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Biomedical subjects

A M Moses

Publications and source records attributed to A M Moses.

At least 55 records · Page 3Linked to original sources
PubMed1981

Antidiuretic responses to injected desmopressin, alone and with indomethacin.

Desmopressin (dDAVP) is a synthetic analog of arginine vasopressin which generally has been very effective, used intranasally, in the treatment of diabetes insipidus. There are several clinical situations, however, where a parenteral route of administration would be preferable. Using 6 patients with diabetes insipidus, we have shown a dose-response relationship between 0.5 and 4 microgram of dDAVP injected sc. The nonsteroidal, antiinflammatory agent, indomethacin, augments the magnitude, but not the duration, of the response to 0.5 microgram dDAVP. These observations suggest that injected dDAVP, generally in the amount of 1 or 2 microgram, would be a valuable agent in the treatment of diabetes insipidus and that combined therapy with indomethacin is probably not warranted.

Adult↗
PubMed1980

Studies on the attainment of normocalcemia in patients with pseudohypoparathyroidism.

Basal serum calcium and parathyroid hormone (PTH) levels were measured, and urinary excretion of cyclic adenosine monophosphate (AMP) and phosphate was determined before and after the infusion of 250 U of PTH in four patients with pseudohypoparathyroidism when they were hypocalcemic and again when they spontaneously became normocalcemic. These data were compared to those observed in a group of patients with pseudohypoparathyroidism before and after they became normocalcemic after treatment with vitamin D and calcium. Serum PTH levels were very high in patients with untreated pseudohypoparathyroidism and decreased, although not to normal, when normocalcemia occurred either spontaneously or through treatment. Of the four patients who became normocalcemic spontaneously, basal and PTH-stimulated urinary excretion of cyclic AMP, and clearance of phosphate increased. These changes were all significantly different from the changes which occurred when patients became normocalcemic as a result of treatment with vitamin D anc calcium. The factors which govern the apparent increased renal sensitivity to endogenous and exogenous PTH when normocalcemia develops spontaneously in patients with pseudohypoparathyroidism remain to be explained. However, these changes are dissimilar from those which occur from treatment with vitamin D anc calcium.

Adult↗
PubMed1980

Augmentation by chlorpropamide of 1-deamino-8-D-arginine vasopressin-induced antidiuresis and stimulation of renal medullary adenylate cyclase and accumulation of adenosine 3',5'-monophosphate.

The effect of chlorpropamide was determined in Brattleboro diabetes insipidus (DI) rats that were injected with 1-deamino-8-D-arginine vasopressin (dDAVP). Chlorpropamide augmented the antidiuretic responses to 0.78 and 1.56 ng dDAVP but not to larger doses. In an effort to explain this observation we investigated the effect of chlorpropamide on renal medullary adenylate cyclase activation by dDAVP and on phosphodiesterase activity. We found that the injection of chlorpropamide increased adenylate cyclase activation by dDAVP added in vitro to renal medullary cell membrane preparations from Brattleboro DI rats but had no effect on phosphodiesterase activity. When kidneys from Brattleboro DI rats, treated and not treated with chlorpropamide, were perfused in vitro, we found that 10(-4) M dDAVP increased the concentration of cAMP in comparison to untreated and chlorpropamide-treated groups, and that chlorpropamide plus dDAVP resulted in a greater concentration of renal cAMP than was found with dDAVP alone. We believe that treatment with chlorpropamide increases dDAVP-stimulated renal medullary adenylate cyclase activity without altering phosphodiesterase activity and that this leads to increased renal cAMP concentrations. This, in turn, causes an augmented antidiuresis in response to dDAVP.

Adenylyl Cyclases↗
PubMed1980

Permanent diabetes insipidus following head trauma: observations on ten patients and an approach to diagnosis.

Permanent diabetes insipidus following head trauma is uncommon, but potentially fatal. The neurologic, roentgenographic, and endocrinologic findings in ten patients with this condition are reported. Eight of the patients were males under the age of 35 years. Unconsciousness (nine) and skull fracture (seven) were frequent findings. Cranial nerve damage (four) and anterior pituitary hormone deficiency requiring replacement (one) were less frequent. An automobile accident caused the trauma in six patients. Standard water deprivation tests revealed that five of the patients had total deficiency of antidiuretic hormone (ADH), and the other five had partial deficiency. The diagnosis of diabetes insipidus was markedly simplified by using a new screening test based on comparing urine and plasma osmolality in candidates with those of normal subjects.

Adult↗
PubMed1979

Fulminating hypercalcemia and markedly increased nephrogenous cyclic AMP in a patient with transitional cell carcinoma of the bladder.

Refractory hypercalcemia developed suddenly in a patient who had undergone a radical cystectomy for an anaplastic transitional cell carcinoma of the bladder. A normal serum parathyroid hormone (PTH) value was obtained by immunoassay while the patient had hypercalcemia and unimpaired renal function. This normal PTH value in the presence of hypercalcemia was consistent with his hypercalcemia being secondary to excessive amounts of circulating PTH. The finding of increased nephrogenous cyclic AMP, however, provided the definitive diagnosis of hyyperparathyroidism. Since autopsy revealed that there was no residual tumor in the bladder area, only evidence of metastatic disease, and since the parathyroid glands were not hyperplastic or adenomatous, we attributed this patient's hypercalcemia to hyperparathyroidism due to the ectopic production of PTH by a metastasis from the transitional cell carcinoma of the bladder.

