Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Osteodystrophy is almost universally present in chronic renal failure. Mild, but detectable, abnormalities--especially in parathyroid hormone (PTH) secretion--occur even when the glomerular filtration rate is greater than 30 cc/min. Osteomalacia is common in areas in which vitamin D intake and exposure to sunlight are minimal; when these factors are plentiful, osteitis fibrosa predominates. Osteoporosis is seen with increasing frequency in hemodialyzed patients. Nonosseous complications of secondary hyper-parathyroidism include hypercalcemia, metastatic calcification and pruritus. The most important factor in the medical therapy of osteodystrophy is control of serum phosphate levels. Next, a positive calcium balance must be provided either by giving vitamin D as dihyrdotachysterol, raising dialysate calcium or administering calcium orally. Parathyroidectomy is sometimes indicated, especially when the patients are transplant candidates and manifest hypercalcemia. Whether or not transplant is contemplated, patients with persistently high calcium-phosphate products, severe metastatic calcification or rapidly progressive osteodystrophy should be considered for parathyroidectomy. Newer, experimental vitamin D preparations, such as 1,25-dihydroxycholecalciferol or 1-alpha-hydroxycholecalciferol, should improve the managemet of patients with renal osteodystrophy and decrease the need for parathyroidectomies.
 ...
PMID:Calcium metabolism in renal failure. 109 Jan 50

We have reported of a case of generalised sarcoidosis with primary hyperparathyroidism. A pathogenetic relation between sarcoidosis associated with hypercalcemia and the development of parathyroid adenoma will be discussed and a causal connection will be proposed. According to our hypothesis every primary hyperparathyroidism could have developed from regulatory hyperfunction. This is illustrated by sarcoidosis with hypercalcemia and hypercalcuria. In this case a disturbance in vitamin D dependent calcium metabolism induces hyperplasia of the parathyroid which later leads to the development of a parathyroid adenoma. In addition a review of literature describing similar cases is given.
 ...
PMID:[A case of sarcoidosis with simultaneous primary hyperparathyroidism, coincedence or consequnce?]. 109 56

1. Hypo- and hypercalcemia can be explained as derangements of the calcium homeostasis. Hypocalcemic tetany usually alarming the patient tremendously is, at least in adults, rarely life-threatening. Hypercalcemia leads in 30% of the cases to clinical symptoms which may inadvertedly pass into a state of hypercalcemic crisis. This latter requires an often difficult emergency treatment. 2. Hypocalcemic tetany may be reversed by administering calcium i.v. or, in severe cases, by a calcium infusion. Only rarely are magnesium supplements necessary to let the tetany disappear. Vitamin D or dihydrotachysterol (DHT) do not correct hypocalcemia immediately, since their effects may be delayed up to 15-25 days. In order to normalize the serum calcium permanently, vitamin D or DHT treatment should be instituted as rarely as possible. 3. Initially, hypercalcemic crisis is best treated by forced intravenous fluid administration with normal saline (and furosemide) in combination with high doses of prednisone. Fluid-, sodium- and potassium balances ought to be checked during this type of treatment. A first evaluation of the effectiveness of these measures is recommended after 24 hours: treatment is continued in patients who respond favorably, while subjects who do not show a significant decrease of the serum calcium may either be given a phosphate infusion or mithramycine as a bolus. Calcitonin appears to be useful only to start treatment before institution of a phosphate infusion.
 ...
PMID:[Hypo and hypercalcemia as an emergency]. 110 94

Although the biologically active metabolite of vitamin D, 1,25-dihydroxycholecalciferol, is synthesized exclusively by kidney tissue, severe hypercalcemia developed in an anephric child treated with large doses of vitamin D. Treatment by calcium-free peritoneal dialysis acutely reduced serum calcium from 17.2 to 14.2 mg/100 ml. This decrement was effected by removal of three times the total calcium in extracellular fluid, suggesting enhanced bone resorption. Oral prednisolone for 7 days reduced serum calcium to 13 mg/100 ml, but hypercalcemia recurred rapidly after prednisolone was stopped. Calcitonin, given for only 4 one-half days, produced normocalcemia. Maximum serum 25-hydroxyvitamin D (25-OHD), observed immediately after vitamin D was stopped, was 635 ng/ml (normal range 23-32 ng/ml) and subsequently decreased with an initial half-time of 10 days. Losses in peritoneal dialysate may have contributed to disappearance of serum 25-OHD. Because of the high serum levels of 25-OHD and absence of renal tissue, 25-OHD was the likely metabolite that caused hypercalcemia, probably by stimulation of bone resorption, though contribution to hypercalcemia by another vitamin D metabolite cannot be absolutely excluded.
 ...
PMID:Vitamin D intoxication in an anephric child. 111 41

A 43-year-old man with alopecia maligna was treated for 4 weeks with a total of 130 mg vitamin D3. Two weeks later, after intensive exposure to the sun, he developed a hypercalcaemic crisis and died 5 weeks later of acute cardiac failure. The hypercalcaemia proved treatment-resistant despite good diuresis. Causes other than vitamin D intoxication were excluded clinically and on histopathological investigations. It is suggested that vitamin D should be administered only on the strictest indications and with regular control of the patient.
 ...
PMID:[Fatal vitamin D intoxication]. 111 67

In three women intoxication with vitamin D or dihydrotachysterol occurred. Two patients died from complications despite successful lowering of the serum calcium, the third died after a pulmonary embolus during hypercalcaemia 5 months after cessation of vitamin D. Correct observation of the narrow therapeutic range of vitamin D preparations appears most important in the treatment of hypoparathyroidism and other indications. Particular attention should be given to the prophylaxis of over dosage. Apart from regular serum calcium estimations instruction of the patient and relatives as to the dangers and symptoms of intoxication is recommended. The issuing of a therapy identity card would meet these requirements.
 ...
PMID:[Observations in vitamin D and dihydrotachysterol poisoning]. 111 68

