Objective: To explore the expulsion effect of sodium dimercaptopropanesulfonate (DMPS) on mercury in different organs of mercury poisoning and the therapeutic effect of glutathione (GSH) combined with antioxidant therapy on mercury poisoning. Methods: In February 2019, 50 SPF male SD rats were randomly divided into 5 groups, 10 rats in each group: A (saline negative control group) , B (HgCL2 positive control group) , treatment group (C: intramuscular injection of DMPS 15 mg/kg treatment, D: intramuscular injection of DMPS30 mg/kg treatment, E: intramuscular injection of DMPS 15 mg/kg and intraperitoneal injection of GSH200 mg/kg treatment) . Rats in group B, C, D and E were subcutaneously injected with mercury chloride solution (1 mg/kg) to establish a rat model of subacute mercury poisoning kidney injury. Rats in group A were subcutaneously injected with normal saline. After the establishment of the model, rats in the treatment group were injected with DMPS and GSH. Rats in group A and group B were injected with normal saline. At 21 d (treatment 7 d) and 28 d (treatment 14 d) after exposure, urine and blood samples of 5 rats in each group were collected. Blood biochemistry, urine mercury, urine microalbumin and mercury content in renal cortex, cerebral cortex and cerebellum were detected. Results: After exposure to mercury, the contents of mercury in renal cortex, cerebrum and cerebellum of rats in group B, C, D and E increased, and urine microalbumin increased. Pathology showed renal tubular injury and renal interstitial inflammation. Compared with group B, urinary mercury and renal cortex mercury in group C, D and E decreased rapidly after DMPS treatment, and there was no significant decrease in mercury levels in cerebellum and cerebral cortex of rats, accompanied by transient increase in urinary albumin after DMPS treatment (P<0.05) ; the renal interstitial inflammation in group E was improved after GSH treatment. There was a positive correlation between urinary mercury and the contents of mercury in renal cortex, cerebral cortex and cerebellum (r=0.61, 0.47, 0.48, P<0.05) . Conclusion: DMPS mercury expulsion treatment can significantly reduce the level of metal mercury in the kidney, and there is no significant change in the level of metal mercury in the cortex and cerebellum.
Animals ; Brain/drug effects* ; Glutathione ; Inflammation ; Kidney/drug effects* ; Kidney Diseases/chemically induced* ; Male ; Mercuric Chloride/therapeutic use* ; Mercury/urine* ; Mercury Poisoning/drug therapy* ; Rats ; Rats, Sprague-Dawley ; Saline Solution/therapeutic use* ; Unithiol/therapeutic use*

Toxic leucoencephalopathy (TLE) is a rare neurological complication of heroin abuse. 'Chasing the dragon' is an inhalational mode of heroin abuse that originated in Southeast Asia. Intriguingly, no cases of TLE have been reported from this region, although the inhalational mode of heroin abuse is common. We herein report the case of a middle-aged man with a history of polysubstance abuse who presented with progressive neurological symptoms and progressed to an uncommunicative state. While the initial impression was that of iatrogenic parkinsonism, diffuse leucoencephalopathy with sparing of the cerebellum was noted on magnetic resonance imaging. In view of his history of inhalational heroin abuse close to the onset of the neurological symptoms, a diagnosis of TLE was made. No clinical improvement was noted with administration of a dopaminergic agent. This is the first known case of delayed TLE following heroin inhalation from Southeast Asia with the unusual feature of cerebellar sparing.
Administration, Inhalation ; Brain ; pathology ; Disease Progression ; Heroin ; administration & dosage ; Heroin Dependence ; complications ; Humans ; Leukoencephalopathies ; chemically induced ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Nervous System Diseases ; chemically induced ; Singapore

OBJECTIVEWe report the first case of acute encephalopathy induced by vaccination in an infant with methylmalonic aciduria cblA in China.

METHODThe clinical presentation, blood acylcarnitines analysis, urine organic acids analysis and gene studies of the patient were summarized.

