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)

Neuromuscular function was evaluated in six patients with osteomalacia or secondary hyperparathyroidism, or both, as demonstrated by bone biopsy showing osteomalacia or increased immunoreactive parathyroid hormone, or both. Each patient had weakness, atrophy, and fatigability of proximal muscles, especially of the lower extremities. Most also showed involuntary fine movements of the tongue, hyperactive tendon reflexes with abnormal spread, and decreased vibration sensation, abnormalities similar to those observed in primary hyperparathyroidism. Every patient studies had evidence of neuropathic muscle disease, either on electromyography or muscle biopsy studies histochemically or both. Muscle biopsies showed no definite myopathic features. Treatment of the osteomalacia improved muscle strength. Patients with osteomalacia therefore have a treatable neuromuscular disease that is neuropathic in nature and resembles closely that found in primary hyperparathyroidism.
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PMID:Neuromuscular disease in secondary hyperparathyroidism. 4 34

There is much individual variability in the clinical manifestations of hypocalcemia. The rapidly of the development of hypocalcemia will determine whether or not symptoms will be present. Signs and symptoms of hypocalcemia consisted of tetany (Chvostek's and Trousseau's signs), seizures, diminshed to absent deep tendon reflexes, papilledema, mental changes (weakness, fatigue, irritability, memory loss, confusion, delusion, hallucination), and skin changes. Etiologic factors for hypocalcemia in man include (1) decreased calcium absorption or increased loss from the gastrointestinal tract; (2) parathyroid hormone deficiency; (3) skeletal resistance to parathyroid hormone; (4) ineffective parathyroid hormone; (5) decreased production or increased degradation of 25-hydroxycholecalciferol or 1,25-dihydroxycholecalciferol; (6) increased complex formation with calcium; (7) increased skeletal uptake of calcium; (8) hypomagnesemic state; and (9) direct inhibition of bone resorption. Measurement of total and ionic calcium, magnesium, parathyroid hormone, vitamin D metabolites (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol), and nephrogenous cyclic adenosine monophosphate are especially helpful in the laboratory evaluation of the hypocalcemic patient.
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PMID:Hypocalcemia. Differential diagnosis and mechanisms. 22 22

A study is presented of 14 patients with hyperparathyroid crisis treated at the Massachusetts General Hospital between 1964 and 1978. These patients showed diverse clinical manifestations that were indistinguishable from those in patients with pseudohyperparathyroidism. Their symptoms varied from progressive fatigue, malaise, and weakness to those related to the gastrointestinal and urinary tracts. The one biochemical alteration commonly found among these patients was the rapid increase in the serum calcium. There was a concomitant rise in the BUN in 50% of the patients and in the creatinine in 80%. The diagnosis was established by an elevated immunoreactive parathyroid hormone (PTH) level in all eight patients (100%) who had the radioimmunoassay; by the presence of subperiosteal resorption of the phalanges in six of the eight patients (75%); and in three of four patients (75%) by the loss of the lamina dura of the teeth. The 12 patients who had surgery all survived; the two who did not died. Thirteen patients (93%) had a neoplasm--an adenoma in 12 and a carcinoma in one. One patient had hyperplasia (7%). Nine patients (64%) received hypocalcemic drug therapy. The serum calcium temporarily fell to 12 mg/100 ml in five patients (56%) but failed to budge in four (44%). Simultaneous treatment with saline infusion, furosemide and with hypocalcemic drugs over a prolonged period compounded the difficulty at operation by increasing interstitial edema. Our findings from this study show prompt surgical intervention as the ideal treatment for hyperparathyroid crisis, preferably, within 72 hours of the acute onset of symptoms.
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PMID:Hyperparathyroid crisis: clinical and pathologic studies of 14 patients. 51 79

Thirty-five patients with bone disease and chronic renal failure (twenty-four on maintenance haemodialysis) were treated for 7--39 months with 1alpha-hydroxyvitamin D3, 2--2.5 microgram daily by mouth. Symptoms (bone pain and muscle weakness) and radiographic appearances improved and plasma alkaline phosphatase returned to normal in the majority of patients (87, 76 and 75% respectively). In contrast, histological appearances in bone improved in only 46% twenty-three patients from whom paired biopsies were available, and this change was not greatly different from that seen in a comparable group of untreated patients. Significant correlations were noted in individual patients between the changes in symptoms, X-rays, plasma alkaline phosphatase and immunoreactive parathyroid hormone and these, in turn, were related to histological changes in bone, although these latter changes were often small. It is concluded that 1alpha-hydroxyvitamin D3 is a useful new drug in the treatment of renal bone disease, but that the evaluation of the response depends critically on the method of assessment used.
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PMID:Correlation of clinical, biochemical and skeletal responses to 1alpha-hydroxyvitamin D3 in renal bone disease. 60 24

A 17 year old man with longstanding hypocalcemia and hyperphosphatemia presented with incapacitating bone pain and progressive weakness nad bowing of the legs. The serum abnormalities were due to idiopathic hypoparathyroidism as evidenced by a decreased serum concentration of parathyroid hormone and an appropriate rise in urinary cyclic AMP and phosphate excretion, and serum calcium concentration, in response to exogenously administered parathyroid extract. The serum concentration of 1,25-dihydroxycholecalciferol was appropriately decreased. The bone findings were due to osteomalacia as documented by physical findings, bone roentgenograms, and bone biopsy. Normal renal tubular function, blood pH, and serum concentration of 25-hydroxycholecalciferol and elevated serum alkaline phosphatase excluded the common causes of osteomalacia. The data are consistent with the hypothsis that lack of parathyroid hormone causes both hypocalcemia and a decreased serum concentration of 1,25-dihydroxycholecalciferol which, in turn, limit the availability of calcium and cause defective synthesis of bone matrix resulting in abnormal mineralization.
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PMID:Hypoparathyroidism: a possible cause of osteomalacia . 87 58

