Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 27-year old African woman with history of regular chloroquine ingestion presented with progressive deterioration of vision, easy fatiguability, dyspnoea, dizziness progressing to syncopal attacks. Ophthalmological assessment revealed features of chloroquine retinopathy, cardiac assessment revealed features of heart failure and a complete heart block with right bundle branch block pattern. The heart block was treated by pacemaker insertion and the heart failure resolved spontaneously following chloroquine discontinuation. She however remains blind.
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PMID:Chloroquine related complete heart block with blindness: case report. 162 52

Iloprost, a stable prostacyclin analog, was evaluated clinically for its ability to ameliorate the symptoms of peripheral neuropathy associated with diabetes. In an open, nonrandomized trial, 13 diabetic patients with neuropathy but without proliferative retinopathy received an intravenous infusion of Iloprost at a dose of 10 micrograms, at a rate of 0.1 micrograms/kg/h, twice daily for two weeks. The administration of Iloprost relieved the majority of such subjective symptoms as pain, numbness or sensation of cold and to a lesser extent, such autonomic symptoms as dizziness. In contrast, there was little evidence of objective improvement, e.g., in motor nerve conduction velocity. Iloprost treatment significantly inhibited the platelet aggregation rate stimulated by collagen in vitro. In the one patient tested, thermography revealed an increase in skin temperature by more than 2 degrees C. Side effects associated with Iloprost included headache (3 patients) or aggravation of pain in the extremities (2 patients) and could be ameliorated by slowing the infusion rate or by discontinuing the drug (one patient). Iloprost appears to be safe and effective for relieving the symptoms of diabetic neuropathy. Our results provide the rationale for a double-blind, clinical trial in larger populations of diabetics with peripheral neuropathy.
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PMID:Clinical efficacy of a stable prostacyclin analog, iloprost, in diabetic neuropathy. 170 9

We have treated 128 patients aged 40 +/- 9 years (60 males and 68 females), all with essential hypertension (W.H.O. I and II), over a period of 10 yr. The treatment was performed with clonidine at a dose that ranged from 0.150 to 1,200 mg (twice daily). Forty-two patients also received a diuretic (HCTZ 25 mg daily). Mean blood pressure decreased significantly from 169 +/- 10 mm Hg systolic, 107 +/- 3 diastolic to 145 +/- 6 mm Hg (p less than 0.001) 90 +/- 3 mm Hg diastolic (p less than 0.001). Side effects occurred during the first month. These were drowsiness 28%, dry mouth 35%, constipation 13%, dizziness 9%, postural hypotension 2%, and male impotence 3.3% (2/60). Side effects still present after 120 months of treatment were drowsiness 11.7%, dry mouth 26.6%, constipation 14.1%, dizziness 4.7%, and male impotence 1.7% (1/59). The number of patients who discontinued treatment resulting from side effects were 3.34%, all of them within the first 6 months. There were no changes in renal or liver function or in serum electrolytes or lipids. Retinopathy improved in most patients. Electrocardiogram (ECG) improved in 45 patients with LVH. It is concluded that clonidine provided sustained blood pressure control with minimum side effects during 10-year therapy for hypertension.
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PMID:Safety aspects of long-term antihypertensive therapy (10 years) with clonidine. 245 59

A 19-year-old woman with insulin-dependent diabetes mellitus (IDDM) of 3.5 years duration had been suffering from recurrent episodes of diabetic ketoacidosis (DKA), dizziness, and weight loss (16 kg, 29%) for 6 months. History and physical examination gave evidence of severe peripheral and autonomic neuropathy. Radionuclide retention on gastric emptying test at 60 min was greater than 90% (normal < 60%). On autonomic cardiovascular testing there was evidence of both parasympathetic and sympathetic damage. There was no evidence of nephropathy or retinopathy. Optimal diabetic control using 4 insulin injections (2 u/kg/day) and high-dose cisapride terminated the vomiting, and she regained the weight lost within 5 months. This case is unique in that severe diabetic neuropathy followed relatively soon after onset of disease, without other microvascular complications. The correct diagnosis of gastroparesis as the cause of the recurrent DKA and weight loss, and the specific prokinetic therapy and nearly normoglycemic control of the diabetes led to dramatic clinical and functional improvement. Specific prokinetic therapy and the nearly normoglycemic control of the diabetes led to dramatic clinical and functional improvement. Gastroparesis can cause recurrent DKA even in young patients with IDDM of short duration.
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PMID:[Severe neuropathy in a young diabetic]. 784 56

