Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirteen outbreaks of food-borne botulism occurred between 1970 and 1984. Fifty patients were affected, with 30 of them requiring hospitalization. The number of patients per outbreak ranged from one to ten (mean, 3.8). All outbreaks were caused by home-prepared foods: nine by smoked ham, one by bacon, one by sausage, and one by mussels; contaminated food was not found in one outbreak. Bacteriologic study was performed in 11 outbreaks and type B toxin, the only found, was detected in eight of them. Generalized muscular weakness, visual disturbances, extreme dry mouth, and severe constipation were observed in all inpatients. Palpebral ptosis, dysphonia, urinary retention, postural hypotension, and respiratory impairment were also reported, but not in all inpatients. Identical, but less severe, manifestations were registered in the 20 ambulatory patients. Electromyographic study showed decreased motor action potential and posttetanic facilitation. Pulmonary function, studied in four inpatients, was decreased in three. All patients recovered fully. Management consisted of supportive measures, symptomatic treatment, and nursing care. Equine antitoxin was not administered and assisted ventilation was unnecessary.
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PMID:Food-borne botulism. A review of 13 outbreaks. 334 59

Vincristine is an antineoplastic drug with a broad spectrum of activity against haematological malignancies and childhood sarcomas. Besides useful activity, it lacks the usual emetic and myelotoxicity of anticancer drugs, but its use is limited by neurotoxicity. The neurotoxicity commonly manifests as reduced motility of the intestines resulting in constipation, and peripheral neuropathy which is predominantly sensory in nature. The early symptoms include numbness and tingling of hands and feet which is accompanied by loss of deep tendon reflexes. In its more severe form, muscle weakness develops which is more marked in distal muscles of the hands and feet. Other manifestations of neurotoxicity include ocular palsies, hoarseness of voice, and autonomic neuropathy in the form of postural hypotension and atony of the urinary bladder. The neurotoxicity is dose related and cumulative with repeated dosage such that the drug therapy has to be stopped after a cumulative dose of 30 to 50 mg. The neurotoxicity is usually reversible on interruption of the therapy, but the recovery is slow and takes several months. There are no specific antidotes which have established usefulness against neurotoxicity.
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PMID:Vincristine neurotoxicity. Pathophysiology and management. 354 May 19

Health effects of occupational exposure to lead were investigated among 92 exposed workers in lead-acid battery factory and 40 nonexposed workers serving as a control group from an oil mill in Khartoum North industrial area. The two groups were closely similar in age, stature, body weight, and socioeconomic conditions. A highly significant increase (P less than .01) was recorded in blood lead, urinary coproporphyrin, and basophilic stippled red blood cells of the exposed group in comparison to the control group. Central nervous system symptoms (insomnia, fatigue, weakness, and drowsiness) were reported by 50% and other symptoms such as abdominal colic and constipation were reported by 41% of the exposed group. Blue line on the gum was detected only on 2% of the exposed group. Strong associations between exposure to lead and the prevalence of central nervous system symptoms, abdominal colic, and constipation were recorded. Exposure to exceedingly high levels of lead in the working environment causes adverse health effects.
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PMID:Effects of exposure to lead among lead-acid battery factory workers in Sudan. 376 35

Forty-four cases of botulism occurred in infants in Southeastern Pennsylvania between 1976 and 1983. Forty-three were caused by Clostridium botulinum type B. Progressive weakness necessitated ventilatory support in 39 infants. Complications during hospitalization included otitis media in 13 patients and aspiration pneumonia in 11. Eight infants developed the syndrome of inappropriate secretion of antidiuretic hormone and two developed adult respiratory distress syndrome. One infant died of progressive bradycardia despite adequate control of ventilation. Manifestations of autonomic nervous system dysfunction recognized on admission to the hospital were constipation, distention of the urinary bladder, and decreased salivation and tearing. During hospitalization, some infants had unexpected fluctuations of skin color, blood pressure, and heart rate. Infants' strength improved despite persistent intestinal elaboration of toxin. C botulinum was isolated from seven of nine home or work environments sampled. All 44 infants were white and were receiving breast milk at the time of onset of symptoms. The majority had first feedings of nonhuman food substances within 4 weeks prior to onset of symptoms. Delineation of fecal flora in seven infants revealed predominance of enterobacteriaceae. Perturbations of intestinal flora during infancy, especially at weaning, may cause transient permissiveness to colonization by C botulinum.
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PMID:Clinical, laboratory, and environmental features of infant botulism in Southeastern Pennsylvania. 388 19

A phase II trial of prolonged IV infusions of vincristine was conducted in 21 patients with refractory acute leukemia. Patients received 0.25-0.50 mg/m2 by infusion daily for 5 days after an initial 0.5-mg bolus. A partial response was observed in one of two patients with acute lymphoblastic leukemia. Of 14 patients with acute nonlymphoblastic leukemia, a complete response lasting for 2.5 months occurred in one patient and a partial response lasting 1.3 months was observed in a second. No objective responses were noted in five patients with blast crisis of chronic granulocytic leukemia. Nonhematologic toxicity was minimal and, when present, generally consisted of a feeling of weakness; constipation, mucositis, and areflexia were also observed. Hematologic toxicity consisted mainly of mild to moderate reduction of platelets in most patients; marked thrombocytopenia (less than 50,000/mm3) occurred in two patients whose pretreatment platelet count was greater than 100,000/mm3. Although generally well tolerated, prolonged infusion of vincristine appears to have limited activity in the treatment of refractory acute nonlymphoblastic leukemia and blast crisis of chronic granulocytic leukemia; further evaluation is needed in acute lymphoblastic leukemia refractory to conventional bolus injection.
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PMID:Phase II trial of vincristine infusion in acute leukemia. 396 57

