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1.
Arch Endocrinol Metab ; 68: e230254, 2024 Apr 19.
Artigo em Inglês | MEDLINE | ID: mdl-38652700

RESUMO

Thyroid storm is a rare but well-known life-threatening complication that occurs due to acute exacerbation of thyrotoxicosis with the increased levels of circulating thyroid hormones. Reports of metabolic encephalopathy associated with thyroid storm are scarce. We describe the case of a 23-year-old male patient with no previous history of abnormal thyroid function who had consumed excessive amounts of alcohol before disease onset. The patient was found unconscious and febrile on a roadside by a passerby and was admitted to our hospital's emergency department. His primary clinical presentation included hyperthermia (40.8 °C), nodal tachycardia (180 beats/min), seizures, coma, and hypoglycemia (2.18 mmol/L). The hypoglycemia was quickly corrected after admission, but his level of consciousness showed no improvement. With aggressive screening, the patient was found to have severe thyroid dysfunction (T3 = 6.67 nmol/L, T4 = 252.00 nmol/L, free T3 = 29.20 pmol/L, free T4 = 65.30 pmol/L, and TSH = 0.001 µIU/mL). After medical treatment, plasmapheresis, hemofiltration, and hemoperfusion, the patient showed substantial improvement in thyroid hormone levels and stabilization of vital signs, but the impaired consciousness and seizures persisted. Multiple computed tomography scans revealed brain abnormalities. Magnetic resonance imaging performed after tracheal extubation revealed bilateral frontal lobe lesions. We reported a case of metabolic encephalopathy in a patient with life-threatening thyroid storm and bilateral frontal lobe lesions. Hypoglycemia may have been involved in the development of encephalopathy in our patient. Health care providers should consider thyroid storm in the differential diagnosis of hyperthermia, seizures, and coma. Early plasmapheresis, hemofiltration, and hemoperfusion can lower T4 levels and improve prognosis in patients with thyroid storm and encephalopathy.


Assuntos
Lobo Frontal , Crise Tireóidea , Humanos , Masculino , Crise Tireóidea/complicações , Adulto Jovem , Lobo Frontal/diagnóstico por imagem , Imageamento por Ressonância Magnética , Encefalopatias/etiologia
2.
Arch. endocrinol. metab. (Online) ; 68: e230254, 2024. graf
Artigo em Inglês | LILACS-Express | LILACS | ID: biblio-1556953

RESUMO

SUMMARY Thyroid storm is a rare but well-known life-threatening complication that occurs due to acute exacerbation of thyrotoxicosis with the increased levels of circulating thyroid hormones. Reports of metabolic encephalopathy associated with thyroid storm are scarce. We describe the case of a 23-year-old male patient with no previous history of abnormal thyroid function who had consumed excessive amounts of alcohol before disease onset. The patient was found unconscious and febrile on a roadside by a passerby and was admitted to our hospital's emergency department. His primary clinical presentation included hyperthermia (40.8 °C), nodal tachycardia (180 beats/min), seizures, coma, and hypoglycemia (2.18 mmol/L). The hypoglycemia was quickly corrected after admission, but his level of consciousness showed no improvement. With aggressive screening, the patient was found to have severe thyroid dysfunction (T3 = 6.67 nmol/L, T4 = 252.00 nmol/L, free T3 = 29.20 pmol/L, free T4 = 65.30 pmol/L, and TSH = 0.001 μIU/mL). After medical treatment, plasmapheresis, hemofiltration, and hemoperfusion, the patient showed substantial improvement in thyroid hormone levels and stabilization of vital signs, but the impaired consciousness and seizures persisted. Multiple computed tomography scans revealed brain abnormalities. Magnetic resonance imaging performed after tracheal extubation revealed bilateral frontal lobe lesions. We reported a case of metabolic encephalopathy in a patient with life-threatening thyroid storm and bilateral frontal lobe lesions. Hypoglycemia may have been involved in the development of encephalopathy in our patient. Health care providers should consider thyroid storm in the differential diagnosis of hyperthermia, seizures, and coma. Early plasmapheresis, hemofiltration, and hemoperfusion can lower T4 levels and improve prognosis in patients with thyroid storm and encephalopathy.