Epalrestat is a carboxylic acid derivative which inhibits aldose reductase, an enzyme of the sorbitol (polyol) pathway. Under hyperglycaemic conditions epalrestat reduces intracellular sorbitol accumulation, which has been implicated in the pathogenesis of late-onset complications of diabetes mellitus. Epalrestat 150 mg/day for 12 weeks improved motor and sensory nerve conduction velocity, and vibration threshold compared with baseline and placebo in patients with diabetic neuropathy. Subjective symptoms including pain, numbness, hyperaesthesia, coldness in the extremities, muscular weakness, dizziness, and orthostatic fainting were also improved. Similar benefits were seen in a comparison with historical controls. Epalrestat 300 mg/day for 1 or 3 years was also significantly superior to placebo or no treatment in improving electroretinogram parameters and photo stress recovery time in patients with diabetic retinopathy. Improvements were also documented by funduscopy and fluorescein angiography. Epalrestat appeared most effective in patients with less severe diabetes mellitus and more recent development of late-onset complications. Epalrestat is apparently well tolerated with predominantly minor adverse events reported in clinical trials. Liver enzyme elevations were most commonly reported but generally resolved spontaneously on dose reduction or discontinuation. The effects of age and renal impairment on the efficacy and tolerability of epalrestat require clarification, and data on its use in other late-onset complications of diabetes such as nephropathy are also lacking. Comparisons with other aldose reductase inhibitors are also required to fully determine the role of epalrestat. The suggested ability of epalrestat to prevent the onset of diabetic complications should also be investigated. Thus, available data suggest epalrestat produces some improvement in the late-onset neuropathy and retinopathy associated with diabetes mellitus, although additional trials are required to determine whether ongoing therapy is necessary to maintain the improvements achieved and to confirm tolerability in the long term. Nevertheless, preliminary results suggest that epalrestat may be a useful drug in an area where there is a need for effective therapy.
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PMID:Epalrestat. A review of its pharmacology, and therapeutic potential in late-onset complications of diabetes mellitus. 831 78

A cross-sectional study was designed to identify a relationship between the presence of symptoms usually related to nervous system involvement as well as other chronic complications of diabetes with three objectively defined degrees of autonomic neuropathy (AN). Symptoms usually related to peripheral sensitive neuropathy and AN were assessed using a questionnaire applied to 132 diabetics (38 IDDM and 94 NIDDM), 65 without and 67 with AN. AN was classified as follows according to 5 cardiovascular autonomic tests described by Ewing: 1) early involvement-1 abnormal test (N = 27); 2) definite involvement-2 or 3 abnormal tests (N = 26); 3) severe involvement-4 or 5 abnormal tests (N = 14). A statistically significant association was observed between degree of autonomic involvement and the presence of the following symptoms: dizziness on standing, dysphagia, vomiting, diarrhea, fecal incontinence, gustatory sweating, urinary retention, numbness and hyperesthesia of the feet or legs. Constipation and cystitis were not significantly related to cardiovascular AN. Only 3% of the patients without neuropathy and with early involvement had four or more than four of the symptoms. The prevalence of proliferative retinopathy and nephropathy was increased among patients with more severe degrees of AN. For IDDM patients there was a positive correlation between the degree of cardiovascular AN and the duration of diabetes. We conclude that: 1) severe cardiovascular AN is usually related to 4 or more of the evaluated symptoms and those patients usually have the other complications of diabetes; 2) severe AN could be a risk factor or an indicator of the same underlying process that determines the beginning of proliferative retinopathy and/or nephropathy.
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PMID:Relationship between the degree of cardiovascular autonomic dysfunction and symptoms of neuropathy and other complications of diabetes mellitus. 858 Aug 65

What are the earliest indications of cancer? What prompts an apparently healthy person to suspect that 'something may be wrong'? The first manifestations may involve a growing awareness of neuronal dysfunction, such as headaches, dizziness, physical degeneration or vision abnormalities. While denial may extend the time between the patient's appreciation of the health hazard, particularly if the indications are subtle, a sudden decline in vision may be one of the most readily perceived, and provide the strongest stimulation to seek medical help. Cancer-induced neuropathies are rare but provide much information on the genesis of a defined group of autoimmune reactions, and the biological mechanisms involved. The secondary effects of neoplasia, collectively termed paraneoplasia, are often the first indication of cancer. Sudden weight loss is one of the most recognised early signs, and is known to result from biochemical effects on tissues distant from the site of the growth. More recently, immunologic phenomena have been implicated in a series of different paraneoplasia. Examples, such as Lambert-Eaton myasthenic syndrome (LEMS), paraneoplastic cerebellar degenerations (PCD) and cancer-associated retinopathy (CAR) can be identified immunologically through the detection of autoantibody reactions with defined proteins. Interest in the clinical significance of paraneoplastic-associated immunologic reactions increased following the recognition of their strong disease association; PCD patients produce autoantibodies reactive with brain proteins, LEMS patients with muscle components and CAR patients with ocular antigens. Blood tests designed to detect these unusual autoantibody reactions are now in commercial use to identify different forms of paraneoplasia, sometimes before the neoplasm responsible has been identified. The cause of paraneoplasia-related autoimmune reactions has, in some cases, been traced to the patient's cancer, an immunologic connection based upon research findings and published reports of biopsies and cultures that actively express the key proteins involved in cancer-associated organ-specific hypersensitivity.
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PMID:Cancer-induced retinal hypersensitivity. 891 51

