Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003615 (appendicitis)
4,439 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the case of a 28-year-old woman who presented simultaneously with superior sagittal sinus thrombosis and thyroid crisis, and was subsequently found to have protein C deficiency. February 3, 2003, she admitted complaining of abdominal pain. The diagnosis of appendicitis was made, and she was operated on under lumbar anaesthesia. Day 7, she developed acute headache and distal weakness of the left lower limb. On examination she was alert, with a temperature of 38 degrees C, a sinus tachycardia of 124/min and blood pressure 164/84 mmHg. Neurological examination revealed neck stiffness and left hemiparesis, predominantly in her lower limb. Gadlinium-enhanced brain MRI revealed extensive superior sagittal sinus thrombosis. CT scan demonstrated infarction in the right frontal cortex, and subarachnoid hemorrhage adjacent to the right cerebellar tentorium. The patient was treated with a free radical scavenger edarabon, and glycerin. No anticoagulant therapy was instituted. Over the next 24 hours, her condition worsened. She became comatose, as well as developing a generalized tonic-clonic seizure. Day 12, laboratory examinations revealed an undetectable TSH-level CTSH (thyroid stimulating hormone) <0.005 mcIU/ml), with a level of free thyroxin 7.77 ng/dl (0.9-1.7), free triiodothyronin 29.6 pg/ml (2.3-4.3), and positive anti-TSH receptor antibodies determined subsequently. Coagulation factor VIII activity was 155% (normal range 60-150). Protein C deficiency (antigen 59%, activity 49%) was also present, suggesting a congenital type I heterozygous deficiency. A diagnosis of thyroid crisis on the basis of Graves' disease was made. The patient remained comatose and died on Day 16, with renal failure. The patient had protein C deficiency, a well-established risk factor for cerebral venous thrombosis (CVT). However, additional risk factors are required in most cases to precipitate CVT. In our case, this trigger was most likely thyroid crisis, suggesting that thyrotoxicosis, probably through hypercoagulability, may be a predisposing factor for the development of CVT.
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PMID:[Thyroid crisis and protein C deficiency in a case of superior sagittal sinus thrombosis]. 1737 Jun 53

A 73-year-old female patient developed a generalized tonic-clonic seizure on the 6th day after treatment with moxifloxacin 400 mg daily intravenously for appendicitis. This patient had atrial fibrillation and history of a surgery for intracerebral hemorrhage, with impaired renal function and liver function, but without history of seizures. Moxifloxacin was discontinued and switched to cefuroxime. The patient remained seizure-free at discharge four days later. The naranjo adverse drug reaction probability scale score was 4, indicating a possible adverse reaction to moxifloxacin. The potential risk factors related to moxifloxacin-induced seizures are discussed. It highlights that preexisting central nervous system disease, elderly female with lower bodyweight and severe renal impairment may be the risk factors involved in moxifloxacin-induced seizures.
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PMID:Moxifloxacin Induced Seizures -A Case Report. 2617 84