Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
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We report the case of a 32-year-old man who presented at the emergency department with severe chest pressure, left arm pain, and dizziness. These symptoms were described as intermittent, occurring after exercise and at rest. He had undergone several stress tests during the past 8 years, but no objective evidence of ischemia was produced. His history of hyperlipidemia and increasing frequency of symptoms prompted us to perform coronary angiography, which showed a single coronary artery with an ostium at the right sinus of Valsalva. The vessel had an initial, mixed common trunk that gave rise to both the right coronary artery proper and to the left coronary artery. The left main trunk followed a prepulmonic course. The anatomic features were eventually confirmed by computed tomographic angiography. The left main stem had a fixed 50% to 60% area narrowing, at baseline study. A treadmill stress myocardial perfusion study showed no evidence of ischemia. The patient was referred to a 2nd facility, where intravascular ultrasonography, at baseline, revealed 63% left main narrowing without evidence of atherosclerosis. Acetylcholine provocation demonstrated worsening of the stenosis to about 80%, with reproduction of angina and ST-segment depression, which indicated that medical management of spasm might provide symptomatic relief.
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PMID:Single coronary artery with prepulmonic coursing left main coronary artery manifesting as prinzmetal's angina. 1817 28

We present a 46-year-old patient who suffered from cardiac arrest and subsequently underwent placement of an implantable cardioverter defibrillator (ICD). The patient underwent a cardiac catheterization which revealed no significant coronary artery disease. About 1 year later he experienced appropriated and frequent ICD discharges due to monomorphic ventricular tachycardia (VT) with left bundle branch block morphology. His prodromal symptoms were mild dizziness and lightheadedness with no chest pain. Amiodarone, mexiletine, sotalol and dofetilide as well as ablation of two inducible ventricular tachycardias in the electrophysiology studies were unsuccessful in controlling the arrhythmias and ICD discharges. During the last episode, he experienced a mild burning sensation in his chest and was given nitroglycerin 0.4 mg sublingually, which relived his symptoms and aborted the VT. This led to a second cardiac catheterization to investigate whether the VT was being induced by myocardial ischemia. This second coronary angiogram spontaneously revealed significant coronary vasospasm and simultaneously, the patient's cardiac rhythm showed short runs of VT with left bundle branch block morphology. Intracoronary nitroglycerine relieved the coronary vasospasm and terminated the arrhythmia. The patient was treated with isosorbide mononitrate and diltiazem. He remained symptom free with no ICD discharges and no VT in ICD interrogations for more than 2 years. Coronary vasospasm may be silent and with no chest pain which creates a difficult clinical situation particularly if it is associated with ventricular tachycardia and sudden cardiac death. The mechanisms of VT in the setting of coronary vasospasm are not known and increased automaticity, focal discharges, functional unidirectional block with reentry, or a combination of these mechanisms may contribute to inducing the VT during the transient ischemia or rarely in the reperfusion phase. It is important to perform provocative tests to diagnose silent coronary vasospasm in unexplained sudden cardiac arrests.
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PMID:Multiple episodes of ventricular tachycardia induced by silent coronary vasospasm. 1829 82

Methyl bromide is a highly toxic gas with poor olfactory warning properties. It is widely used as insecticidal fumigant for dry foodstuffs and can be toxic to central and peripheral nervous systems. Most neurological manifestations of methyl bromide intoxication occur from inhalation. Acute toxicity characterized by headache, dizziness, abdominal pain, nausea, vomiting and visual disturbances. Tremor, convulsion, unconsciousness and permanent brain damage may occur in severe poisoning. Chronic exposure can cause neuropathy, pyramidal and cerebellar dysfunction, as well as neuropsychiatric disturbances. The first case of methyl bromide intoxication in Thailand has been described. The patient was a 24-year-old man who worked in a warehouse of imported vegetables fumigated with methyl bromide. He presented with unstable gait, vertigo and paresthesia of both feet, for two weeks. He had a history of chronic exposure to methyl bromide for three years. His fourteen co-workers also developed the same symptoms but less in severity. Neurological examination revealed ataxic gait, decreased pain and vibratory sense on both feet, impaired cerebellar signs and hyperactive reflex in all extremities. The serum concentration of methyl bromide was 8.18 mg/dl. Electrophysilogical study was normal. Magnetic resonance imaging of the brain (MRI) revealed bilateral symmetrical lesion of abnormal hypersignal intensity on T2 and fluid-attenuation inversion recovery (FLAIR) sequences at bilateral dentate nuclei of cerebellum and periventricular area of the fourth ventricle. This incident stresses the need for improvement of worker education and safety precautions during all stages of methyl bromide fumigation.
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PMID:Neurological manifestation of methyl bromide intoxication. 1857 99