3.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-910602

RESUMO

Objective:To study the efficacy and safety of early abdominal puncture drainage (APD) in severe acute pancreatitis (SAP).Methods:A retrospective study was conducted on 189 patients with SAP who were managed at the Department of Intensive Medicine of the Second Affiliated Hospital of Anhui Medical University from January 2013 to May 2020. According to whether ultrasound-guided APD was performed within one week after admission to ICU, these patients were divided into 2 groups: patients treated with APD (the APD group) and patients treated without APD (the non-APD group). Clinical data, including the acute physiological and chronic health status (APACHE) Ⅱ score, modified Marshall score, sequential organ failure evaluation (SOFA) score, and prognostic indicators including the retroperitoneal percutaneous drainage (PCD) rate and length of hospital stay, were compared between the two groups before and 1 week after surgery.Results:Of the 189 SAP patients in this study, there were 110 males and 79 females, aged (52.5±17.4) years old. On admission to ICU, the blood amylase, C-reactive protein, procalcalonin, interleukin-6, APACHE II score, modified Marshall score and SOFA score in the APD group were significantly higher than those in the non-APD group. After 1 week of treatment, most clinical indicators in the 2 groups were significantly improved, and there were no significant differences between these indicators (all P>0.05). There were no significant differences in the abdominal infection, retroperitoneal PCD and mortality rates between the APD group and the non-APD group ( P>0.05). The length of hospital stay [29 (18, 45) vs 21 (15, 32) d] and ICU stay [5 (3, 11) vs. 7 (5, 17) d] in the APD group were significantly higher than those in the non-APD group ( P<0.05). Conclusion:For patients with SAP with peritoneal effusion, early APD effectively improved the condition and prognosis without increasing the peritoneal infection and mortality rates.

4.
Basic & Clinical Medicine ; (12): 668-675, 2017.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-512378

RESUMO

Objective To investigate the mechanism of IL-1β in promoting glial scar formation after spinal cord injury.Methods The experimental model of SCI was created by extradural compression of the spinal cord using an aneurysm clip.Rats were randomly divided into model group, sham operation group, IL-1β inhibitor IL-1RA group, IL-1β group and IL-1β+JAK2-STAT3 inhibitor AG490 group, according to different interventions, then were given normal saline, IL-1RA, IL-1β and IL-1β+AG490 every 10 μL respectively, sham group received only laminectomy.The motion function of the hindlimbs of rats was measured by Basso Beattie Bresnahan(BBB) scores and the expression of GFAP, vimentin and p-STAT3 were detected by Western blot technique, immunofluorescence assay and immunohistochemistry technique at corresponding time points(at the 8th, 12th hour, 1st, 3rd, 7th and 14th day after SCI).Results The expression trend of p-STAT3(at the 8th and 12th hour after SCI),GFAP and vimentin(at the 7th and 14th day after SCI)was: the expressions of p-STAT3, GFAP and vimentin in the model group were significantly higher compared with the sham group(P<0.01), the expression of p-STAT3,GFAP andvimentin in the IL-1RA group were significantly lower compared with the model group(P<0.05) whereas significantly higher compared with the sham group(P<0.05);the expressions of p-STAT3, GFAP and vimentin in the IL-1β+AG490 group were significantly lower compared with the model group(P<0.05)whereas significantly higher compared with the sham group(P<0.05), the expressions of p-STAT3, GFAP and vimentin in the IL-1β group were significantly higher compared with the model group(P<0.05).Conclusions IL-1β can improve glial scar formation via JAK2-STAT3 signal.Inhibition of IL-1β or JAK2-STAT3 can reduce glial scar formation and promote functional recovery of spinal nerve.

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