Rash and cholestatic liver injury caused by methimazole in a woman with Turner syndrome and Graves's disease: a case report and literature review.

BACKGROUND: Rash and cholestatic liver injury caused by methimazole (MMI) in patients with Turner syndrome (TS) and Graves's disease (GD) are rarely reported, and there is a paucity of reports on the management of this condition. It is not clear whether propylthiouracil (PTU) can be used as a safe alternative in this case. CASE PRESENTATION: A 37-year-old woman was admitted to our hospital with rash, severe pruritus and a change in urine colour after 2 months of GD treatment with MMI. Physical examination showed rash scattered over the limbs and torso, mild jaundice of the sclera and skin, short stature, facial moles, immature external genitals and diffuse thyroid gland enlargement. Liver function tests indicated an increase in total bilirubin, direct bilirubin, total bile acid, glutamic pyruvic transaminase, glutamic oxaloacetic transaminase and alkaline phosphatase. The level of sex hormones suggested female hypergonadotropic hypogonadism. The karyotype of peripheral blood was 46, X, i(X)(q10)/45, X. After excluding biliary obstruction and other common causes of liver injury, combined with rash and abnormal liver function following oral administration of MMI, the patient was diagnosed as having TS with GD and rash and cholestatic liver injury caused by MMI. MMI was immediately discontinued, and eleven days after treatment with antihistamine and hepatoprotective agents was initiated, the rash subsided, and liver function returned to nearly normal. Because the patient did not consent to administration of 131I or thyroid surgery, hyperthyroidism was successfully controlled with PTU. No adverse drug reactions were observed after switching to PTU. CONCLUSIONS: While patients with TS and GD are undergoing treatment with MMI, their clinical manifestations, liver functions, and other routine blood test results should be closely monitored. When patients with TS and GD manifest adverse reactions to MMI such as rash and cholestatic liver injury, it is necessary to discontinue MMI and treat with antihistamine and hepatoprotective agents. After the rash subsides and liver function returns to nearly normal, PTU can effectively control hyperthyroidism without adverse drug reactions.

Diabetic ketoacidosis complicated by emphysematous pyelonephritis: a case report and literature review.

BACKGROUND: The management of emphysematous pyelonephritis (EPN) includes conservative medical treatment, percutaneous drainage, and surgical resection of the involved kidney. EPN with diabetic ketoacidosis(DKA) is very rare, in which the clinical management of refusing surgical drainage is inexperienced. CASE PRESENTATION: A 34-year-old woman presented with abdominal pain, chills, fever, nausea, vomiting, chest tightness, and shortness of breath. Blood test results were consistent with diabetic ketoacidosis. Urinary computed tomography scan showed multiple stones in the right kidney and lower ureter, with right hydronephrosis. Blood culture demonstrated Escherichia coli bacteremia, and EPN was diagnosed. Considering the need for a second percutaneous nephrolithotomy, the patient refused percutaneous drainage. After continuous intravenous infusion of small doses of insulin and antibiotic treatment, the ketoacidosis resolved. The patient's temperature returned to normal and abdominal pain was alleviated, and liver and kidney functions were also back to normal. After hospital discharge, the patient underwent two percutaneous nephrolithotomy in the department of urology. CONCLUSIONS: EPN with diabetic ketoacidosis should be diagnosed as soon as possible. For patients with Class 1 and Class 2 EPN with diabetic ketoacidosis and urinary tract obstruction, if surgical drainage is refused, it is particularly important to rapidly correct diabetic ketoacidosis and intravenous use of sensitive antibiotics, so as to create conditions for follow-up percutaneous nephrolithotomy.

Endogenous chemicals guard health through inhibiting ferroptotic cell death.

Ferroptosis is a new form of regulated cell death caused by iron-dependent accumulation of lethal polyunsaturated phospholipids peroxidation. It has received considerable attention owing to its putative involvement in a wide range of pathophysiological processes such as organ injury, cardiac ischemia/reperfusion, degenerative disease and its prevalence in plants, invertebrates, yeasts, bacteria, and archaea. To counter ferroptosis, living organisms have evolved a myriad of intrinsic efficient defense systems, such as cyst(e)ine-glutathione-glutathione peroxidase 4 system (cyst(e)ine-GPX4 system), guanosine triphosphate cyclohydrolase 1/tetrahydrobiopterin (BH4) system (GCH1/BH4 system), ferroptosis suppressor protein 1/coenzyme Q10 system (FSP1/CoQ10 system), and so forth. Among these, GPX4 serves as the only enzymatic protection system through the reduction of lipid hydroperoxides, while other defense systems ultimately rely on small compounds to scavenge lipid radicals and prevent ferroptotic cell death. In this article, we systematically summarize the chemical biology of lipid radical trapping process by endogenous chemicals, such as coenzyme Q10 (CoQ10), BH4, hydropersulfides, vitamin K, vitamin E, 7-dehydrocholesterol, with the aim of guiding the discovery of novel ferroptosis inhibitors.

Surface charge modulation boosts electrocatalytic water splitting over iridium catalysts on a polyimide support.

Developing high-performance iridium (Ir)-based catalysts with minimal precious Ir metal is a significant but challenging step towards the acidic oxygen evolution reaction (OER). Here, we report a high-performance OER catalyst with Ir nanoparticles on a polyimide support, where the polyimide support can effectively modulate the electronic structures of the Ir active sites for decreased thermodynamic barriers, but also enrich the local proton concentration near the Ir active sites, enhancing the OER rates.