Carcinoma, Transitional Cell↗
PubMed1979

Albright's osteodystrophy in a patient with renal hypercalciuria.

We have investigated an 18-yr-old hypercalciuric female with features of both renal hypercalciuria and pseudohypoparathyroidism. She had increased circulating parathyroid hormone levels, which are common to both diseases. She also had a modest hypocalcemia and low normal basal cAMP excretion, both of which are more likely to occur in pseudohypoparathyroidism. She also had Albright's osteodystrophy, which is frequent in patients with pseudohypoparathyroidism and has never been reported in patients with renal hypercalciuria. In contrast to patients with pseudohypoparathyroidism, her serum 1,25-dihydroxycholecalciferol level was increased and her renal responses to parathyroid hormone infusion, including renal calcium reabsorption, were normal. This patient, therefore, raises the possibility that some patients with renal hyperalciuria may have a forme fruste of pseudohypoparathyroidism.

Adolescent↗
PubMed1979

Chlorpropamide-induced changes in patients with hyperparathyroidism.

Ten patients with primary hyperparathyroidism were placed on a constant 30 mEq of calcium and 120 meq of sodium diet, and alterations in their calcium balance in response to standard oral doses of chlorpropamide were studied over a 4 day control period and a 4 day treatment period. The 10 patients treated with chlorpropamide significantly increased the urinary excretion of calcium and sodium and decreased the excretion of cyclic adenosine monophosphate (AMP). The serum calcium was lowered in six of the patients treated with chlorpropamide, and three of these patients, who had diabetes mellitus and either refused or were too ill for parathyroidectomy, continued to receive chlorpropamide for periods of 9 to 36 months. These three patients experienced prolonged lowering of the serum calcium level and became less confused, lethargic, and fatigued. The interrelationships between the chlorpropamide-induced changes in excretion of calcium, sodium, and cyclic AMP still must be clarified.

Adenosine Monophosphate↗
PubMed1976

Renal responses to PTH in patients with hormone-resistant (pseudo) hypoparathyroidism.

Five patients with pseudohypoparathyroidism were compared to normal subjects and patients with hypoparathyroidism in their ability to respond to the infusion of parathyroid hormone (PTH) by altering excretion of calcium, sodium, potassium, phosphate and bicarbonate. In patients with pseudohypoparathyroidism, impairment in renal responses to PTH was more generalized than has been recognized. The patterns of response varied from patient to patient. The most commonly observed abnormality, aside from lack of increase in urinary cyclic adenosine 5'-monophosphate (AMP) was failure to decrease the calcium to sodium clearance ratio, and indication of impaired renal calcium reabsorption. The responses which most closely approximated normal, including a normal decrease in the calcium to sodium clearance ratio, occurred in a patient (Case 1) who had the largest, although impaired, response in cyclic AMP excretion. Conversely, the most abnormal responses occurred in three patients (Cases 2, 4 and 5) who had the smallest increases in cyclic AMP excretion after the administration of PTH. The impaired renal reabsorption of calcium after the administration of PTH (lack of decrease in calcium to sodium clearance ratio) may, when present, be in part responsible for hypocalcemia.

Absorption↗
PubMed1976

Pathophysiologic and pharmacologic alterations in the release and action of ADH.

The physiologic factors involved in vaseopressin (ADH) release and action are reviewed with emphasis on the interaction between osmotic and volume stimuli to the discharge of ADH. Abnormalities in reception of stimuli to ADH release, and in the impaired synthesis and release of ADH, are reviewed in relation to the causes of diabetes insipidus, and information on the biochemical changes which have been described in patients with nephrogenic diabetes insipidus is also discussed. We summarize the pathologic lesions and associated diseases found in 54 of our patients with diabetes insipidus. Criteria for establishing the diagnosis of diabetes insipdus are reviewed with emphasis on the dehydration test, including the importance of measuring plasma osmolality at the conclusion of water deprivation. Treatment of diabetes insipidus is briefly discussed with emphasis on the use of DDAVP and oral agents. The syndrome of inappropriate ADH secretion (SIADH) is reviewed including our experience with 39 patients. The differential diagnosis of SIADH, including the value of water loading and the measurement of ADH levels, is discussed. We comment on treatment of these patients including the use of investigational drugs. Lastly, we review the pharmacologic features and clinical relevance of some drugs which alter the release and action of ADH.

Analgesics↗
PubMed1976

The role of volume contraction in the hypocalciuric action of chlorothiazide.

Thiazide-induced hypocalciuria usually requires two to four days of drug treatment for its full expression. The present experiments were designed to test the possibility that an immediate hypocalciuria could be produced in subjects whose extracellular volumes were already contracted. In previously untreated subjects, chlorothiazide (2 g/day) did not produce hypocalciuria on the first day of treatment. Hypocalciuria occurred on the second day and was somewhat enhanced on the third and fourth days of treatment. In subjects pretreated with furosemide (40 mg two or three times a day for two days), chlorothiazide produced hypocalciuria on the first day of its use. Under the influence of chlorothiazide, there was a strong linear correlation between the changes in the excretion of calcium and sodium. The results are consistent with the idea that chlorothiazide enhances the ratio of calcium to sodium reabsorptions and that this tendency for absolute hypocalciuria can be overridden by a large natriuretic response to the drug. Volume contraction, which minimizes the natriretic response to diuretics, allows a more immediate and pronounced hypocalciuric response to thiazides.

Adult↗