Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the prognosis of acute porphyria among 206 adult Finnish patients with acute intermittent porphyria (AIP) or variegate porphyria (VP). The series represents all known patients with these porphyrias in Finland. Of the 47 patients who had a total of 117 acute attacks during the period 1967-1989, 6 died during an attack and 21 attacks were associated with paresis; the frequency of severe attacks was significantly smaller than before 1967 (p = 0.00002). Most pareses and deaths occurred because of a delay in diagnosis and inappropriate treatment of porphyria. For those patients who were symptom-free at the time of diagnosis (1365 follow-up years), the risk of the first subsequent attack was significantly smaller than for those who had had an acute attack before the diagnosis of porphyria (1047 follow-up years, p = 0.005). In addition, milder symptoms of porphyria were more common among those who had had previous attacks than among those who had not (p less than 0.00001). In AIP the risk of attacks correlated with the excretion of porphobilinogen in the urine during remission among adults (p = 0.03); a low rate of excretion predicted freedom from acute attacks. A regular use of many precipitating drugs was never associated with symptoms of porphyria. Two percent of the surgical operations and 4% of the pregnancies were associated with acute attacks. Nearly one-third of the women had symptoms of porphyria associated with the menstrual cycle, but these seldom proceeded to an acute attack. Forty-six percent of the women had used sex-hormone preparations regularly; 2 of them (4.5%) experienced associated acute attacks. Patients with AIP or VP showed increased incidences of hepatocellular carcinoma, and probably also chronic renal failure and hypertension.
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PMID:Prognosis of acute porphyria: occurrence of acute attacks, precipitating factors, and associated diseases. 154 56

We report on 7 patients (2 women, 5 men) with chronic renal failure, who developed under a high dosage of the new diuretic muzolimine (range 240 to 1440 mg per day) fatal neuromyeloencephalopathy. Clinical neurophysiological and neuroradiological findings and finally neuropathological studies in 2 patients resembled those found in vitamin-B12-deficiency-syndrome with a predominant affection of the spinal posterior column and the corticospinal tracts. The first neurological symptoms like paraesthesia, severe hyperpathia of the legs and mild to heavy spinal ataxia occurred after an average time of treatment of 78 days and a mean dosage of 52 g. The most progressive neurological deficits like severe tetraspastic paresis, were seen only in the nondialytic renal insufficient group (3 patients), while the others had a more benign course of the disease. This lead to the hypothesis of a partially dialysable toxic metabolite of muzolimine. After a follow-up of more than 2 1/2 years no significant recovery was seen in these cases.
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PMID:Muzolimine-induced severe neuromyeloencephalopathy: report of seven cases. 184 34

We report on 7 patients suffering from chronic renal failure (2 females, 5 males; aged 35-75 (phi 53.5) years) who showed severe neuromyeloencephalopathy (NME) after high doses of a new Henle's loop diuretic, Muzolimine. The temporal and phenomenological development of these systems was strikingly parallel. The neurological deficit was revealed on neurophysiological, neuroradiological and in 2 cases on neuropathological tests (gross demyelinisation of the posterior column, mainly of the fasciculus gracilis, less in the lateral corticospinal tract and in some spinal roots). The critical drug dose for first neurological impairment was 52 g on average; at this point the patients had been treated for 78 days. The maximal daily dose was 1.440 mg. Dominant clinical features were pallhypaesthesia, ataxia, signs of peripheral neuropathy in combination with hyperreflexia and progressive para- to tetraspastic paresis. Constellation of symptoms, course of disease and findings of additional investigations, especially those of neuropathology, very much resemble Vitamin B12 deficiency and SMON-(Subacute Myelo Optic Neuropathy) syndrome. The rare entity of Muzolimine-NME is discussed in respect to other endogenous and exotoxic neuromyelopathies. We present the hypothesis of a toxic, partially dialysable metabolite of Muzolimine.
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PMID:[Neuromyeloencephalopathy caused by high-dose muzolimine medication in patients with renal failure]. 215 46

Chronic renal failure can produce malfunction of multiple organs, including auditory and vestibular apparatus. Twelve patients of chronic renal failure of varying etiologies treated conservatively were subjected to vestibular function tests. Only 33% of the patients had normal ENG data. Fifty-eight per cent of the patients had canal paresis and 8% showed hyperactive response. Ototoxic drugs like furosemide may be most important factor in aetiology of vestibular dysfunction in chronic renal failure.
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PMID:Vestibular functions in conservatively treated chronic renal failure. 280 93

We report a 70-year-old man who had a sudden onset of right hemiparesis and mutism. The lower extremity was more involved than the upper one. He had a long history of diabetes and chronic renal failure for which hemodialysis was necessary. On August 30, 1990, he had an sudden onset of right hemiparesis and mutism. Neurological examination revealed awake but mute in no acute distress. He could only respond to very simple commands such as opening his mouth or protruding his tongue. He did not appear to understand more difficult questions. In addition, he could not answer verbally. He was totally mute. Cranial nerves appeared intact except for slight right central facial paresis and severe diabetic retinopathy. He had complete paralysis of his right leg and a moderate weakness in his right upper extremity. Deep reflexes were diminished in both upper extremities and absent in the lower limbs. Frotal signs such as grasp and snout reflexes were present. Cranial CT scans revealed an ill-defined low density area in the left parasagittal subcortical area and a part of the anterior cerebral artery territory. The supplementary motor area appeared at least in part to be involved. He was treated with glycerol and other supportive cares, however, his clinical course was complicated by pneumonia, heart failure, septicemia, and he expired two months after his stroke. The patient was discussed in a neurological CPC, and the chief discussant arrived at a conclusion that he had an artery-to-artery embolism at the internal carotid bifurcation resulting in the cerebral infarction mainly in the territory of the anterior cerebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 70-year-old man with right hemiparesis and mutism]. 836 54

