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)

The records of 72 pediatric and adolescent patients with multiple hypothalamic and/or pituitary hormone deficiencies of nontumoral origin who were followed up for years and receiving somatotropin, thyroxine, and sex hormones at the appropriate age have been reviewed. According to their corticotropin-releasing factor-corticotropin-cortisol (CAC) axis function as evaluated by basal plasma cortisol levels and the response of cortisol to insulin hypoglycemia and to corticotropin-releasing factor, the patients were divided into three groups: group 1 (n = 25), patients with multiple hypothalamic and/or pituitary hormone deficiencies with normal CAC axis; group 2 (n = 38), patients with partial CAC deficiency without cortisol replacement therapy (hydrocortisone); and group 3 (n = 9), patients with CAC deficiency receiving hydrocortisone therapy (5 to 10 mg/d). Repeated CAC axis evaluation in patients of group 2 over years revealed a progressive decrease in the basal and stimulated cortisol levels with age and pubertal advancement. Despite the low cortisol levels and the low cortisol response to insulin hypoglycemia, these patients did not have clinical symptoms until the end of puberty when nine of 24 patients complained of abdominal pain, weakness, or anorexia. Linear growth, which was followed up in all patients at regular intervals, showed a lower growth velocity and irregular growth in response to somatotropin treatment in the patients receiving low doses of hydrocortisone (group 3 patients when compared with group 2 patients not receiving hydrocortisone).
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PMID:When should hydrocortisone therapy be instituted in children with hypopituitarism? 283 78

A 45-year-old man with type I diabetes mellitus of 25-yr duration and well controlled by conventional insulin therapy developed an isolated adrenocorticotropic hormone (ACTH) deficiency. He presented with a 3-month history of weight loss, weakness, anorexia and persistent tendency to hypoglycemia that he had never experienced before. Basal and dynamic endocrine testing disclosed absent cortisol secretion caused by an isolated ACTH deficiency due to a primary pituitary defect. Corticosteroid replacement therapy allowed again a good glycometabolic control. The possible causes of hypoglycemia in insulin-treated diabetes and the pathogenetic basis of the reported association are discussed.
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PMID:Development of isolated ACTH deficiency in a man with type I diabetes mellitus. 284 79

A nine-year-old mixed breed dog was presented with a history of mild generalized seizures, weakness, and muscle fasciculations, following periods of excitement and exercise. Investigative procedures included haematology, chemical pathology, faecal analysis, urinalysis, cerebrospinal fluid analysis, hormone assays, computerized axial tomography and scintigraphic imaging. Results of these investigations revealed hypoglycaemia (blood glucose 1.9 mmol l-1, hyperinsulinism (111 muu ml-1) and an amended insulin-glucose ratio of 2643. The glucagon tolerance test was typical for an insulin producing pancreatic islet cell tumour and pancreas scintigraphic imaging revealed focal lesions in the pancreas and liver. Seizures were initially controlled by dietary means and by limiting exercise. Eventual control was obtained by treatment with prednisolone (1 mg kg-1 on alternate days) and diazoxide (10 mg kg-1 in divided doses daily). Post mortem examination confirmed the presence of a pancreatic islet cell adenocarcinoma with hepatic metastasis.
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PMID:An insulinoma causing hypoglycaemia and seizures in a dog: case report and literature review. 285 64

The session on 'The Muscles and Their Neural Control' comprised papers that covered an extremely broad field, ranging from single membrane channels to integration at the motor unit level. To start with the molecular mechanisms, slow noninactivating sodium channels were postulated to be the common denominator in a number of myopathies, their activation causing depolarization and thus muscle weakness. New ideas were presented regarding muscle insulin receptors as the main target for neurotrophic influences, as well as transmitter release at nonmammalian motor nerve terminals. Changes in muscle compliance seem to be involved in adaptation of spindle sensitivity and reflex activity. Also, data were presented in favor of a neurotoxic component in myotrophic lateral sclerosis. Analysis of stationary motor unit discharges can differentiate parkinsonian patients without tremor from normal controls. Long-term use-dependent factors that change muscle properties have considerable effects on the way in which contractile force is graded.
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PMID:Muscles and their neural control. 288 22

