Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The restless legs syndrome is generally benign but is occasionally associated with anemia, metabolic disorder, or polyneuropathy. Leg restlessness with disruptive nocturnal myoclonus has been described as a sleep disorder. We report two patients with complex partial and secondarily generalized seizures, who developed restless legs while taking methsuximide and phenytoin. They had no evidence of metabolic disturbance or neuromuscular disease, although one patient had fragmented sleep and disruptive myoclonus on polysomnography, and leg restlessness subsided with change of antiepileptic drugs. These symptoms could reflect transient alteration in peripheral nerve function not evident by examination or electrophysiologic studies, sleep disturbance by antiepileptic drugs or the effects of temporal lobe seizure foci on perception of the physiologic state of nerves and muscles.
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PMID:Restless legs with antiepileptic drug therapy. 314 64

Haemolytic transfusion reactions can be defined as the occurrence after transfusion of measurably increased destruction of red cells, of donor or recipient, by alloantibodies. They may be acute (occurring within 24 hours of transfusion) or delayed (when signs of red cell destruction do not occur until 4 to 10 days after transfusion). The severest signs and symptoms of acute reactions follow intravascular red cell lysis and progress to anaemia, fever, haemoglobinuria and jaundice. The subjective responses of pain, restlessness, nausea, skin flushing, dyspnoea and shock are mediated by cleavage products of complement (C3a, C5a) activated by red cell antigen-antibody reaction. The bleeding and renal failure complications that follow are multi-factoral in aetiology but also stem from the activation of intravascular clotting and from the vasomotor disturbances following histamine and kinin release.
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PMID:Clinical presentation of haemolytic transfusion reactions. 739 74

Prolonged latency in the appearance of REM sleep as a marker of depression has been demonstrated in patients with the sickle-cell disease. To detect the possible existence of depressive disturbances in patients with sickle-cell disease, the Hamilton rating scale for depression (17 items) was used in 30 patients with homozygote sickle-cell disease and 31 carriers of the sickle-cell trait, treated or not with vasodilator drugs. None of the 61 subjects studied presented a score of 18 or more on the Hamilton rating scale, this being the threshold value for confirming the existence of moderate depression. However, analysis of variance showed an increase in mental dullness, agitation and somatization disorder. Dullness was related to the extent of anemia and the number of sickle-cell crises per year. Treatment had an effect on agitation in patients, with pentoxyfylline having a soothing effect unlike cinepazide maleate. Women complained of insomnia in the middle of the night and somatic anxiety and presented higher total scores than men. Men exhibited a higher degree of mental dullness. The findings of this preliminary study indicate that while not associated with frank depression, the sickle-cell gene has psychological repercussions on various depressive parameters and that these patients can benefit from treatment with pentoxyfylline.
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PMID:[Sickle cell disease and depression: preliminary study using the Hamilton rating scale for depression]. 819 26

We present a 81-year old male who developed dementia, gait disturbance and right hemiparesis. He was well until the age of 74 when he developed a hemorrhagic infarction in the right occipital region, which left him left homonymous hemianopsia. One year later he had one TIA attack consisting of dizziness, headache, and some clouding of consciousness. At that time, atrial fibrillation was found. At age 79, he was attacked by right hemiparesis. Cranial CT scans revealed a lesion consistent with a hemorrhagic infarct in the left middle cerebral artery territory. Two months prior to his final admission, he had a gradual onset of forgetfulness, labile affect, nocturnal agitation and hallucination which were followed by gait disturbance and urinary incontinence. On admission, he was alert but moderately demented. In addition he showed difficulty in repetition, limb kinetic and ideomotor apraxia of the left hand indicative of sympathetic apraxia, and constructional apraxia bilaterally. Granial nerves appeared intact except for left homonymous hemianopsia. His gait was wide-based and small stepped. No weakness or ataxia was noted. Deep reflexes were diminished on the left side. Plantar reflex was equivocally extensor of the left. Light touch and pain was slightly diminished on the right side. Cranial CT scans revealed a large low density area in the left fronto-temporo-parietal region. Also ventricular dilatation, diffuse low density change in the subcortical white matter, and diffuse cortical atrophy were seen. His clinical course was complicated by melena, anemia, pneumonia, cardiac failure and renal failure. He expired 2 months after his admission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 81-year-old man with dementia, gait disturbance, hemiparesis, and sympathetic apraxia]. 833 25

We prospectively investigated drug-induced headaches (HA) among 60 epileptic patients receiving felbamate (FBM). Twenty patients (33%) experienced HA. HA was pounding in 11 (55%), steady in 9 (45%), moderate or severe in 19 (95%), occurred at least once a week in all patients, and was relieved by nonnarcotic analgesics in 14 (70%). Mean duration on FBM before HA onset was 19 days. HA occurred with higher FBM doses and was relieved in 8 of 13 patients (62%) with FBM dose reduction. FBM was discontinued in most cases because of risks of anemia or hepatitis; not because of HA. Other side effects included insomnia (25%), gastrointestinal symptoms (27%), and agitation or restlessness (23%). HA is a common dose-related complication of FBM, occurs early after initiation of FBM treatment, and is relieved by dose reduction.
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PMID:Felbamate-induced headache. 861 82