EGb 761 is a standardized extract of dried leaves of Ginkgo biloba containing 24% ginkgo-flavonol glycosides, 6% terpene lactones such as ginkgolides A, B, C, J and bilobalide. Its broad spectrum of pharmacological activities allows it to be in adequacy to the numerous pathological requirements--hemodynamic, hemorheological, metabolic--which occur in cerebral, retinal, cochleovestibular, cardiac or peripheral ischemia. Moreover, EGb 761 has direct effects against necrosis and apoptosis of neurons and improves neural plasticity as evidenced in vestibular compensation. At the molecular and the cellular levels, some evidence obtained with animal models indicates that EGb 761 can interact as a free radical-scavenger and a inhibitor of lipid peroxidation with all, or nearly all reactive oxygen species; maintains ATP content by a protection of mitochondrial respiration and preservation of oxidative phosphorylations; exerts arterial and venous vasoregulator effects involving the release of endothelial factors and the catecholaminergic system. Moreover, EGb 761 regulates ionic balance in damaged cells and exerts a specific and potent Platelet-activating factor antagonist activity. Numerous well-controlled clinical studies, realized in Europe and in USA, have revealed that EGb 761 is an effective therapy for a wide variety of disturbances of cerebral function, ranging from cerebral impairment of ischemic vascular origins (i.e. multi infarct dementia), early cognitive decline to mild-to-moderate cases of the more severe types of senile dementias (including Alzheimer's disease) or mixed origins (i.e. psychoorganic origin). Improvement of signs and symptoms have been demonstrated for cognitive functions, particularly for memory loss, attention, alertness, vigilance, arousal and mental fluidity. Some clinical studies have showed that EGb 761 treatment may improve the capacity of geriatric patients to cope with the stressful demands of daily life. The explanation is a dual stress-alleviating action of EGb 761: its facilitates behavioral adaptation to stress and may decrease the excess of cortisol release to stress. Moreover, EGb 761 shows a specific neuroprotective effects to hippocampic cells. Regarding the visual system, experimental studies have shown that EGb 761 can inhibit or reduce the functional retinal impairments resulting from ischemia-reperfusion, photo-degeneration, diabetic or proliferative retinopathy. Clinical studies have revealed that EGb 761 may be useful in treating visual activity impairments and damages to the visual field associated with chronic cerebrovascular insufficiency, senile macular degeneration and diabete mellitus. Regarding the vestibular and auditory systems, experimental and clinical studies have shown the efficacy of EGb 761 in treating hypoacusis, tinnitus, vertigo, dizziness and other symptoms of vestibulocochlear disorders. At least, adequatly controlled studies in patients with peripheral arterial occlusive disease have provided good evidence for therapeutic efficacy in intermittent claudication. The future of EGb 761 is undoubtedly in the promise in slowing the progression of Alzheimer's disease. Indeed, two recent american clinical studies have shown the efficacy and safety of EGb 761 in patients with mild to severe Alzheimer's disease and multi-infarct dementia. In clinical terms, progression of symptoms was delayed by approximately 6 months. Actually new clinical studies are undertaken in USA and Europe. At the dawn of the third millenium (the Sixth for Ginkgo biloba) we propose a state of art about it.
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PMID:[Ginkgo biloba extract (EGb 761). State of knowledge in the dawn of the year 2000]. 1048 50

An autopsy case of a patient with diffuse brainstem glioma associated with Laurence-Moon-(Bardet-)Biedl syndrome is described. The subject was a 25-year-old woman who had been suffering from mental retardation, pigmented retinopathy, obesity, hexadactyly, amenorrhea and renal cysts. She developed dizziness, headache and consequent consciousness disturbance. Magnetic resonance images disclosed marked swelling of the pons without contrast enhancement. By means of combined chemotherapy and radiation, she survived for 15 months. Histopathological diagnosis for postmortem specimens obtained from the brainstem was glioblastoma multiforme. No pathogenetic association between the syndrome and brainstem gliomas is known, and the literature contains no cases of patients with this coincidence.
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PMID:Diffuse brainstem glioma in a patient with Laurence-Moon-(Bardet-)Biedl syndrome. 1118 44

The Kearns-Sayre (K-S) syndrome which includes the triad of progressive external ophthalmoplegia, pigment retinopathy, and disorder of cardiac conduction was first described in 1958. The mitochondria disorder is believed to be the cause of this syndrome. Involvement of the cardiac conduction system is the most importent prognostic factor in K-S syndrome. A 34-year-old male K-S syndrome patient, manifesting as ptosis and weakness of limbs since the age of 15 years, suffered from dizziness and weakness. Twelve-lead eletrocardiography (ECG) showed a 2:1 atrioventricular (AV) block with slow ventricular rate. Intermittent complete AV block, complete left bundle branch block and torsades de pointes were noted in Holter ECG. The electrophysiology study demonstrated prolonged HV interval (85 ms) on conduction beat and infra-His block on non-conduction beat. A VVIR mode of permanent pacemaker was implanted and the patient's condition was stable during this period of follow-up.
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PMID:Atrioventricular block in Kearns-Sayre syndrome: a case report. 1155 73


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