Serum immunoreactive parathyroid hormone (iPTH) levels were increased in a 15 year old girl with pseudohypoparathyroidism, hypocalcemia, hyperphosphatemia, and minimal phosphaturic and absent hypercalcemic responses to exogenous parathyroid extract (PTE). Following normalization of the serum calcium concentration with vitamin D, serum iPTH and phosphate concentrations returned to the normal range, and phosphaturia could be clearly stimulated and hypercalcemia induced by PTE. On the other hand, the urinary cyclic adenosine 3',5'-monophosphate (cyclic AMP) excretion could not be stimulated, suggesting that in this case, there appears to be no relationship between the urinary excretion of cyclic AMP and the phosphaturic effect of PTE. The minimal phosphaturic effect and the lack of hypercalcemic effects of PTE in untreated pseudohypoparathyroidism can be explained by the secondary hyperparathyroidism causing elevated iPTH levels rather than by a defect at the level of the receptor sites. A requirement of pharmacologic amounts of vitamin D per se, however, for the responsiveness of patients with pseudohypoparathyroidism to PTE cannot be ruled out.
 ...
PMID:Pseudohypoparathyroidism. Disappearance of the resistance to parathyroid extract during treatment with vitamin D. 113 47

1. The bivalent cation-binding agent, cellulose phosphate, together with a low calcium diet was given for 6 days to nine patients with primary hyperparathyroidism subsequently verified at surgery. 2. Urinary calcium fell promptly by 8-4 mmol/24 h, and by 70% and reached amounts below 4-0 mmol/24 h in five of the nine patients. The magnitude of fall may have been related to increased synthesis of vitamin D by the skin in a sub-tropical environment. Plasma magnesium fell steadily and urinary magnesium fell by 80%. 3. The plasma calcium showed two types of response. In five patients there was no significant change because a reduction in calcium load was offset by a further increase in the already high tubular reabsorption of calcium. In the remaining four patients, the tubular reabsorption of calcium was at a higher level initially and failed to increase further on the experimental regime, with a corresponding fall in plasma calcium. 4. The hypercalcaemia of primary hyperparathyroidism can be explained by increased renal tubular reabsorption of calcium; net bone resorption makes only a small contribution but an additional factor dependent on the blood-bone equilibrium is not ruled out. 5. Comparison with other published data suggests that the fall in urinary calcium in response to a calcium-depleting regimen is prevented by concurrent depletion of inorganic phosphate and may be enhanced by concurrent depletion of magnesium. 6. Persistence of hypercalcaemia combined with an increase in tubular reabsorption of calcium in response to cellulose phosphate may be of diagnostic value in suspected primary hyperparathyroidism. 7. Cellulose phosphate may be of value in stone prevention in patients with primary hyperparathyroidism who are unsuitable for surgical treatment.
 ...
PMID:Effect of cellulose phosphate and dietary calcium restriction in primary hyperparathyroidism. 114 6

Ten years of experience with daily prophylaxis of rickets brought about isolated knowledge which corrected old mistakes and demands a revision of older attitudes towards the usual prophylaxis. Prophylaxis of vitamin D according to the most modern and reliable knowledge in the best way promotes the growth and mineralisation of the skeleton with dosages of 400 to 800 I.U. smaller or higher dosages are disadvantageous. By observing the above given dosage, rickets and hypercalcaemia are rare and only conceivable under special pathological conditions. The diagnosis of beginning rickets must be well known, otherwise unspecific symptoms of rickets may induce the administration of unnecessarily high amounts of vitamin D. The symptoms of rickets show a gradual increase: the increase of serum alkaline phosphatase precedes the clinical and radiological symptoms. The reliable radiographic deformities of the hand can first be seen at the Ulna, then at the Radius and later at the secondary centers of Metacarpals. Among the relatively reliable clinical symptoms there its first the rosary later the Marfan-sign and eventually the deformation of the long bones. For infants protected by vitamin D, craniotabes as a sign of rickets is completely unreliable as well as the Harrison grooves and rachitic kyphosis. If one observes all these rules and rachitic kyphosis. If one observes all these rules and criterions vitamin D is as reliable in the prophylaxis as in the therapy of vitamin D deficiency rickets.
 ...
PMID:[Ten years' daily prophylaxis against rickets--review and outlook (author's transl)]. 119 21

Facial paralyses in children may be grouped under headings displaying a certain amount of individuality. Chronologically, first to be described are neonatal facial paralyses. These are common and are nearly always cured within a few days. Some of these cases are due to the mastoid being crushed at birth with or without the use of forceps. The intra-osseous pathway of the facial nerve is then affected throughout its length. However, a cure is often spontaneous. When this desirable development does not take place within three months, the nerve should be freed by decompressive surgery. The special anatomy of the facial nerve in the new-born baby makes this a delicate operation. Later, in all stages of acute otitis, acute mastoiditis or chronic otitis, facial paralysis can be seen. Treatment depends on the stage reached by the otitis: paracentesis, mastoidectomy, various scraping procedures, and, of course, antibiotherapy. The other causes of facial paralysis in children are very much less common: a frigore or viral, traumatic, occur ring in the course of acute poliomyelitis, shingles or tumours of the middle ear. To these must be added exceptional causes such as vitamin D intoxication, idiopathic hypercalcaemia and certain haemopathies.
 ...
PMID:[Facial paralysis in children]. 121 18


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>