Fatigue and muscular weakness are prevalent symptoms in patients with primary hyperparathyroidism. This study examined muscular strength before and after operation in a group of eight patients with hyperparathyroidism and in a control group of seven patients with benign thyroid lesions. The maximum power grip, pronation and supination, and endurance for the same muscular movements, were studied by means of a computer program. Patients with hyperparathyroidism had impaired muscular strength compared with the controls but 12 months after operation a significant improvement of all muscular performance was observed. No such improvement was detectable among the controls. There was no correlation between the levels of serum calcium and parathyroid hormone and the measurements recorded before and after operation. Muscular impairment in hyperparathyroidism is measurable by an objective technique. Improvement occurs after surgery.
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PMID:Muscle strength is improved after parathyroidectomy in patients with primary hyperparathyroidism. 155 67

We describe a neonate with distal renal tubular acidosis with secondary hyperparathyroidism manifesting as hyperchloraemia, hypercalcaemia, elevated serum parathyroid hormone (PTH) and life-threatening metabolic acidosis. He exhibited general weakness, tachypnoea, dry skin and weight loss. Urinary excretion of titratable acid and ammonium was decreased. Daily alkali (2.5 mEq/kg body weight) was required to maintain a normal plasma bicarbonate (HCO3-). With alkali therapy, the fractional excretion of HCO3- was below 5%. Serum calcium and PTH were restored to normal promptly on initiation of alkali therapy. After 5 months of alkali therapy, normal growth and urine acidifying ability were restored and alkali therapy was discontinued. The acidification defect in this patient was transient. We consider this patient to be consistent with Lightwood's syndrome of "transient infantile renal tubular acidosis".
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PMID:Transient neonatal distal renal tubular acidosis with secondary hyperparathyroidism. 161 37

Over the last 25 years, the perceived clinical spectrum of primary hyperparathyroidism (HPT) has changed dramatically from a disorder characterized by severe bone and renal disease to one typically manifested by few or mild symptoms and little evidence of organ damage. Reasons for this change in spectrum include changing demographics (primary HPT is primarily a disease of the middle-aged and elderly), diffusion of medical knowledge leading to a higher index of suspicion, and improved clinical laboratory technology (especially inexpensive and accurate determination of serum calcium and parathyroid hormone). In the first 343 cases of primary HPT seen at the Massachusetts General Hospital, 57% had renal stones, 23% had hyperparathyroid bone disease, and less than 1% had no symptoms. By contrast, studies dating from the availability of automated serum calcium measurement found renal stones and hyperparathyroid bone disease in less than 5% of cases, and about half of cases had few or no symptoms. Most patients with primary HPT today have mild, nonspecific symptoms, such as weakness, fatigue, and mental depression, and such signs as arterial hypertension and osteopenia, and detection of their hypercalcemia is generally serendipitous. The mildness and slow progression seen in many cases of primary HPT has resulted in much controversy about appropriate management.
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PMID:Clinical spectrum of primary hyperparathyroidism: evolution with changes in medical practice and technology. 176 71

A 29-year-old insulin-dependent diabetic woman developed phosphate depletion, nephrolithiasis and bilateral ureteric obstruction due to antacid abuse. Unlike previous descriptions of chronic phosphate depletion, myalgia, weakness and bone pain were absent. Biochemical features included hypophosphataemia, hypercalciuria, hypophosphaturia, elevated plasma, 1,25-dihydroxyvitamin D and low plasma intact parathyroid hormone. These abnormalities were corrected when antacid ingestion was reduced and phosphate intake supplemented. We propose that phosphate depletion secondary to antacid abuse caused 1 alpha-hydroxylase activation and elevation of the plasma 1,25-dihydroxyvitamin D level, leading to marked hypercalciuria. Once diagnosed, antacid abuse is a readily reversible cause of hypercalciuria and renal stones. Moreover, antacid-induced phosphate depletion may present with nephrolithiasis in the absence of musculoskeletal symptoms. This report is intended to draw attention to this important cause of renal stone disease.
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PMID:Antacid-induced phosphate depletion syndrome presenting as nephrolithiasis. 229 30

A myopathy basically involving proximal respiratory muscles can develop in uremia. To evaluate respiratory muscle force in uremia, maximal inspiratory pressure (MIP) was measured in 27 patients with renal failure. MIP was very limited in patients with a creatinine clearance (Crc) lower than 10/ml/min 1.73 m2 not treated with hemodialysis (HD) and in patients on HD who were not treated with 1.25 (OH)2D3 (45 +/- 9 and 43 +/- 5 cm H2O, respectively), moderately reduced in patients on HD treated with 1.25 (OH)2D3 (58 +/- 5 cmH2O) and normal in patients with Crc higher than 10 ml/min 1.73 m2 (86 +/- 6 cmH2O). The treatment with 1.25 (OH)2D3 during 3 months promoted a significant increase in MIP and serum calcium level and a reduction in parathyroid hormone in patients with Crc lower than 10 ml/min. It was concluded that, in uremia, a respiratory muscle weakness partially reversible with vitamin D therapy may be found.
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PMID:[Chronic kidney insufficiency and respiratory muscle function. Changes induced by treatment with 1,25(OH)2D3]. 232 53


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