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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Classic renal tubular acidosis is characterized by a primary defect in establishment of a large hydrogen ion gradient across the distal renal tubule. Thus the development of hyperchlorenic metabolic acidosis follows. In addition, hypokalemia results from renal potassium wasting secondary hyperaldosteronism from sodium wasting and contraction of the extracellular fluid. The presenting signs and symptoms are growth retardation, fatigue, periodic paralysis, polyuria, polydipsia, vomiting and constipation as well as nephrocalcinosis and nephrolithiasis. It is suggested that effective treatment with alkali therapy requires markedly higher doses than formerly recommended, and may related to a higher rate of endogenous acid production from (1) intermediary metabolism of sulfur amino acids and organic acids, (2) impaired tubular reabsorption of bicarbonate and (3) hydrogen ion release from hydroxyapatite formation. It is also suggested that acidosis may interfere with vitamin D metabolism and thus play an important role in the pathoetiology of the growth failure in children with this disorder.
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PMID:Acid-base, calcium, potassium and aldosterone metabolism in renal tubular acidosis. 3 60

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

The possibility (based on the recognised existence of anticonvulsant osteomalacia), of an osteomalacic origin of a number of subjective symptoms in epileptics (back pain, tiredness, sleepiness, irritability, and giddiness) was tested during a controlled therapeutic trial in 226 outpatients. There was no correlation between subjective symptoms and objective pathological indices of osteomalacia, and group treated with vitamin D (2000 international units daily for 3 months) showed no amelioration of subjective symptoms above that seen in the placebo group. The findings do not support the view that all epileptic patients on anticonvulsant therapy should be treated prophylactically with vitamin D.
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PMID:Subjective symptoms in epileptic patients on anticonvulsant drugs. A controlled therapeutic trial on the effect of vitamin d. 109 58

The atrophy produced by endocrine disorders is primarily due to alterations in protein and carbohydrate metabolism. Type II muscle fibers are more severely affected than are Type I fibers. Steroid myopathy and the myopathy associated with excess ACTH have a typical pattern of proximal weakness affecting the legs more than the arms. Steroid myopathy is usually not apparent until other signs of glucocorticoid excess are present. Treatments of steroid myopathy are as follows: Lower the dose of steroid, use a nonfluorinated glucocorticoid, and exercise or physical therapy. Adrenal insufficiency produces generalized weakness, muscle cramping, and fatigue in 50 per cent of patients. Some patients also develop hyperkalemic paralysis. The treatment is hormone replacement. Thyrotoxicosis produces myopathy caused by net protein catabolism, accelerated basal metabolic rate and impaired carbohydrate metabolism. Shortening of contraction time may result from accelerated myosin ATPase activity and enhanced calcium uptake by the sarcoplasmic reticulum. Depolarization of the muscle fiber and impaired Na-K activity in muscle may predispose to thyrotoxic periodic paralysis. Neuromuscular presynaptic impairment may account for the worsening of myasthenia gravis by thyrotoxicosis. In hypothyroidism, impaired energy metabolism may limit force generation. Slow contraction and relaxation reflect reduction in myosin ATPase activity and impaired calcium uptake by the sarcoplasmic reticulum. Treatment for thyroid-associated muscle disorders is restoration of a euthyroid state. Muscle weakness associated with hypopituitarism is due to loss of thyroid and adrenal cortical hormones. Children require growth hormone for muscle development. T3 and growth hormone synergize to maintain normal protein synthesis. Primary and secondary hyperparathyroidism and osteomalacia are often associated with proximal weakness and fatigability. The myopathy improves with restoration of normal PTH levels and vitamin D replacement. Hypoparathyroidism and pseudohypothyroidism are associated with tetany. Tetany is worsened by alkalosis and is treated by calcium and magnesium replacement.
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PMID:Endocrine myopathies. 306 2

A cervical lymph node enlarged since 3 weeks was to be removed in a 12-year-old boy, whose only complaint was slight fatigue. Routine screening revealed hypercalcemia of 7.3-8.1 mval/l. This rose to 9.2 mval/l despite furosemide-induced high fluid turnover and prednisone while diagnostic evaluation proceeded. Serum phosphate was low consistently. Malignancy, vitamin D-intoxication, immobilisation and familial conditions could be ruled out as causes. Highly elevated serum-parathormone levels inspite of hypercalcemia, and ultrasonography of the neck were the most helpful evidence of a parathyroid adenoma. Calcitonin was effective in lowering serum-calcium to 6-7 mval/l preoperatively.
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PMID:[Asymptomatic, excessive hypercalcemia n a 12-year-old boy]. 685 83

A 1-year prospective study of seasonal mood changes was conducted in 250 female Boston area residents, aged 43 to 72, who were participants in a study of vitamin D supplementation. Each woman completed the Profile of Mood States questionnaire at four study visits. There were significant changes over the year in scores for Tension-Anxiety, Depression-Dejection, Anger-Hostility, Fatigue-Inertia, and Confusion-Bewilderment. These scores were all highest or "worst" in the fall and lowest in the spring or summer. Worse mood scores were associated with fewer hours of sleep. Serum thyroxine was positively associated with higher Depression-Dejection scores in August through November and with higher (better) Vigor-Activity scores in February through May. Supplementation with 400 IU of vitamin D did not appear to affect levels or changes in mood scores.
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PMID:Seasonal mood changes in 250 normal women. 814 Jan 83

