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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On the basis of positive results obtained in the treatment of Sudeck's atrophy with calcitonin, the authors extended their investigation to other forms of localised osteoporosis. Six patients were examined affected by osteoporosis secondary to immobilisation, three patients with osteoporosis of the lower limbs from paralysis of the sciatic nerve and six patients with migrant osteoporosis. Treatment was as follows: pig calcitonin (Calcitar) in doses of 160 u MRC/daily + calcium gluconate in doses of 3 gr/daily. The duration of treatment averaged forty five days. In osteoporosis from immobilisation and nerve lesions the calcitonin treatment did not influence the condition and there was no change in radiographic appearances nor was there any analgesic action. On the other hand, the results were clearly positive in migrant osteoporosis: in all the patients treated there was complete regression of pain, cutaneous trophic changes, and functional loss. At a later stage, normal radiographic appearances were restored.
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PMID:Pig calcitonin in the treatment of localised osteoporosis. 6 20

Biochemical and bone morphometric measurements were evaluated in 12 patients who were on long-term anticonvulsant therapy with barbiturates. Half of the patients had no symptomatic bone disease, and half presented with bone disease and pain. Serum biochemical values were normal except for a few patients who had an elevated serum level of parathyroid hormone; the concentration of serum 25-hydroxy vitamin D was decreased in the majority of patients in whom it was measured. Bone absorptiometric values were normal but proved to be misleading: the Singh Index and videodensitometric measurements indicated that bone mass was below normal in all patients. Bone morphometric data indicated that bone resorption was 3 times greater than normal, and there was no evidence of osteomalacia. Vitamin D and possibly calcium have been suggested as potentially useful agents in the treatment of the bone disease associated with chronic anticonvulsant therapy.
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PMID:The frequency of bone abnormality in patients on anticonvulsant therapy. 7 73

In the differential diagnosis of intermittent claudication some rare myopathies have to be considered. The most frequent is phosphorylase deficiency (McArdle's disease). Exercise-induced muscular pain, weakness, contractures and occasionally myoglobinuria are the most prominent clinical signs. Serum creatine phosphokinase, aldolase and lactic dehydrogenase may be elevated after exertion. In the ischemic forearm test there is no rise of serum lactic acid. The enzyme deficiency can be demonstrated by histochemical and biochemical examination of a muscle specimen. Further, but more infrequent, enzymatic disturbances of glycolysis are phosphofructokinase deficiency and phosphohexoisomerase inhibitor, which also yield an abnormal ischemic forearm test and must be demonstrated histochemically and biochemically. Apart from muscular signs, myopathy with lactic acidosis is associated with palpitation, dyspnea and exhaustion, and a disproportionate rise in serum lactic acid level after exertion. Histochemically and electronmicroscopically demonstrable fat accumulation in the muscle can be a sign of a disturbance in lipid metabolism. This type of exercise-induced myopathy has been reported only in a few cases with carnitine-pylmityltransferase deficiency, which has to be demonstrated biochemically. Muscular contractures also exercise-induced but painless and reversible within seconds may be due to deficient uptake of sarcoplasmic calcium in the tubular system. Dyskalemic paralysis causes painless paresis within minutes of hours after exertion, which disappears within hours to a few days. Myopathy with tubular aggregates can be differentiated from other exercise-induced myopathies by morphology. Myotonia combined with painful contractures characterizes myopathia myotonica.
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PMID:[Exercise-induced muscular weakness, myalgia and contractures. I. A clinical review]. 13 80

In an adult with sporadic idiopathic osteomalacia an increased phosphate clearance, hypophosphataemia, normocalcaemia, normal serum-25-hydroxycalciferol and an only slightly increased immunoreactive parathormone were found. Intestinal 47Ca absorption was clearly decreased. Radiologically and histologically there was a clear-cut defect of skeletal mineralisation. Under treatment with daily doses of 1-1.25 mg of vitamin D3 the 25-hydroxycalciferol level increased markedly, the immunoreactive parathormone decreased slightly. Serum calcium and hypophosphataemia remained unchanged and intestinal 47Ca absorption was improved. Already 4 weeks after commencing treatment pain and defective gait of the patient disappeared. Radiologically skeletal changes were improved after 7 months. However, histologically no significant bone healing had occurred. The biochemical findings of this disease correspond to those of familial hypophosphataemic (vitamin-D-resistant) rickets. The therapeutic effects of pharmacological doses of vitamin D resemble those in pseudo-vitamin-D-deficient rickets. The pathogenesis of idiopathic osteomalacia of the adult remains unclear. Vitamin D metabolism is unchanged as far as the stage of 25-hydroxycholecalciferol. It is unknown if a disorder of the renal synthesis of 1,25-dihydroxycholecalciferol or a peripheral resistance to the effects of this metabolite exists. In addition a defect of the tubular phosphate reabsorption independent of parathormone and vitamin D is assumed.
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PMID:[Idiopathic hypophosphataemic osteomalacia (author's transl)]. 18 46

The action of the adenyl compounds adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and adenosine was studied on the human blister base preparation. All 4 adenyl compounds produced pain which was slow in onset and not maintained. The threshold concentration for pain was of the order of 1-3 micron. The slopes of log concentration:pain intensity plots were relatively shallow and for moderate to severe pain a 100-fold increase of the threshold concentration was required. The adenyl compounds resembled 5-hydroxytryptamine and bradykinin with respect to onset and duration of action but were less potent. On the other hand, for threshold effects they were more potent than acetylcholine or potassium. Evidence was found for an interaction of adenyl compounds with 5-hydroxytryptamine but not with potassium, acetylcholine or bradykinin. Cyclic adenosine 3',5'-monophosphate or the chelation of extracellular calcium or magnesium were shown not to be involved in the algogenic action of adenyl compounds and the action of adenyl compounds on the rabbit isolated jejunum too was found to be unrelated to their algogenic action on the human blister base preparation.
Pain 1977 Aug
PMID:Observations on the algogenic actions of adenosine compounds on the human blister base preparation. 19 25