Traditional centrally acting antihypertensives have been associated with a high incidence of adverse effects and are no longer recommended as first-line therapy. The newer imidazoline receptor agonists must overcome this reputation if they are to gain recognition as potential first-line agents for hypertension. Methyldopa, a centrally acting alpha(2)-agonist, is characterized by a number of serious adverse reactions that limit its use. Although unpredictable idiosyncratic or hypersensitivity reactions are uncommon, these include hepatitis, myocarditis, and hemolytic anaemia. Less serious problems such as abnormal liver function tests, positive Coombs test, drug-induced fever, and pancreatitis also occur. Central side effects include drowsiness, fatigue, lethargy, sedation, depression, psychotic reactions, nasal stuffiness, impotence, and exacerbation of Parkinsonism. In hypertensive men, methyldopa is less well tolerated than either captopril or propranolol, and up to 20% of patients discontinue therapy because of adverse effects. Clonidine acts primarily as an alpha(2)-agonist but also acts as an agonist at imidazoline receptors in the rostroventrolateral medulla. It is equipotent to most other antihypertensives but is considerably less well-tolerated in comparative trials. The principal adverse effects of clonidine are drowsiness, sedation, lethargy and dry mouth. Reserpine acts primarily by depleting central catecholamine neurotransmitter stores. It was very extensively used in early hypertension trials, but its central side effects of sedation, nasal stuffiness, and severe depression are now considered so undesirable that the drug is seldom prescribed. The imidazoline (I1) agonists moxonidine and rilmenidine act selectively and have very little central alpha(2)-agonist activity. In comparative studies against placebo and other reference antihypertensives, the only adverse effect consistently associated with these drugs was dry mouth (approximate placebo-corrected incidence 10%). Sedation was not pronounced. Withdrawal syndromes are complex pathophysiologic processes and occur with a variety of antihypertensive drugs. Cessation of therapy with clonidine and, to a lesser extent, methyldopa may result in a severe withdrawal syndrome characterized by restlessness, sweating, anxiety, tremor, palpitations, and headache. There may be a rapid rise in blood pressure, often with a true "rebound" to higher than pretreatment levels. Plasma and urinary catecholamine levels are increased, and fatalities have been reported. It is important to stress that such a syndrome has not been recorded, in animal or human studies, with either moxonidine or rilmenidine.
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PMID:Aspects of tolerability of centrally acting antihypertensive drugs. 887 99

Adequate prehospital care of the severely traumatised patient is important to prevent or attenuate early as well as late life threatening complications, such as tissue hypoxia, ischemia/reperfusion injury and finally multiple organ failure. A mismatch of oxygen supply and oxygen demand is a hallmark in the pathophysiology of multiple trauma. Oxygen supply may be diminished by the following factors: shock-related decrease of cardiac output, anemia and hypoxia. On the other hand, oxygen demand may be increased by pain, panic, and agitation. Hence, it is a central point in prehospital care to reduce this supply-demand imbalance by identification and prompt reversal of the underlying causes. Most often, shock is caused by hypovolaemia and tissue injury ("traumatic-hemorrhagic shock"). However, shock may also be a result of central nervous system injury (neurogenic shock as a special form of distributive shock) or circulatory obstruction, e.g tension pneumothorax or cardiac tamponade (obstructive shock). Volume resuscitation by means of crystalloid or colloid solutions is an essential part in the therapy of the traumatic-haemorrhagic shock. In addition, catecholamines may be necessary in order to achieve an adequate arterial pressure. However, if bleeding cannot be controlled in the prehospital setting, only moderate volume support and permissive hypotension as well as rapid transportation into the next hospital may be preferable. This may be the case in penetrating thoracic or abdominal injuries as well as in traumatic amputations of the proximal limb. On the contrary, in patients with severe head injury, hypotension must be avoided by all means. Obstructive shock has to be treated urgently by insertion of a chest drain or drainage of the pericardium, respectively. Under all circumstances, it is an essential part of prehospital therapy to provide sufficient analgesia as soon as possible. Prehospital anesthesia, combined with artificial ventilation may be necessary for optimal patient management. Furthermore, ventilatory support is indicated when respiratory failure, loss of consciousness, or severe shock are present. Additional oxygen should be given whenever possible, even in the absence of an overt hypoxic state. Important additional measures are cervical spine immobilisation and reposition as well as splinting of long bone fractures or luxations, in order to avoid secondary injury of the spinal cord or ongoing tissue and vascular damage.
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PMID:[Emergency management of polytrauma patients]. 902 49

