A 90-year-old man experienced chest oppressive sensation at 12:30 AM for the first time. Electrocardiography showed a newly developed inversion of the terminal T-wave in the V2-5 leads. A left coronary angiogram showed no significant atherosclerotic stenosis. A myocardial bridge was found in the mid-left anterior descending artery (LAD). Myocardial scintigraphy with 123I beta-methyl 15-para-iodophenyl 3(R,S)-methylpentadecanoic acid revealed a reduced uptake in the apical and septal areas. Based on these findings, we suspected new-onset vasospastic angina complicated by a myocardial bridge in the territory of the LAD. He remained in good condition without recurrent anginal attacks after nifedipine was started before bedtime.

Mechanical pain sensing, adipogenesis, and STING-dependent innate immunity seem three distinct biological processes without substantial relationships. Intriguingly, TMEM120A, a transmembrane protein, has been shown to detect mechanical pain stimuli as a mechanosensitive channel, contribute to adipocyte differentiation/function by regulating genome organization and promote STING trafficking to active cellular innate immune response. However, the role of TMEM120A as a mechanosensitive channel was challenged by recent studies which cannot reproduce data supporting its role in mechanosensing. Furthermore, the molecular mechanism by which TMEM120A contributes to adipocyte differentiation/function and promotes STING trafficking remains elusive. In this review, we discuss these multiple proposed functions of TMEM120A and hypothesize the molecular mechanism underlying TMEM120A\'s role in fatty acid metabolism and STING signaling.

BACKGROUND: Glutaric acidemia is a type of multiple acyl-coenzyme A dehydrogenase deficiency, an inborn error in fatty acid metabolism. In patients with glutaric acidemia, during the perioperative period, prolonged fasting, stress, and pain have been identified as risk factors for the induction of metabolic derangement. This report describes the surgical and anesthetic management of a patient with glutaric acidemia.
METHODS: A 56-year-old male patient with glutaric acidemia type 2 underwent a series of surgeries. During the initial off-pump coronary artery bypass surgery, the patient developed renal failure due to rhabdomyolysis upon receiving glucose at 2 mg/kg/min. However, in the second laparoscopic cholecystectomy, rhabdomyolysis was avoided by administering glucose at 4 mg/kg/min.
CONCLUSIONS: To avoid catabolism in patients with glutaric acidemia, appropriate glucose administration is important, depending on the surgical risk.

We present a case of high anion gap metabolic acidosis with an unusual aetiology in a 75-year-old lady with hypoglycaemia, encephalopathy and relatively preserved renal function. Full toxicology and biochemical analysis suggested that she had an inborn error of metabolism, riboflavin-responsive multiple acyl-CoA dehydrogenase deficiency that can predispose to severe acidosis in situations where calorific intake is reduced. We believe this to be one of the few published cases and is remarkable for the presentation in late adulthood in addition to the requirement for emergency haemodialysis due to the severity of the metabolic disturbance.

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