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)

For ten years, severe physical exercise in a 24 year old male patient had been an almost constant trigger of frequent attacks of pareses which were mostly accompanied by complete tetraplegia and once by the occurrence of cardiac arrest with atrial fibrillation. During the attack, the serum potassium concentration fell to 1.2 mmol/l, whereas the intraleukocytic potassium concentration rose from 136 mmol/l to 149 mmol/l. The catecholamine excretion in the urine was raised during the first 24 hours after admission as an emergency (189 micrograms noradrenalin and 54 micrograms adrenalin). After intravenous adrenalin infusion (0.01-0.1 microgram/kg X min) during the symptom-free interval, there was a major fall of the serum potassium concentration from 3.9 mmol/l to 3.1 mmol/l. This was not accompanied by a raised insulin excretion and could be prevented by prior administration of the nonselective beta blocker propranolol. On the basis of these results, the patient was treated prophylactically with three times 40 mg/d p.o. propranolol. Pareses requiring treatment no longer occurred under this therapy.
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PMID:[Severe periodic hypokalemic paralysis. Prevention using beta-receptor blockade]. 288 27

The case of a 42-year-old man is reported, who on four occasions developed a hypokalaemic periodic paralysis after an intramuscular injection of "Ambene". The detailed examination of this patient shows, that it is the primary, autosomal dominant inherited form of hypokalaemic periodic paralysis, and not the secondary form, which is caused by a renal or gastrointestinal loss of potassium. Clinical and electrophysiological, as well as histopathological and electron microscopic findings are presented, showing the typical vacuolar myopathy with submicroscopic tubular structures. In the literature there is evidence for an increased sensitivity of the muscle membrane to insulin with an increased potassium-shift inside the cell in hypokalaemic periodic paralysis. "Ambene" is a combination, which contains amongst other substances dexamethasone and the local anaesthetic drug lidocain. In the present case the paresis was possibly caused by a combined effect of dexamethasone with a consequent hyperglycaemia and lidocain with a change in the excitability of the muscle membrane. The pathophysiological mechanism of hypokalaemic periodic paralysis is discussed in terms of the release by the combination of these two drugs. It has not previously been reported that "Ambene" can provoke a hypokalaemic periodic paralysis. This is a severe side effect because of the resulting cardiac and respiratory problems.
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PMID:[Hypokalemic periodic paralysis provoked by "Ambene"]. 293 67

In 40 patients with insulin-dependent diabetes mellitus, the number of gastrin cells in the mucous membrane of the antrum of the stomach was measured by immunohistochemistry according to the method of L. Sternberger. The number of the cells depended on the gravity of antral gastritis, namely their number decreased as the lesion was aggravated. The basal level of serum gastrin was determined by radioimmunoassay in 144 patients with insulin-dependent diabetes mellitus. The high basal level of gastrin was recorded in patients with achlorhydria. However, no correlation was established between the gravity of antral gastritis and the basal level of serum gastrin. If the basal gastrin level is too high, the possibility of asymptomatic paresis of the stomach should be taken into account together with the other factors.
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PMID:[Gastrin cells and the basal level of serum gastrin in patients with insulin-dependent diabetes mellitus]. 351 19

Twenty patients with adult-onset diabetes mellitus and malignant external otitis (MEO) were treated at the Mount Sinai Medical Center, New York, over a seven-year period (August 1976 to October 1983). A retrospective analysis compared patients who received an antipseudomonal cephalosporin as monotherapy (group A) with those who received conventional antipseudomonal therapy (group B). Pseudomonas aeruginosa was isolated in all patients. Differences (group B less than group A) included insulin dependence, underlying vascular disease, total number of cranial nerve palsies or paresis, and surgical procedures. The overall clinical outcome was similar in both groups; 64% of patients in group A (7/11) and 70% in group B (7/10) were cured at a follow-up period of five to 57 months. A more favorable outcome was found in patients with less extensive infection in both groups. Monotherapy compared favorably with conventional antipseudomonal therapy for the treatment of patients with MEO and moderate infection.
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PMID:Malignant external otitis. Comparison of monotherapy vs combination therapy. 360 49

Insulin-induced hypoglycemia provokes polyribosome disaggregation and accumulation of monomeric ribosomes in the brain of rats with hypoglycemic paresis and coma. The extent of brain polyribosome disaggregation depends on the decrease of blood glucose concentration, and in comatose animals on the duration of hypoglycemia. Cycloheximide prevents the disaggregation of brain polyribosomes induced by hypoglycemia, indicating that hypoglycemia affects brain protein synthesis, decreasing the rate of initiation relative to the rate of elongation of polypeptide chain synthesis.
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PMID:Effects of hypoglycemia on rat brain polyribosome sedimentation pattern. 389 18

The effect of sustained insulin-induced hypoglycemia on peripheral nerve function and structure was examined in rats. After a period of hypoglycemia (less than 2.5 mmol/L) of at least 72 h, axonal degeneration and reduction of the maximal amplitude of the evoked muscle action potential occurred, the two abnormalities being correlated negatively (r = -0.99, 2P = 0.00097). One of five rats developed paresis of both hindlegs as well as nerve damage and perikaryal alterations of lower motor neurons.
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PMID:Peripheral neuropathy in rats induced by insulin treatment. 629 68