Myasthenia gravis (MG) is a chronic neuromuscular disease which leads to varying degrees of weakness in the skeletal muscles. Some of the symptoms of the disorder include weakness of the eye muscles, difficulty in swallowing and slurred speech. When only the muscles of the eyes are affected, the illness is termed ocular myasthenia, which is often characterized by abrupt onset of diplopia and ptosis of the eyelid. In most patients with ocular-onset MG, there is a progression to involvement of other muscle groups within the first two years (generalized myasthenia). In the case reported here, a 39-year-old male of Ecuadorian descent complained of difficulty seeing, double vision, dizziness, unsteady gait, difficulty maintaining balance and fatigue for the previous two days. Neurological examination was remarkable for total external ophthalmoplegia. There was no external bulbar muscle paralysis, motor weakness, muscle wasting, sensory deficits or sphincter dysfunction. His laboratory workup was significant for elevated acetylcholine receptor antibody. He was diagnosed with ocular MG after differential diagnoses were ruled out based on the onset and presentation of symptoms, the patient's age and a normal magnetic resonance imaging exam. No signs of generalized myasthenia were detected. His symptoms improved dramatically after treatment with Acetyl cholinesterase (AchE) inhibitors and steroids, regaining much of his ocular mobility and ability to walk without gait imbalance. At follow-up visits, the patient remained healthy with no evidence development of other myasthenic signs. This case is atypical since ocular MG does not normally occur in the absence of other myasthenic forms.
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PMID:An atypical course of myasthenia gravis. 1860 52

A case of a giant intracranial varix arising from an arteriovenous (AV) fistula is reported. This 16 year old boy presented with a sudden onset of headache and dizziness. The patient had suffered from intermittent seizure attacks since the age of 4. Brain computed tomography (CT), taken 2 years prior to admission, showed compression of the quadrigeminal plate by a suspicious mass lesion. His brain CT, magnetic resonance imaging (MRI), and cerebral angiography on admission demonstrated a giant varix with evidence of haemorrhage in the cerebellum. The varix was fed from branches of the posterior cerebral artery and drained through a dilated vein into the vein of Galen. It was resected surgically. Surgery and/or endovascular obliteration of the AV fistula is required because the varix which develops from an AV fistula can enlarge and rupture.
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PMID:Giant intracranial varix arising from an arteriovenous fistula. 1863 7

A 40-year-old male military Veteran* presents to a family physician with chronic symptoms that include recurrent headaches, dizziness, depression, memory problems, difficulty sleeping, and relationship troubles. He has not had a family physician since leaving the military 2 years ago. His Military Occupation Classification had been infantry. He explains that he had been deployed to war zones and that during a firefight several years earlier an enemy weapon exploded nearby, killing a fellow soldier and wounding others. He does not recall being injured, but remembers feeling a thump and that his "computer had to reboot." This was followed by headaches and a few days of ringing in his ears. He also suffered a concussion during a military hockey game. He was assessed and treated for persistent headaches in the service and recalls that results of a head computed tomography scan were negative. Veterans Affairs Canada (VAC) granted him a disability award for posttraumatic headache and provided certain treatment benefits. He took medication for the headaches. Following transition to civilian life he had difficulty holding jobs, but had been reluctant to seek help. He saw stories on television about blast-induced minor traumatic brain injury in Iraq and Afghanistan, and wonders if he "has MTBI." Findings from his physical examination, bloodwork, and Mini Mental State Examination are normal, but his Montreal Cognitive Assessment score is 24, suggesting possible cognitive impairment. The physician organizes follow-up appointments and a neurology consultation. After reading about Canada's military-aware operational stress injury (OSI) clinics in a medical journal, he refers the Veteran to a VAC district office for access to mental health assessment.
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PMID:Battlefield brain: unexplained symptoms and blast-related mild traumatic brain injury. 1900 4