Two hundred and eighty-nine patients operated on for primary hyperparathyroidism (PHPT) in the years 1956-79 have been followed up for a mean period of 5 years. The aim of the study was to investigate the symptomatology of PHPT and the disappearance of the symptoms after operative treatment. Of the presenting symptoms hypercalcaemic crisis and cystic bone changes were cured, and none of the patients with pancreatitis as presenting symptom had a recurrence. In the renal stone group, 10% of the patients had recurring stones during the follow-up period. The presenting symptom disappeared in 84% of the patients. Thirty-five% of the patients had no presenting symptom and were classified as "asymptomatic", though, on questioning, most of them had various symptoms which disappeared postoperatively. Malaise, fatigue and muscular weakness disappeared in 79% of the patients, upper abdominal pains in 66%, constipation in 63%, pains in the extremities in 51% depression in 65%. Hypertension increased by 28% during the follow-up period; only three of the 90 patients with hypertension has discontinued antihypertensive treatment postoperatively. During the follow-up study, 6% of the patients were hypercalcaemic, though the serum calcium was only slightly elevated in almost all of these patients (mean +/- SD 2.75 +/- 0.09 mmol/l) and most of them had the multiglandular form of PHPT. The renal function did not deteriorate as much as was expected on the basis of earlier reports; only two patients had a serum creatinine over 500 mumol/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term effect of surgical treatment on the symptoms of primary hyperparathyroidism. 407 2

While sacrococcygeal teratoma presents typically at birth as a mass lesion, we had a case of late presentation with the classical triad of urinary retention, constipation and weakness of legs. Interesting enough, a tuft of hair together with a small lump was noted at birth and an associated small meningocoele was found at operation. We review the literature with regard to pathogenesis, clinical features, differential diagnosis, malignant change and treatment of the tumour.
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PMID:An unusual case of sacrococcygeal teratoma and a short review. 408 5

Early-lactation Holstein cows fed a corn silage-based diet low in chloride and supplemented with sodium bicarbonate were observed for clinical, metabolic, and production alterations over the course of 8 to 11 weeks. In 3 of the more severely affected cows, metabolic derangements included a rapidly developing primary hypochloremic, secondary hypokalemic and hyponatremic metabolic alkalosis, and hemoconcentration. Clinical signs included severe hypophagia, weight loss, muscle weakness, hypogalactia, dehydration, constipation, cardiopulmonary depression, and a depraved appetite. It was concluded that the rapid progression of these derangements, apart from any anatomic abnormalities or infectious causes, emphasizes the need for rapid assessment and therapeutic intervention in primary imbalance associated with body chloride depletion and metabolic alkalosis.
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PMID:Effects of dietary chloride restriction in lactating dairy cows. 608 55

Twenty-nine patients with non-small cell lung cancer refractory to prior therapy were treated with either vindesine (VDS) alone (3 mg/m2 every week) or the combination of VDS plus cisplatin (DDP) (100 mg/m2 every 28 days). Serial blood and urine samples were collected to assess the pharmacokinetics of VDS and DDP. All patients were evaluable for toxicity and 27 were evaluable for response. No objective antitumor responses were observed. Peripheral neuropathy manifested by paresthesias, muscle weakness, and constipation were observed in 20 treated patients, and hematologic toxicity consisting of thrombocytopenia and/or leukopenia occurred in 18 patients. The plasma and urinary pharmacokinetics of VDS and DDP measured in this study indicate that VDS and DDP do not interfere with each other and that the pharmacokinetics in previously treated and untreated patients are similar. The antitumor responses and degree of toxicity observed in this trial compare unfavorably with previously reported VDS and VDS-DDP trials in previously untreated patients with this disease and suggest that prior exposure to chemotherapy might both decrease antitumor activity and enhance toxicity of these chemotherapeutic agents.
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PMID:Therapeutic efficacy and pharmacokinetics of vindesine and vindesine-cisplatin in previously treated patients with non-small cell lung carcinoma. 629 98

Acute intermittent porphyria is caused by an inherent error of porphyrin metabolism characterized by a deficiency of porphobilinogen deaminase and increased activity of delta-aminolevulinic acid synthase, key enzymes necessary for the biosynthesis of heme. During an attack patients may have abdominal pain, vomiting, muscle weakness, constipation and neuropsychiatric symptoms. In the majority of individuals the disease remains clinically latent throughout life. Various drugs and chemicals, hormones and nutritional factors predispose to clinical attacks, probably by inducing hepatic delta-aminolevulinic acid synthase. Avoidance of these substances is important in preventing attacks. Screening of family members to detect genetic carriers permits precautionary measures. Management of attacks includes symptomatic therapy, high carbohydrate intake and intravenous administration of hematin.
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PMID:Acute intermittent porphyria: pathophysiology and treatment. 637 48


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