In this randomized, double-blind study, we compared the anesthetic characteristics and pulmonary function changes of 0.33% bupivacaine and 0.33% ropivacaine used for interscalene brachial plexus (IBP) anesthesia in patients with chronic renal failure. Forty-two patients undergoing IBP anesthesia for creation of arteriovenous fistulas were randomly allocated to receive either 30 mL of 0.33% bupivacaine (Group B) or 0.33% ropivacaine (Group R). Block onset time, diaphragmatic excursion (ultrasonographic evaluation), and free plasma concentrations of bupivacaine and ropivacaine were evaluated. Negative motion or immobility of the ipsilateral hemidiaphragm and a decrease of >10 mm in positive motion were defined as diaphragmatic paresis. The pulmonary function variables were measured by bedside spirometry equipment. Seven patients needed supplemental local anesthetic, one with total spinal block; these patients were excluded from the study. The success rate was 80.9%. Block quality was similar in the two groups. Ipsilateral hemidiaphragmatic excursion was decreased in both groups compared with baseline values (P < 0.05). Diaphragmatic paresis was identified in 10 of 16 patients and 8 of 18 patients in Groups B and R, respectively (P > 0.05). Pulmonary function significantly decreased from baseline in both groups (forced vital capacity (FVC) 30%, forced expiratory volume at 1 second (FEV(1)) 32%, and peak expiratory flow (PEF) 31% in Group B and FVC 17%, FEV(1) 17%, and PEF 5% in Group R) (P < 0.001). The decreases in Group B were larger than those in Group R (P < 0.05). Three patients in Group B and one in Group R had mild respiratory problems (P > 0.05). Concentrations of bupivacaine and ropivacaine were below toxic levels rather than "normal range." We conclude that pulmonary function decreased more after IBP with 0.33% bupivacaine than with 0.33% ropivacaine.
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PMID:Interscalene brachial plexus block with bupivacaine and ropivacaine in patients with chronic renal failure: diaphragmatic excursion and pulmonary function changes. 1642 91

The percutaneous ethanol injection (PEI) with ultrasound guidance has been suggested for the treatment of patients with hyperparathyroidism who are on dialysis, with the aim of selectively treating the parathyroid glands with nodular hyperplasia. We present our experience in 25 patients with chronic renal failure followed during 13.4 +/- 10.6 months. A decrease in the levels of parathormone (PTH) (1,236.32 +/- 129.8 vs. 721.66 +/- 142.24 pg/ml), phosphatemia (6.16 +/- 0.35 vs. 4.93 +/- 0.36 mg/dl) and calcium-phosphorous product (60.82 +/- 3.81 vs. 46.47 +/- 3.46 mg2/dl2) was verified. In 56% of patients, PTH levels decreased (>50% of the baseline value) and 36% had final values <300 pg/ml. Patients in whom ultrasound showed a single gland responded better than those with more than one gland (83.3 vs. 30.8% of responders in each group). The procedures performed had a 4.9% complication rate: hematoma, symptomatic hypocalcemia, temporary paresis of the vocal cords. In summary, treatment with PEI is useful for the management of patients with hyperparathyroidism who are on dialysis, and the results achieved are better in patients who have a single gland identified by ultrasonography.
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PMID:Treatment of uremic hyperparathyroidism with percutaneous ethanol injection. 1594 51

The term chronic renal failure (CRF) usually means the final stage of chronic kidney disease (CKD) with a decline in glomerular filtration rate (GF) below 0.25 mL/s. CRF is a world-wide serious health and economic issue with an increasing incidence and prevalence. CRF patients are, in comparison to other patients, hospitalized more often and for longer and, despite improvements in care, their quality of life is usually low and morbidity and mortality high. We present an overview of the most important CKD risk factors and the diseases most likely to result in CRF. Diabetic nephropathy, followed by various forms ofischemic renal disease and primary and secondary glomerulopathy, chronic tubulointerstitial nephritis and autosomal dominant polycystic kidney disease are the leading causes of CRF. We provide a brief overview of other disease states that may result in renal failure. Clinical manifestations of CRF are discussed, mainly cardiovascular, gastrointestinal, haematological and neurological symptoms. Breathlessness is a consequence of hypervolaemia, metabolic acidosis and anaemia. The disease often presents with symptoms, such as headache and visual disturbances, resulting from arterial hypertension. Gastrointestinal symptoms and fatigue, usually caused by anaemia, are frequent. Platelet dysfunction is manifested as an increased bleeding time. Paradoxically, apart form tendency to abnormal bleeding, CRF also tends to be associated with thromboembolic complications. Patients may experience itching, bone, joint and muscle aches, are more prone to infections. They may suffer from insomnia, concentration disorders and apathy. The signs of peripheral mixed sensory-motor neuropathy include paraesthesia, paresis and restless leg syndrome. However, renal failure may also be oligosymptomatic or asymptomatic. Cardiovascular complications are the most frequent cause of morbidity and mortality of CRF patients.
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PMID:[Aetiology and a clinical picture of chronic renal failure]. 2187 93