Search

A 56-year-old man with a long history of alcoholism and a palpable raised mass about 23 cm × 12 cm in size on his neck was diagnosed with Madelung’s disease (MD); the patient also had hyperuricemia. On day 1, he underwent neck lipoma tissue resection and suddenly had dyspnea 9 h after the operation, which was followed by cardiac arrest. After heart rate resuscitation, he developed a heartbeat, but he remained in a coma and died 9 days after the operation. No obvious pathological tracheal compression from a hematoma was observed while evaluating the patient’s neck on autopsy. On microscopy, the patient had an extensive pulmonary fat embolism, partial alveolar septal rupture and hemorrhage, and fat particles, and there was extensive infiltration of macrophages, which had phagocytosed fat particles, in the alveolar cavity. There was also evidence of pulmonary infection and hypoxic-ischemic encephalopathy. The cause of death was postoperative pulmonary fat embolism resulting in pneumonia and central nervous system injury. This is the first report of a patient with MD who died of a fatal pulmonary fat embolism after neck lipoma tissue resection. Medicolegal experts and clinicians should pay sufficient attention to this case.

Methamphetamine (METH) is a major psychostimulant drug of abuse worldwide, and its neurotoxicity has been studied extensively. In addition to neurotoxicity, METH can also induce hepatotoxicity. The underlying mechanism of intestinal microorganisms in METH-induced hepatotoxicity remains unclear. In this study, mice have received antibiotics intragastrically or PBS once each day for 1 week, followed by METH or saline. The antibiotics attenuated METH-induced hepatotoxicity as evidenced by histopathological observation and biochemical analysis; furthermore, they alleviated METH-induced oxidative stress. The effect of antibiotics on METH-induced hepatotoxicity was investigated using RNA-sequencing (RNA-seq). The RNA-seq results demonstrated that antibiotics could regulate 580 differentially expressed genes (DEGs), of which 319 were upregulated after METH treatment and then downregulated with antibiotic pretreatment and 237 were first downregulated after METH administration and then upregulated after antibiotic pretreatment, in addition to 11 upregulated and 13 downregulated ones simultaneously in METH and antibiotic-pretreated groups. RNA-seq analyses revealed that TLR4 is one of the hub genes. Western blot analysis indicated that antibiotics inhibited the increase of TLR4, MyD88 and Traf6 induced by METH. This research suggests that antibiotics may play an important role in preventing METH-induced liver injury by regulating oxidative stress and TLR4/MyD88/Traf6 axis, though further investigation is required.

A full-term female baby born with an Apgar score of 10 exhibited a continual decrease in blood glucose and acid-base imbalance until she died at 40 h postpartum despite emergency rescue efforts. Autopsy showed a highly oedematous brain and a swollen liver. The cells of the myocardium, liver and kidney exhibited extensive microscopic vacuolar degeneration. The cardiac muscle and liver and kidney tissues were positive for Sudan III staining. Tandem mass spectrometry analysis revealed that the deceased was deficient in free carnitine, accompanied by an increase in multiple acylcarnitines. Genetic testing showed the parents of the deceased to be ETFDH mutation carriers, and the deceased carried a complex heterozygous mutation in ETFDH. Therefore, based on the results of autopsy, specific staining, genetic metabolic disease testing and genetic testing, we speculated that glutaric aciduria type IIc was the cause of death.

Misuse of the psychostimulant methamphetamine (METH) could induce serious hepatotoxicity. Our previous study revealed the effects of luteolin on alleviating METH-induced hepatotoxicity, however, the detailed mechanisms have not been elucidated. In this study, rats were orally pretreated with 100 mg/kg luteolin or sodium dodecyl sulfate water, and then METH (15 mg/kg, intraperitoneal [i.p.]) or saline was administered. Histopathological and biochemical analyses were used to determine the alleviative effects of luteolin. Based on the RNA-sequencing data, METH induced 1859 differentially expressed genes (DEGs) in comparison with the control group, which were enriched into 11 signaling pathways. Among these DEGs, 497 DEGs could be regulated through luteolin treatment and enriched into 16 pathways. The p53 signaling pathway was enriched in both METH administered and luteolin pretreated rats. Meanwhile, luteolin significantly suppressed METH-induced elevation of p53, caspase9, caspase3, cleaved caspase3, the ratio of Bax/Beclin-2, as well as autophagy-related Beclin-1, Atg5, and LC3-II. Luteolin also relieved METH-induced hepatotoxicity by decreasing inflammation factors, including TNF-α, IL-1β, and IL-18. Moreover, the levels of PI3K, p-Akt, and the normalized ratio of p-Akt/Akt declined after METH administration, whereas luteolin pretreatment failed to reverse these effects. Our results suggest that luteolin alleviates METH-induced hepatic apoptosis, autophagy, and inflammation through repressing the p53 pathway. It further illustrates the protective mechanisms of luteolin on METH-induced hepatotoxicity and provides a research basis for clinical treatment.

We report a case of nontraumatic fat embolism syndrome with large amounts of macrophages with phagocytized fat droplets in the alveoli. A 46-year-old male presented with a glass-cut injury in his little finger. The wound was debrided and sutured at the hospital, but he was found dead 43 h after treatment. Autopsy results showed that the patient had steatohepatitis, accompanied by histological findings of fat droplets in the pulmonary capillaries. In the alveoli, we found a large number of macrophages with phagocytized fat droplets that showed stained. To the best of our knowledge, this is the first report of such a case, and the paper proposes that fat droplets phagocytized by a large number of macrophages may be a characteristic feature of fat embolism, which may be relevant to forensic pathology practice.