RESULTThe proband, a boy, was admitted at the age of 15 months because of recurrent vomiting, acidosis and development delay for 8 months. The previously healthy boy presented vomiting and coma just one hour after hepatitis B vaccination at the age of seven months. Moderate dehydration, electrolyte disturbance and metabolic acidosis had been found. Although his acute metabolic crisis had been corrected soon after intravenous transfusion, psychomotor retardation and recurrent vomiting had been observed. When he was 15 months old, vomiting and lethargy occurred again 3 hours after DTaP vaccination. He was weakened as the illness became worse and got coma with dyspnea 7 days later. He was hospitalized with the suspected diagnosis of viral encephalitis. Blood acylcarnitines analysis, urine organic acids analysis and gene study had been performed for the etiologic investigation.His blood propionylcarnitine (16.3 µmol/L vs. normal range 1.0-5.0 µmol/L) and propionylcarnitine/free carnitine ratio (0.27 vs. normal range 0.03 to 0.25) increased. Markedly elevated urinary methylmalonic acid (388.21 mmol/mol creatinine vs. normal range 0.2 to 3.6 mmol/mol creatinine) and normal plasma total homocysteine supported the diagnosis of isolated methylmalonic aciduria. Two mutations, c.650 T>A (p.L217X) and c.742 C>T (p.Q248X), were identified in his MMAA gene, confirmed the diagnosis of cblA. Each parent carried one of the two mutations. Progressive clinical and biochemical improvement has been observed after hydroxylcobalamin injection, protein-restricted diet with the supplements of special formula and L-carnitine. He is currently 2 years and 7 months old with normal development and general condition.

CONCLUSIONA boy with cblA was firstly detected after the acute encephalopathy induced by vaccination in China. It is important to pay more attention to the patients with metabolic crisis or organ damage after vaccination. Metabolic studies are keys to the diagnosis of potential diseases and improve the outcome.

Amino Acid Metabolism, Inborn Errors ; complications ; Brain Diseases ; chemically induced ; Carnitine ; analogs & derivatives ; Diet, Protein-Restricted ; Hepatitis B Vaccines ; adverse effects ; Humans ; Infant ; Male ; Methylmalonic Acid ; urine ; Mutation ; Vaccination ; adverse effects ; Vitamin B Complex ; Vomiting

OBJECTIVETo study the MRI-based characteristics of acute carbon monoxide poisoning (ACOP) and delayed encephalopathy after acute carbon monoxide poisoning (DECAMP), and to compare the degree of brain damage.

METHODSA retrospective analysis was performed on the clinical and MRI data of 27 patients diagnosed with ACOP and 35 patients diagnosed with DECAMP. Ten healthy volunteers were recruited in the normal control group. All subjects received both routine MRI and diffusion-weighted MRI. Apparent diffusion coefficient (ADC) was determined with symmetric measurement of region of interest in the bilateral globus pallidus, white matter around lateral ventricle, and centrum semiovale. ADC values were compared afterwards.

RESULTSThirteen of the 27 ACOP cases were found of symmetrical abnormal signal in the bilateral globus pallidus, among whom 8 patients only showed pallidum region involvement, while the other 5 patients showed involvement of other regions. Eight ACOP patients showed cortical and subcortical white matter involvement, and 4 cases showed diffused abnormal signal around the bilateral ventricles and in the bilateral centrum semiovale. Two cases of ACOP presented with multiple region involvement. Thirty-five DECAMP patients showed diffused swelling and symmetric demyelination in multiple regions of the brain parenchyma. The periventricular white matter and centrum semiovale were involved in 33 cases, the deep brain nuclei were involved in 23 cases, and the cerebral cortex was involved in 3 cases. The ACOP and DECAMP groups had significantly lower ADC values in the periventricular white matter and bilateral centrum semiovale than the normal control group (P < 0.05), and the ADC values were significantly lower in the DECAMP group than in the ACOP group (P < 0.05). The ACOP group had a significantly lower ADC value in the globus pallidus than the DECAMP group and normal control group (P < 0.05); the DECAMP group had a significantly higher ADC value in the globus pallidus than the ACOP group and normal control group (P < 0.05).