Among 28 patients with acute diabetes mellitus of recent onset, long-term remission (25-48 months) was obtained in 14 and medium-term remission (10-24 months) in the other 14. At the onset of the disease these two groups were very similar: remissions were longer in the older patients and shorter in the leaner ones. In patients seen at an early stage, there is no hormonal or immunological data to differentiate between those who will be in remission and those who will not. In our series, insulin secretion was the same in all patients at the onset of diabetes and at the end of the remission period. Further explorations suggested some degree of resistance to insulin, but this was easily overcome by the initial intravenous insulin treatment and by the conventional subcutaneous insulin treatment after the remission had ceased. Our data show the weakness of arguments which separate insulin-dependent from non insulin-dependent patients in acute diabetes mellitus of recent onset.
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PMID:[Long-term remission in fresh acute diabetes mellitus]. 295 31

A 12-year-old female Irish Setter was examined because of recurrent episodes of hindlimb weakness. The dog was not ataxic, but had generalized muscular atrophy, decreased patellar reflexes, and slow proprioception. Blood glucose content was low (32 mg/dl) and the amended insulin-glucose ratio was high (9,600). Electromyographic studies showed evidence of polyneuropathy. The diagnosis was functional islet B-cell tumor with peripheral neuropathy. Exploratory laparotomy was performed. Widespread metastases were observed and the dog was euthanatized because of the poor prognosis. The dog was necropsied and the diagnosis was confirmed on the basis of microscopic findings.
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PMID:Peripheral polyneuropathy in a dog with functional islet B-cell tumor and widespread metastasis. 299 11

In order to better characterize the psychobiology of hypoglycemic symptom production, six normal subjects had physiological/biochemical and symptom ratings at 20, 30 and 40 min after six different doses of intravenous regular insulin (0.0, 0.5, 1.0, 2.0, 3.0 and 4.0 units, in a Latin-square design); subjects also indicated after each dose whether they believed they had received an active or an inactive substance. Choice response switched from inactive to active substance when plasma glucose fell to the mid to high 50s mg/dl (i.e. whole blood glucose of approximately 50), and plasma epinephrine levels rose to between 100 and 200 pg/ml. Adrenergic symptoms and 'weakness' were most strongly associated with choice; other symptom variables had weaker associations. Symptoms were more strongly correlated with epinephrine than glucose levels, but anxiety was not strongly correlated with the epinephrine increases.
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PMID:Symptoms of insulin-induced hypoglycemia in normal subjects. 304 94

A 12-year-old diabetic girl is reported who developed faintly violaceous nodules on the back of the right thigh. These spread to the posterior aspect of the left thigh and to both legs. She complained of some muscular weakness. A diagnosis of cutaneous polyarteritis nodosa was considered. No blood eosinophilia was detected. Skin biopsy disclosed scattered dermal foci of eosinophilic and granular degeneration of collagen with a palisade of histiocytes and eosinophils in a flame configuration. The lesions did not correspond to the sites of insulin injections. Eight childhood cases of eosinophilic cellulitis were found in the literature, all of them in males. The specificity and meaning of the flame configuration are discussed.
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PMID:[Childhood Wells syndrome]. 305 92

Myotonic dystrophy is an autosomal dominant disorder that results in skeletal muscle weakness and wasting, myotonia, and numerous nonmuscular manifestations including frontal balding, cataracts, gonadal dysfunction, cardiac conduction abnormalities, respiratory insufficiency, and hypersomnolence. Although the gene defect in myotonic dystrophy has been mapped to chromosome 19, the exact metabolic abnormalities responsible for this disorder are unknown. Skeletal muscle has been found to be relatively insulin-resistant in myotonic dystrophy, and a decrease in the anabolic action of insulin on skeletal muscle may be related to muscle wasting in this disorder. Laboratory studies, including electromyography, electrocardiography, and muscle biopsy, are helpful in evaluating patients for this disorder, but the clinical aspects and a careful family history remain the mainstays of diagnosis. A number of management strategies preserve function and prevent complications in myotonic dystrophy.
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PMID:Myotonic dystrophy. 306 94

A 16-year-old boy with insulin-dependent diabetes mellitus since age five years was admitted with severe ketoacidosis, and suffered a cardiorespiratory arrest from which he made a full recovery. He subsequently developed the typical clinical picture of diabetic amyotrophy with painful asymmetrical weakness and wasting of proximal lower limb muscles. Cerebrospinal fluid protein was elevated, and electromyography showed typical changes. Diabetic amyotrophy has not previously been reported in this age group.
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PMID:Adolescent diabetic amyotrophy. 320 32


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