A 63-year-old man was admitted because of dizziness, polydipsia, polyuria, and diminished libido. His brain MRI showed swelling of the pituitary gland. Because of panhypopituitarism suggested by hormonal examination, hydrocortisone, desmopressin and levothyroxine sodium were started as hormone replacement therapy. He was given a clinical diagnosis of central neurosarcoidosis with panhypopituitarism because of the presence of an abnormal lung shadow, positive gallium scintigram in bilateral hilar lymph nodes, negative tuberculin skin test, lymphocytosis and a high CD4/8 ratio in bronchoalveolar lavage fluid. After prednisolone therapy, his lung shadow and pituitary swelling reduced significantly. Anti-diuretic hormones and anterior pituitary hormones tended to increase, and his urine volume also decreased. This case suggested that endocrinological abnormalities in central neurosarcoidosis might be improved by prednisolone therapy even if the initiation of treatment is delayed.
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PMID:[Case of central neurosarcoidosis with panhypopituitalism]. 1904 32

A 65-year-old man was referred with Stage IV rectal cancer with lung and liver metastasis. He had done low anterior resection. One month after operation, he was administered anti-cancer drugs of FOLFOX4 protocol. Six months after operation, partial response was obtained of abdominal CT scan evaluation. Nine months after operation, FOLFOX4 was stopped by peripheral nerve injuries. FOLFIRI protocol started as second-line chemotherapy. Nineteen months after operation, he was diagnosed left hydro-nephrosis by retro peritoneal lymph-node metastasis. He was treated by urethral stenting, and FOLFOX protocol was re-started. Twenty one months after operation, FOLFOX4 was stopped by drug allergy, and changed to FOLFIRI protocol. Twenty five months after operation, He felt difficulty of walking and dizziness. He was diagnosed meningeal carcinomatosis by brain CT scan. He was administered glycerol and steroid. His neurological symptoms was improved. Although he died of disease progression at twenty six months after operation.
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PMID:[A fatal case of meningeal carcinomatosis in a stage IV rectal cancer patient who had long time survival by multi- line chemotherapy]. 1929 83

There is an increasing interest in the health risks related to the use of herbal remedies. Although most consumers think that phytomedicines are safe and without side effects, interactions between complementary alternative and conventional medicines are being described. The aim of this clinical case report is to highlight the importance of the safe use of herbal remedies by providing a clinical interaction study between pharmaceutical medicines and herbal medicinal products. The case of a patient self-medicated with Valeriana officinalis L. and Passiflora incarnata L. while he was on lorazepam treatment is described. Handshaking, dizziness, throbbing and muscular fatigue were reported within the 32 h before clinical diagnosis. The analysis of family medical history ruled out essential tremor, Parkinson's disease, Wilson's disease and other symptom-related pathologies. His medical history revealed a generalized anxiety disorder and medicinal plant consumption but no neurological disorder. Appropriate physical examination was carried out. An additive or synergistic effect is suspected to have produced these symptoms. The active principles of Valerian and passionflower might increase the inhibitory activity of benzodiazepines binding to the GABA receptors, causing severe secondary effects. Due to the increase in herbal product self-medication, the use of herbal remedies should be registered while taking the personal clinical history. Multidisciplinary teams should be created to raise studies on medicinal plants with impact on medical praxis.
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PMID:Interactions of Valeriana officinalis L. and Passiflora incarnata L. in a patient treated with lorazepam. 1944 Oct 67

A 76-year-old man with squamous cell lung cancer underwent right lower lobectomy in November, 2005. He was diagnosed with pT2N0M0, stage I B, and tegafur/uracil (UFT) was administered. On July, 2007, right hilar lymphadenopathy was detected and considered to be a recurrence. UFT was discontinued, and gemcitabine (GEM) and docetaxel (DOC) combination chemotherapy was initiated on August 21. He began to complain of fatigue, palpitation and dizziness since the fifth day of the administration, and anemia (hemoglobin: Hb 8.7 g/dL) was detected on the fifteenth day. On the twenty-second day of the administration, he was admitted to our hospital because of aggravation of anemia (Hb 6.5 g/dL). His anemia was diagnosed as immune hemolytic anemia based on the laboratory findings including a positive Coombs' test. He showed improvement with prednisolone therapy. The anemia was considered to be drug-induced. This case was extremely rare, and there are no reports on immune hemolytic anemia related to GEM and/or DOC.
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PMID:[A squamous cell lung cancer patient who developed immune hemolytic anemia after gemcitabine and docetaxel administration]. 1962 Aug 5


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