CONCLUSIONRoutine MRI and ADC value can evaluate the degree of brain damage in ACOP and DECAMP patients based on lesion involvement on a more microscopic scale. It can provide valuable information for therapy selection and prognostic evaluation.

Adult ; Aged ; Brain Diseases ; chemically induced ; diagnosis ; Carbon Monoxide Poisoning ; complications ; diagnosis ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Retrospective Studies ; Young Adult

Gefitinib is regarded as a relatively safe agent for the treatment of an advanced non-small cell lung cancer (NSCLC). Pulmonary toxicity such as interstitial lung disease associated with gefitinib is uncommon with an estimated all time incidence around 1% worldwide. Moreover, a case of gefitinib associated with pulmonary cystic changes has not been reported yet. In this report we present a case of progressive multiple air cystic changes in both lungs in a patient with NSCLC and intrapulmonary metastases who underwent a gefitinib therapy.
Antineoplastic Agents/*adverse effects ; Brain Neoplasms/secondary ; Carcinoma, Non-Small-Cell Lung/*drug therapy/secondary ; Cysts/*chemically induced ; Female ; Humans ; Lung/pathology ; Lung Diseases/*chemically induced ; Lung Diseases, Interstitial ; Lung Neoplasms/*drug therapy ; Middle Aged ; Quinazolines/*adverse effects

Two cats were presented with vestibular signs and seizures. Both cats were diagnosed with thiamine deficiency. The transverse and dorsal T2-weighted magnetic resonance (MR) images revealed the presence of bilateral hyperintense lesions at specific nuclei of the midbrain, cerebellum, and brainstem. After thiamine supplementation, the clinical signs gradually improved. Repeated MR images taken 3 weeks after thiamine supplementation had started showed that the lesions were nearly resolved. This case report describes the clinical and MR findings associated with thiamine deficiency in two cats.
Animals ; Brain Stem/pathology ; Cat Diseases/chemically induced/*diagnosis/*drug therapy ; Cats ; Cerebellum/pathology ; Diet/veterinary ; Dietary Supplements/analysis ; Female ; Magnetic Resonance Imaging/veterinary ; Male ; Mesencephalon/pathology ; Seizures/chemically induced/pathology/veterinary ; Thiamine/administration & dosage/*therapeutic use ; Thiamine Deficiency/chemically induced/diagnosis/drug therapy/*veterinary ; Treatment Outcome

Appropriate selection and measurement of lead biomarkers of exposure are critically important for health care management purposes, public health decision making, and primary prevention synthesis. Lead is one of the neurotoxicants that seems to be involved in the etiology of psychologies. Biomarkers are generally classified into three groups: biomarkers of exposure, effect, and susceptibility.The main body compartments that store lead are the blood, soft tissues, and bone; the half-life of lead in these tissues is measured in weeks for blood, months for soft tissues, and years for bone. Within the brain, lead-induced damage in the prefrontal cerebral cortex, hippocampus, and cerebellum can lead to a variety of neurological disorders, such as brain damage, mental retardation, behavioral problems, nerve damage, and possibly Alzheimer's disease, Parkinsons disease, and schizophrenia. This paper presents an overview of biomarkers of lead exposure and discusses the neurotoxic effects of lead with regard to children and adults.
Alzheimer Disease ; chemically induced ; metabolism ; pathology ; physiopathology ; psychology ; Animals ; Behavior ; drug effects ; Biomarkers ; metabolism ; Brain ; metabolism ; pathology ; physiopathology ; Brain Diseases ; chemically induced ; pathology ; physiopathology ; Environmental Exposure ; adverse effects ; Humans ; Lead ; pharmacokinetics ; toxicity ; Lead Poisoning ; etiology ; metabolism ; pathology ; physiopathology ; psychology ; Neurotoxicity Syndromes ; etiology ; metabolism ; pathology ; physiopathology ; psychology ; Parkinson Disease, Secondary ; chemically induced ; metabolism ; pathology ; physiopathology ; psychology ; Schizophrenia ; chemically induced ; metabolism ; pathology ; physiopathology

OBJECTIVETo study the MRI features of 1,2-dichloroethane Chronic Toxic Encephalopathy of 10 cases.

