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1.
Int J Clin Pharmacol Ther ; 61(10): 437-444, 2023 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-37548458

RESUMEN

OBJECTIVE: Among fibrates as triglyceride-lowering agents, bezafibrate and fenofibrate are predominantly renally excreted, while pemafibrate is mainly hepatically metabolized and biliary excreted. To elucidate possible different properties among fibrates, this retrospective observational study examined the changes in clinical laboratory parameters, including indices of renal function and glucose metabolism, in cases of switching from bezafibrate to pemafibrate. MATERIALS AND METHODS: In 93 patients with hypertriglyceridemia, the average values of laboratory parameters including serum creatinine, estimated glomerular filtration rate (eGFR), plasma glucose, and hemoglobin A1c on respective two occasions before and after switching from bezafibrate to pemafibrate were evaluated. RESULTS: Triglycerides, low-density and high-density lipoprotein cholesterol, creatine kinase, and uric acid did not change before and after switching from bezafibrate to pemafibrate. Serum creatinine significantly decreased and eGFR significantly increased after switching from bezafibrate to pemafibrate (p < 0.001, respectively). Plasma glucose tended to increase (p = 0.070) and hemoglobin A1c significantly increased (p < 0.001) after switching to pemafibrate. The degrees of changes in creatinine, eGFR, glucose, and hemoglobin A1c before and after drug switching were not affected by the presence or absence of coexisting disease, and with or without drug treatment including statin and renin-angiotensin system inhibitor. CONCLUSION: Our findings indicate that switching from bezafibrate to pemafibrate produces a significant decrease in serum creatinine and increases in eGFR and hemoglobin A1c in patients with hypertriglyceridemia, suggesting that the effects on renal function and glucose metabolism differ among fibrates.


Asunto(s)
Bezafibrato , Hipertrigliceridemia , Humanos , Bezafibrato/efectos adversos , Glucemia , Hemoglobina Glucada , Creatinina , Hipertrigliceridemia/diagnóstico , Hipertrigliceridemia/tratamiento farmacológico , Hipertrigliceridemia/metabolismo , Triglicéridos/metabolismo , Triglicéridos/uso terapéutico , Ácidos Fíbricos/uso terapéutico , Glucosa/uso terapéutico , Riñón/fisiología
2.
JMA J ; 5(1): 161-166, 2022 Jan 17.
Artículo en Inglés | MEDLINE | ID: mdl-35224284

RESUMEN

A 39-year-old man presented with worsening fever, cough, and fatigue. He was immediately admitted to the intensive care unit (ICU) and was found to have sepsis, septic pulmonary embolism, right empyema, liver abscess, pyelonephritis, and a prostate abscess, with background diabetes mellitus. While receiving treatment, an ICU nurse noticed that the patient's toe tips were too large to fit the clamp device of pulse oximeters. Thus, we re-examined the patient and confirmed that he had clinical features indicative of acromegaly including bulging eyebrows, enlarged nose and lips, large feet, and prognathism. He and his family had not noticed these features except for his enlarged feet. We evaluated the patient further for acromegaly, and a pituitary mass was detected via contrast-enhanced head magnetic resonance imaging. Whole-body computed tomography also revealed thickened heel pads, cauliflower deformity, frontal sinus enlargement, sella turcica enlargement, and mandibular malocclusion. A 75 g oral glucose tolerance test was performed to investigate abnormal secretion of growth hormone (GH), and the results revealed a paradoxical increase in GH levels. The patient was then diagnosed with acromegaly according to the clinical guidance of the Japan Endocrine Society. Acromegaly develops slowly; thus, to improve patients' prognoses, physicians including internists, family physicians, and endocrinologists should include acromegaly in their differential when signs are apparent.

3.
Prion ; 12(2): 147-149, 2018 03 04.
Artículo en Inglés | MEDLINE | ID: mdl-29411683

RESUMEN

We report a Japanese patient with spinocerebellar ataxia type 31 (SCA31) and sporadic Creutzfeldt-Jakob disease (sCJD). A 52-year-old man developed progressive cognitive impairment after the appearance of cerebellar symptoms. Brain MR diffusion-weighted imaging (DWI) demonstrated a slowly expanding hyperintense lesion in the cerebral cortex. The patient was finally diagnosed as having both SCA31 and sCJD by identification of genetic mutations and by real-time quaking-induced conversion (RT-QUIC) analysis of the cerebrospinal fluid (CSF), respectively. Here, we report the clinical details of this rare combined case, with particular reference to the association between prion protein and the early onset of SCA31.


Asunto(s)
Síndrome de Creutzfeldt-Jakob/patología , Ataxias Espinocerebelosas/patología , Ataxia Cerebelosa/genética , Ataxia Cerebelosa/metabolismo , Ataxia Cerebelosa/patología , Corteza Cerebral/metabolismo , Corteza Cerebral/patología , Síndrome de Creutzfeldt-Jakob/genética , Síndrome de Creutzfeldt-Jakob/metabolismo , Imagen de Difusión por Resonancia Magnética , Humanos , Masculino , Persona de Mediana Edad , Ataxias Espinocerebelosas/genética , Ataxias Espinocerebelosas/metabolismo
4.
Brain Nerve ; 69(8): 957-961, 2017 Aug.
Artículo en Japonés | MEDLINE | ID: mdl-28819079

RESUMEN

A 33-year-old man was admitted to our hospital with bilateral facial nerve paralysis, dysphagia, and muscle weakness in the neck and trunk following fever, headache and throat pain. T2-weighted brain magnetic resonance imaging (MRI) showed hyperintense lesions in the tegmentum of the brain stem and the ventral region of the superior cervical cord. Based on the characteristic findings on the brain MRI, we diagnosed the patient with enteroviral encephalomyelitis. Steroid therapy was administered; however, his bilateral facial nerve paralysis and dysphagia were refractory to this therapy. Subsequently, enterovirus D68 was detected in the serum using polymerase chain reaction (PCR) analysis. At that time, an outbreak of enteroviral D68 infection was reported in Japan. Finally, we diagnosed encephalomyelitis caused by enteroviral D68 infection. Characteristic MRI findings were very useful in narrowing down the differential diagnosis in this patient. (Received March 3, 2017; Accepted April 20, 2017; Published August 1, 2017).


Asunto(s)
Trastornos de Deglución/etiología , Encefalomielitis/etiología , Infecciones por Enterovirus/complicaciones , Nervio Facial , Parálisis Facial/etiología , Adulto , Humanos , Masculino
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