We report a 45-year-old man with monocytosis and right hemiparesis. The patient suffered from an acute myocardial infarction from which he recovered completely when he was 42 years old. One year prior to his death, he was found to have increase in monocyte count (35.5% of leukocytes) in peripheral blood and splenomegaly; he was admitted to the hematology service of our hospital. He was diagnosed as having chronic myelomonocytic leukemia after bone marrow examination. He was treated with radiation therapy with improvement in splenomegaly. In May of 1995, he had fever, anemia, and thrombocytopenia for which he needed daily blood transfusion. In November of 1995, he had an onset of weakness in his right hand, and neurologic consultation was asked for in November 27, 1995. Neurologic examination revealed a chronically ill japanese man in no acute distress. He was alert and not demented. Higher cerebral functions were intact. Cranial nerve examination revealed right facial paresis of the central type. Motor-wise, he was right hemiparetic. Generalized muscle wasting was noted apparently due to the chronic debilitating disease. Deep tendon reflexes were within normal range in the right upper extremity, but were diminished in other areas. Sensation was intact, and no meningeal signs were noted. Pertinent laboratory findings were as follows: Hb 8 g/dl, RBC 238 x 10(4)/microliter, WBC 2,900/microliter (band 1.0%, seg 18.5%, lym 28.0%, mono 44.0%, Baso 2.5%), Plt 13 x 10(4)/microliter, PT 16.6"/10.9", APTT 44.7"/35.0". CSF contained 87 mg/dl of protein, 155 mg/dl of glucose and 2 mononuclear cells/microliter. Bone marrow was slightly hypercellular with mild increase in blast forms. No chromosome abnormality was found. CT and MRI revealed a large mass in the left fronto-parietal region and the meninges showed marked thickening with enhancement after gadolinium-DTPA in MRI. The patient was treated with glycerol and steroid, but the subsequent course was complicated by a seizure, agitation, and pneumonia. He died from respiratory failure on January 13, 1996. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had chronic myelomonocytic leukemia with infiltration of leukemic cells into meninges and the parenchyme of the cerebrum. Thickening of the dura was thought to be in part a reaction to the subdural hematoma as well as to leukemic cells along the meninges. Postmortem examination revealed hypercellular bone marrow with increase in monocytic cells (more than 20%). The lungs showed pneumonia with scattered old tuberculous lesions. The heart showed an old myocardial infarction in the posterior wall of the left ventricle. The brain showed an old chronic subdural hematoma in the left fronto-temporal region and a cystic mass lesion in the left frontoparietal region. The mass was hypercellular and most of them were monocytes. The dura mater showed reactive thickening without leukemic cell infiltration. It was concluded that this patient had chronic myelomonocytic leukemia with a formation of leukemic mass in the brain. Pathologists thought that the mass was a hematogenous spread. It is rare for chronic myelomonocytic leukemia to form a mass lesion in the brain.
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PMID:[A 45-year-old man with peripheral monocytosis and right hemiparesis]. 962 75

Usual causes of intolerance to thyroxine sodium include coronary artery disease, advanced age, untreated adrenal insufficiency, and severe hypothyroidism. We describe 4 patients with iron deficiency anemia and primary hypothyroidism. After treatment with thyroxine sodium, these patients developed palpitations and feelings of restlessness, which necessitated discontinuation of the thyroid hormone. After the anemia was treated with ferrous sulfate for 4 to 7 weeks, they were able to tolerate thyroxine sodium therapy. Iron deficiency anemia coexisting with primary hypothyroidism results in a hyperadrenergic state. In such patients, we postulate that thyroid hormone administration causes palpitations, nervousness, and feelings of restlessness. Correction of any existing pronounced anemia in hypothyroid patients who are intolerant to thyroxine sodium therapy may result in tolerance to this agent.
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PMID:Anemia: a cause of intolerance to thyroxine sodium. 1068 60

The acute toxicity of dried Nerium oleander leaves to Najdi sheep is described in 12 sheep assigned as untreated controls, N. oleander-treated once at 1 and 0.25 g/kg body weight and N. oleander-treated daily at 0.06 g/kg body weight by drench. Single oral doses of 1 or 0.25 g of dried N. oleander leaves/kg body weight caused restlessness, chewing movements of the jaws, dyspnea, ruminal bloat, incoordination of movements, limb paresis, recumbency and death 4-24 hr after dosing. Lesions were widespread congestion or hemorrhage, pulmonary cyanosis and emphysema, hepatorenal fatty change and catarrhal abomasitis and enteritis. The daily oral doses of 0.06 g dried N. oleander leaves/kg body weight caused less severe signs and death occurred between days 3 and 14. In these animals, the main lesions were hepatonephropathy and gelatinization of the renal pelvis and mesentry and were accompanied by significant increases in serum AST and LDH activities, in bilirubin, cholesterol and urea concentrations and significant decreases in total protein and albumin levels, anemia and leucopenia.
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PMID:Acute toxicity of various oral doses of dried Nerium oleander leaves in sheep. 1178 96


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