A case of hypokalemic periodic paralysis, is reported, characterized by a positive family history and by repeated attacks of transient motor weakness since the age of 14 involving one all limbs. An induction test under ECG and EMG monitoring, carried out by infusing glucose and insulin when the patient was symptom-free, provoked motor paresis comparable to the spontaneous attacks and confirmed the diagnosis.
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PMID:Familial hypokalemic paralysis: a case study. 657 50

Goldberger discovered human pellagra was a non-infectious disease, affecting mostly the small and the timid in overcrowded institutions. Symptoms were diarrhoea, dermatitis and dementia. The staff and older children escaped the disease. They ate the meat and left the small and timid with the gravy. The 'Goldberger syndrome' is observed during competitive feeding of livestock, in ketotic animals and in the zinc depleted which are lethargic and pick all day at their feed. The pellagra preventative factor was later found to be nicotinic acid, derived from the amino acid tryptophan. Deficiencies of copper, magnesium, vitamin B6 (activated by a zinc kinase) inhibit the conversion of tryptophan to nicotinic acid. Stresses, including liver diseases, malabsorption, iron overload, porphyria, marasmus, cold stress, pregnancy, lactation, antibiotics and sulfa drugs, all increase dietary needs of nicotinic acid. Elevated free fatty acids and ketone bodies in the blood are associated with ketosis, zinc depletion and the pre-diabetic state. There is a diminished uptake of glucose by the tissues, a condition also found in parturient paresis of dairy cows when elevated hydrocortisone promotes insulin resistance and hyperglycaemia. This defect in insulin response leads to a diabetic-like state. The major predisposing factor in parturient paresis of dairy cows is hypocalcaemia. Gut absorption of dietary calcium may not meet the primary demands of lactation initiation until bone calcium mobilisation is established.
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PMID:Metabolic disorders of cattle. 839

We analysed retrospectively our clinical experience with 36 cases of mucormycosis. They were seen during the last 15 years. The diagnosis suspected on clinical grounds, was confirmed in 31 cases by finding the hyphae in hematoxylin-eosin stained material obtained from aspirated or tissue biopsy or by isolation of the fungus in culture. Rhinocerebral mucormycosis was diagnosed in 22 patients. Diabetes was the underlying disorder in 20 cases, kidney failure in one and myelodysplastic syndrome in one. Nine had stable and 11 unstable diabetes (ketoacidosis in 10 and hyperosmolar coma in 1). The earliest sign was facial edema, followed by proptosis, chemosis and extraocular muscle paresis. They were treated by extensive surgical debridement, insulin and antifungal drugs with 69% of survival rate. The disseminated mucormycosis was diagnosed at the autopsy in 5 cases, acute leukemia was the underlying disease in 2 of them. Pulmonary mucormycosis was diagnosed in 2 cases, cutaneous form in 2, sinuorbital form in 4 and brain abscess in one patient. Eight of these 9 cases survived after therapy. We emphasize the importance of an early diagnosis. This can only be made in the presence of a typical clinical setting confirmed by finding the hyphae in tissue or culture. Antifungal drugs along with treatment of the underlying disorder and aggressive surgical debridement must follow.
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PMID:Rhinocerebral and systemic mucormycosis. Clinical experience with 36 cases. 898 Dec 94

Spinal cord-injured (SCI) subjects exhibit a normal lipolytic rate despite the failure of centrally mediated sympathoexcitatory stimuli to activate lipolysis. Peripheral afferent stimulation below the lesion level induces an exaggerated autonomic reaction in SCI with lesion levels above T5, ie, so-called autonomic dysreflexia. The metabolic effects of induced dysreflexia were investigated in five SCI subjects (age, 35 +/- 8 years; duration of paresis, 15 +/- 7.5 years [mean +/- SD]; lesion level, T3 to T4, n = 2, C7, n = 3) following bladder stimulation. Subcutaneous glycerol concentrations were measured by microdialysis above and below the lesion level. Diurnal plasma noradrenaline (NA) and adrenaline levels were continuously monitored in seven SCI subjects (lesion level T3 to T4, n = 2; C4 to C7, n = 5). Bladder stimulation resulted in an increased mean arterial pressure ([MAP] 81 +/- 8 to 114 +/- 11 mm Hg, P < .05), a decreased heart rate (70 +/- 3 to 54 +/- 4 beats/min, P < .05), and an increased plasma NA (0.70 +/- 0.49 v 3.27 +/- 1.56 nmol/L, P < .05). Interstitial glycerol was increased in the decentralized region (89 +/- 12 to 135 +/- 21 mumol/L, P < .05), whereas no reaction was found in the centrally innervated region. Plasma concentrations of glycerol and insulin increased. Diurnal monitoring showed periods of increased plasma NA sufficient to induce lipolysis (> 1.4 nmol/L) during 20% of the registration period. The data suggest that peripheral afferent stimulation below the lesion level increases NA release and activates lipolysis and that frequent episodes of activation are found in SCI subjects with tetraplegia or high paraplegia.
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PMID:Peripheral afferent stimulation of decentralized sympathetic neurons activates lipolysis in spinal cord-injured subjects. 943 44


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