The authors report the case of a 57 year old man who had taken for several years large quantities of alkaline drugs to relieve pain due to a gastric ulcer. This man presented acute digestive symptoms, and a confusional syndrome explained by various metabolic disturbance and especially hypercalcemia at 145 mg. Stopping the alkalis permitted within a few days the disappearance of the clinical symptoms and the correction of the laboratory disturbances. In the light of this case, the authors study the main clinical cases which have been described either in their acute form or in their chronic form (Burnett's syndrome). They discuss above all the physiopathology of these manifestations and it seems to them that the hypercalcemia is more important than the alkalosis. It remains to be explained why only a small number of subjects are exposed to these metabolic complications. There seems to be an individual hypersensitivity for under normal conditions, excess calcium is not sufficient to induce hypercalcemia.
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PMID:[Complication caused by abuse of alkalies in the treatment of ulcers]. 19 82

Review of the various drugs in current clinical use showed that over 50 of them may cause a purely sensory or mixed sensorimotor neuropathy. These include antimicrobials, such as isoniazid, ethambutol, ethionamide, nitrofurantoin, and metronidazole; antineoplastic agents, particularly vinca alkaloids; cardiovascular drugs, such as perhexiline and hydrallazine; hypnotics and psychotropics, notable methaqualone; antirheumatics, such as gold, indomethacin, and chloroquine; anticonvulsants, particularly phenytoin; and other drugs, including disulfiram, calcium carbimide, and dapsone. Patients receiving drug treatment who complain of paraesthesie, pain, muscle cramps, or other abnormal sensations and those without symptoms who are receiving drugs that are known or suspected to be neurotoxic should undergo neurological examination and studies of motor and sensory nerve conduction. This will allow the incidence of drug-induced peripheral neuropathy to be determined more precisely.
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PMID:Drug-induced peripheral neuropathies. 21 31

The effect of treatment of renal stone formation with 5 to 20 mg./kg. per day oral disodium ethane-1-hydroxy-1,1-diphosphonate for up to 30 months was examined in 12 patients with active renal (calcium) stone disease. The over-all incidence of stone passage decreased from 17.8 stones per year per patient before treatment to 7.7 stones per year per patient during therapy. Of the 12 patients 7 passed fewer stones or no stones during treatment. However, the incidence of stone passage was not changed substantially by disodium ethane-1-hydroxy-1,1-diphosphonate in 5 patients. Symptoms of muscle weakness and pain in the back, hips and shoulders occurred in 3 patients during treatment, 2 patients had an increase in serum alkaline phosphatase and 1 patient had a decrease in bone density. Although disodium ethane-1-hydroxy-1,1-diphosphonate may be clinically useful to manage calcium urolithasis in certain patients its over-all use is limited because of its ineffectiveness in some patients and owing to its potential to induce osteomalacia.
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PMID:Treatment of calcium urolithiasis with diphosphonate: efficacy and hazards. 22 Apr 33

Plasma ascorbic acid (PAA) in normal Labrador Retriever dogs less than one year of age averaged 1.22 +/- 0.05 mg/dl (x +/- sem) and was significantly higher than the value of 0.89 +/- 0.03, for Labrador Retrievers two years of age and older. No significant diurnal variation in PAA was observed. Oral or intravenous administration of 0.5 or 1.0 g of ascorbic acid (AA) elevated PAA for less than 8 hours. Injection of ACTH caused a significant decline in PAA for the initial 2 days, with variable results thereafter. Labrador Retriever puppies fed a ration high in protein, energy and calcium developed the typical skeletal diseases of overnutrition, including hypertrophic osteodystrophy (HOD). The addition or oral AA (0.5 g twice daily) had no ameliorating effect on the skeletal lesions. Instead AA supplementation resulted in relatively higher serum calcium values which, presumably by enhanced hypercalcitoninism, decreased bone resorption. Thus, AA treatment of dogs with HOD is contraindicated, as it can only aggravate the osseous lesions of HOD. The decreased PAA reported in dogs with HOD is interpreted to be the result of stress from pain.
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PMID:Ascorbic acid deficiency and hypertrophic osteodystrophy in the dog: a rebuttal. 23 Sep 38

The purpose of this investigation was to evaluate calcium hydroxide and potassium nitrate individually as densensitizing agents for hypersensitive root surfaces. The apparatus used in the experiment to measure hypersensitivity was (a) a thermo-electric stimulating device to measure hot and cold stimulation quantitatively and (b) a mechanical stimulating device to measure scratch stimulation quantitatively. The conclusions drawn from the study were: 1. Calcium hydroxide was more consistently effective in decreasing sensitivity then was potassium nitrate or the control. 2. Calcium hydroxide as compared to the control was statistically (99% level of significance) more effective in reducing sensitivity to mechanical, hot and cold stimulation immediately and at the conclusion of the experiment (3 months). 3. It appears that calcium hydroxide could be used as a desensitizing agent initially following periodontal surgery to reduce pain from hypersensitive roots in order that proper oral hygiene could be reestablished.
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PMID:Calcium hydroxide and potassium nitrate as desensitizing agents for hypersensitive root surfaces. 26 50


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