METHOD10 cases were examined by MRI, slice thickness 8 mm, layer from 2 mm, axial and coronal line scan, T1WI, T2WI, FLAIR imaging.

RESULTS10 cases show varying degrees of abnormal signal of white matters, low signal intensity on T1WI, high signal intensity on T2WI and FLAIR. MRI could also show extensive abnormal signal in cerebral white matter although the toxic manifestation is mild to moderate. Therefore the symptoms and the shows of MRI could be inconsistent.

CONCLUSIONCombined with a history of exposure, the show of varying degrees of abnormal signal of white matter in 1,2-dichloroethane Chronic Toxic Encephalopathy cases are characteristic.

Adult ; Brain Diseases ; chemically induced ; pathology ; Ethylene Dichlorides ; poisoning ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Occupational Exposure ; Retrospective Studies ; Young Adult

Encephalopathy is a disorder characterized by altered brain function, which can be attributed to various causes. Encephalopathy associated with metronidazole administration occurs rarely and depends on the cumulative metronidazole dose, and most patients with this condition recover rapidly after discontinuation of therapy. Because metronidazole is metabolized in the liver and can be transported by the cerebrospinal fluid and cross the blood-brain barrier, it may induce encephalopathy even at a low cumulative dose in patients with hepatic dysfunction. We experienced a patient who showed ataxic gait and dysarthric speech after receiving metronidazole for the treatment of hepatic encephalopathy that was not controlled by the administration of lactulose. The patient was diagnosed as metronidazole-induced encephalopathy, and stopping drug administration resulted in a complete recovery from encephalopathy. This case shows that caution should be exercised when administering metronidazole because even a low dose can induce encephalopathy in patients with liver cirrhosis.
Anti-Infective Agents/*adverse effects/therapeutic use ; Brain Diseases/*chemically induced/diagnosis ; Hepatic Encephalopathy/*drug therapy/etiology ; Humans ; Liver Cirrhosis/*complications ; Magnetic Resonance Imaging ; Male ; Metronidazole/*adverse effects/therapeutic use ; Middle Aged ; Tomography, X-Ray Computed

OBJECTIVETo develop the organophosphate-induced delayed neuropathy (OPIDN) hen model with 2,4,6-trimethylbenzoyl phenylphosphonate (TOCP), and observe the change of pathology and investigate the alterations of microtubulin associated protein 2 (MAP2).

METHODS48 adult hens were randomly divided into four groups, including three experimental groups and control group (n = 12 each group). The hens in three experimental groups were treated with TOCP by gavage at single dosages of 250, 500 and 750 mg/kg respectively while the control hens received an equivalent volume of corn oil by gavage. All hens were sacrificed after 21 days of treatment. Half hens in each group were dissected for HE examination and myelin straining of brain, spinal cord and sciatic nerve while brains of another half hens were dissected for the determination of MAP2 by western blotting.

RESULTSThe delayed neurotoxicity symptoms of hens both in 500 and 750 mg/kg groups were consistently observed. The pathological changes of brain, spinal cord and sciatic nerve in 500 and 750 mg/kg groups showed nerve cells difference necrosis, increased cytoplasm basophilia, microglia proliferation, mono-nuclear and lymphocyte infiltration, myelin sheath extensive up to part of them disaggregation deletion. Compared with the control group, at 500 and 750 mg/kg respectively the increase of MAP2 was 25% and 23% (P < 0.01 and P < 0.05).

CONCLUSIONSThe histopathologic changes of OPIDN caused by TOCP have dose-response relationship. The changes of MAP2 in nervous system may contribute to the occurrence and development of TOCP induced delayed neurotoxicity.

Animals ; Brain ; metabolism ; pathology ; Chickens ; Female ; Microtubule-Associated Proteins ; metabolism ; Nervous System Diseases ; chemically induced ; metabolism ; pathology ; Organophosphates ; toxicity