Porphyrias are inherited metabolic disorders resulting from a specific enzyme defect in the heme biosynthetic pathway. Porphyrias are induced by various precipitants. Clinical features include abdominal pain, neurologic manifestations, autonomic neuropathy, and mental disturbance. Diagnosis may be delayed because of variable symptoms that mimic other diseases and because of the rarity of of porphyrias. Although most patients with known porphyria can complete anesthesia and surgery safely, undiagnosed porphyric patients are in danger of porphyric crisis due to inadvertent exposure to precipitating drugs and environment. We report a case of a patient who experienced delayed emergence with neurological disturbance after general anesthesia, ultimately diagnosed as acute intermittent porphyria.
Abdominal Pain ; Anesthesia ; Anesthesia, General* ; Biosynthetic Pathways ; Delayed Emergence from Anesthesia ; Diagnosis ; Guillain-Barre Syndrome ; Heme ; Humans ; Neurologic Manifestations* ; Porphyria, Acute Intermittent* ; Porphyrias ; Spine* ; Wernicke Encephalopathy

BACKGROUND: Leptin is an adipokine that is recently reported to be a biomarker of systemic inflammation. Although atherosclerosis causes cardiovascular diseases, it is not clear whether leptin contributes to the acceleration of this process. In this study, we investigated whether alterations of plasma leptin levels were related to diabetic nephropathy and systemic inflammation. In addition, we examined the physiologic action of leptin in cultured vascular smooth muscle cells (VSMCs). METHODS: A total of 126 type 2 diabetic participants and 37 healthy controls were studied. The diabetic participants were divided into three groups according to stage of nephropathy. We investigated whether leptin induced monocyte chemotactic peptide-1 (MCP-1) synthesis through the mitogen-activated protein kinase (MAPK) pathway using cultured VSMCs. RESULTS: Plasma leptin concentrations were significantly higher in the diabetic group than in the controls. Plasma leptin levels were positively correlated with body mass index, fasting and postprandial blood glucose, hemoglobin A1c, total cholesterol, urinary albumin excretion, high-sensitivity C-reactive protein (hsCRP), and MCP-1 plasma levels, and negatively correlated with creatinine clearance values. In cultured VSMCs, leptin increased MCP-1 production in a dose-dependent manner, and this stimulating effect of leptin on MCP-1 expression was reversed by the MAPK (MEK) inhibitor PD98059. In addition, leptin stimulated the phosphorylation of MEK, extracellular signal-regulated kinase, and E26-like transcription factor, which are components of the MAPK pathway. CONCLUSION: Overall, these findings suggest that activation of leptin synthesis may promote MCP-1 activation in a diabetic environment via the MAPK pathway in VSMCs and that it possibly contributes to the acceleration of atherosclerosis.
Acceleration ; Adipokines ; Atherosclerosis ; Blood Glucose ; Body Mass Index ; C-Reactive Protein ; Cardiovascular Diseases ; Cholesterol ; Creatinine ; Diabetes Mellitus ; Diabetic Nephropathies ; Fasting ; Flavonoids ; Hemoglobins ; Humans ; Inflammation ; Leptin ; Monocytes ; Muscle, Smooth, Vascular ; Phosphorylation ; Phosphotransferases ; Plasma ; Protein Kinases ; Transcription Factors

BACKGROUND: An inflammatory mechanism has been suggested to contribute to the progression of diabetic nephropathy. Although retinoid, a known anti-inflammatory agent, has been reported to be beneficial in some experimental renal diseases, it has not been shown whether it prevents disease progression in diabetic nephropathy. Therefore, we investigated whether all-trans retinoic acid inhibits inflammatory changes and improves renal function during the early stages of diabetic nephropathy in streptozotocin-induced diabetic rats. METHODS: We evaluated anti-inflammatory effect of retinoid on streptozotocin-induced diabetic nephropathy. Anti-inflammatory effect was determined by the expression of monocyte chemoattractant peptide-1 (MCP-1). RESULTS: Urinary protein excretion was significantly higher in diabetic rats at four weeks after the induction of diabetes mellitus compared with controls, and proteinuria in the group with retinoic acid treatment was decreased (1.25+/-0.69 vs. 0.78+/-0.72 mg/mg Cr, p=0.056). Urinary excretion of MCP-1 was rapidly increased at two days after induction of diabetes mellitus in diabetic rats, and further increased until four weeks of age compared with control rats. Retinoic acid treatment suppressed to 30% reduction of the urinary level of MCP-1 compared with vehicle treated diabetic rats (119.3+/-74.2 vs. 78.1+/-62.7 pg/mg Cr, p=0.078). Immunohistochemistry revealed a significant increase in staining for MCP-1 protein in the diabetic kidney, and retinoic acid treatment significantly suppressed intrarenal MCP-1 protein synthesis. CONCLUSION: Retinoic acid suppressed proteinuria and inflammatory changes in diabetic rats. These results suggest that retinoic acid may have an anti- inflammatory effect in diabetic nephropathy.
Animals ; Diabetes Mellitus ; Diabetic Nephropathies* ; Disease Progression ; Immunohistochemistry ; Inflammation ; Kidney ; Monocytes ; Proteinuria ; Rats ; Tretinoin

Although fentanyl-induced cough is generally transient and benign, it can give rise to serious problems in patients to whom increasing intracranial, intraocular or intraabdominal pressures may create dangerous situations. This case demonstrates aspiration pneumonia as a complication, exhibiting severe cough induced by intravenous injection of fentanyl.
Cough ; Fentanyl ; Humans ; Injections, Intravenous ; Pneumonia ; Pneumonia, Aspiration ; Vomiting