As with many chronic diseases that express themselves late in life, osteoporosis is distinctly multifactorial both in etiology and in pathophysiology. Osteoporotic fractures occur because of a combination of injury and intrinsic bony fragility. The injury comes most often from a combination of falls, poor postural reflexes that fail to protect bony parts from impact, and reduced soft tissue padding over bony prominences. The bony fragility itself is a composite of geometry, low mass density, severance of microarchitectural connections in trabecular structures, and accumulated fatigue damage. Reduced bone mass, in turn, is caused by varying combinations of gonadal hormone deficiency, inadequate intakes of calcium and vitamin D, decreased physical activity, comorbidity, and the effects of drugs used to treat various unrelated medical conditions. Finally, the often poor outcome from hip fracture in the elderly is partly caused by associated protein-calorie malnutrition. An adequate preventive program for osteoporotic fracture must address as many of these factors as possible, ie, it must be as multifaceted as the disease is multifactorial.
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PMID:Pathophysiology of osteoporosis. 896 13

A 23-year-old man was suffering from high fever and general fatigue 6 months before admission. The levels of serum Ca and intact-parathyroid hormone (PTH) were low. His brain computed tomography (CT) revealed marked calcifications of the basal ganglia, and pelvis magnetic resonance imaging (MRI) showed inflammation of his seminal vesicle. His candida antigen titer was high and antibiotic therapy was unsuccessful. High fever persisted despite fluconazole treatment, however he recovered after treatment with fluconazole and vitamin D (alfacalcitol). Idiopathic hypoparathyroidism hinders the activation of vitamin D via insufficient PTH secretion, and vitamin D has some immunological effects. His decreased natural killer (NK) cell activity improved after alfacalcitol treatment. We suggest the possible immunological effects of vitamin D in this fungal infection.
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PMID:Idiopathic hypoparathyroidism with fungal seminal vesiculitis. 909 93

Primary hyperparathyroidism, characterized by hypersecretion of parathyroid hormone (PTH) leading to hypercalcemia and relative hypophosphatemia, is quite common in the elderly. Most patients with primary hyperparathyroidism have only mild hypercalcemia and are symptomless. But others experience various other organ diseases. Primary hyperparathyroidism is also associated with cardiovascular abnormalities, including QT interval shortening, heart block, cardiac arrhythmias, hypertension, myocardial hypertrophy, myocardial calcification and, though rarely, with valvular heart disease. We described a case of primary hyperparathyroidism associated with cardiac abnormalities. An 82-year-old male presented with the complaints of chest discomfort, fatigue, general weakness, nausea and vomiting over a period of months and was admitted in July 1996. Physical examination with heart auscultation showed a pansystolic murmur over the right sternal border and apex region, and a blowing diastolic murmur over the left sternal border. Biochemistry profiles revealed elevations of serum calcium (14.3 mg/dl) and chloride/phosphate ratio (> 33). Endocrinological studies showed elevations of serum PTH-C (4.8 ng/ml) and PTH-intact (705 pg/ml) concentrations. Kidney ultrasonography revealed a left renal stone. A spine X-ray revealed spondylosis and a compression fracture of the lumbar-spine with osteoporotic change. Thyroid ultrasonography and Thallium (Tl201)-technetium (Tc99m) subtraction scan showed parathyroid adenoma in the low pole of the right thyroid bed. Parathyroid aspiration cytology revealed few and discrete cells. Echocardiogram revealed moderate to severe aortic valvular calcification as well as stenosis with moderate aortic regurgitation, mitral regurgitation and myocardial calcification. The patient received parathyroidectomy one month later. During his postoperative days, he suffered from muscle twitching with positive Trousseau's sign and Chvostek's sign. The patient received calcium carbonate and vitamin D for hypocalcemia, diltiazem and capoten for his heart problems. A repeated echocardiogram two months after surgery showed no improvement of valvular calcification.
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PMID:Primary hyperparathyroidism with cardiac abnormalities: a case report. 950 84

As with many chronic diseases that express themselves late in life, osteoporosis is distinctly multifactorial, both in etiology and pathophysiology. Osteoporotic fractures occur because of a combination of injury and intrinsic bony fragility. Injury comes most often from a combination of falls, falling to the side, poor postural reflexes that fail to protect bony parts from impact, and reduced soft-tissue padding over bony prominences. The bony fragility itself is a composite of geometry, low mass density, severance of microarchitectural connections in trabecular structures, and altered bone material quality. The latter is primarily the result of accumulated fatigue damage, but reduced collagen cross-links and other intrinsic material defects may play a role as well. Reduced bone mass, in turn, is the result of varying combinations of gonadal hormone deficiency, inadequate intakes of calcium and vitamin D, decreased physical activity, comorbidity, and the effects of drugs used to treat various unrelated medical conditions. Finally, the often poor outcome from hip fracture in the elderly is partly due to associated protein-calorie malnutrition. An adequate preventive program for osteoporotic fracture must address as many of these factors as possible and be as multifaceted as the disease is multifactorial.
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PMID:Pathophysiology of osteoporosis. 966 37


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