromised, and cancer patients. Intracranial tuberculomas (ICT) can present with symptoms and signs of focal neurological deficits with or without systemic manifestations. ICT is the least common presentation of CNS TB. Medical management with anti-TB drugs and steroids is the mainstay of treatment, while surgical intervention is usually reserved for refractory cases. Here, we present the case of a 10-year-old Indian American girl with headaches, diplopia, fever, and neck pain diagnosed with ICT and intramedullary spinal cord tuberculoma.

Exertional rhabdomyolysis and acute kidney injury.

Skeletal muscle breakdown occurs normally with exercise, followed by muscle repair and physiologic adaptation. Strenuous, unaccustomed, prolonged, and repetitive exercise, particularly when associated with other risk factors such as hot and humid climate or sickle cell trait can cause clinically significant exertional rhabdomyolysis (ER). Although most cases are asymptomatic and resolve without sequelae, ER is the most common cause of exercise-related myoglobinuric acute renal injury and acute renal failure in athletes. Exercise-related muscle pain, elevated serum creatine kinase (CK), and "cola-colored" urine have been described as a classic presentation of ER. The exact mechanism of ER has not been clearly elucidated. Most studies suggest a cascade of events that include depletion of adenosine triphosphate (ATP), impaired function of the Na+- K+ ATPase system, intracellular excess calcium accumulation, sarcolemma damage, and release of intracellular proteins and other substances into blood. Excess myoglobin that is filtered at the glomerulus can lead to myoglobinuric acute renal injury. Cessation of physical activity, relative rest during clinical recovery, and early aggressive fluid replacement are mainstays of treatment. Return to play after recovery from ER is influenced by associated risk factors that may predispose the athlete to recurrence and is guided by signs, symptoms, and CK levels. This article reviews the definitions, pathophysiology, diagnosis, and management of ER with specific relevance to acute kidney injury.

An unusual case of proton pump inhibitor induced hyperchromograninemia.

Objective: To describe an unusual case of symptomatic hyperchromograninemia associated with proton pump inhibitor (PPI) use. Case Summary: A 55-year-old man with stage 1 follicular lymphoma and GERD on omeprazole presented with symptoms suggesting carcinoid syndrome. The only positive finding on workup was a markedly elevated level of chromogranin A and no carcinoid tumor was identified. Omeprazole was discontinued, following which his symptoms resolved and chromogranin A levels returned to normal. To the best of our knowledge, no symptoms have been previously reported in association with PPI-induced hyperchromograninemia. Discussion: The reliability of chromogranin A as a marker for neuroendocrine tumors is of growing concern. The reasons for the associated symptomatology in this case are unclear but could involve physiologic effects of chromogranin A breakdown products. The role of pharmacogenomics in PPI metabolism is discussed as a potential explanation for the significant hyperchromograninemia. Conclusion: The phenomenon of PPI-induced hyperchromograninemia is highlighted for providers especially in the context of neuroendocrine tumor diagnosis and surveillance. The need for more research into chromogranins is proposed.