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At least 19 recordsLinked to original sources
PubMed1989

The ocular hypotensive effects of demeclocycline, tetracycline and other tetracycline derivatives.

Demeclocycline, tetracycline and other tetracycline derivatives lowered intraocular pressure (IOP) in rabbits following intravitreal injection, but the onset of this effect was not evident until 1 or more days after drug administration. Of the drugs tested, demeclocycline was the most active ocular hypotensive agent. Demeclocycline caused a dose-dependent decrease in IOP. The maximum IOP decrease of approximately 12 mm Hg occurred 5 days after intravitreal administration of 0.5 mg, with the effect persisting for over a week. Demeclocycline did not alter tonographically measured aqueous humor outflow facility or episcleral venous pressure. Based on calculated aqueous humor flow rates following 0.2 mg demeclocycline, a 62% decrease in aqueous humor formation occurred 7 days after intravitreal injection. The flow-to-diffusion ratio for ascorbate was reduced 54% 6 days after the intravitreal administration of demeclocycline, a change also consistent with suppression of aqueous humor formation. Anterior chamber aqueous humor protein concentration was increased 6 days after demeclocycline administration. No histologic changes were present in the treated eyes by light microscopy. Intravitreal demeclocycline similarly lowered IOP in cats, with the duration of effect lasting up to 20 days.

Animals↗
PubMed1980

Effect of prostaglandin inhibition on demeclocycline administration in conscious rats.

Studies were performed in conscious rats to evaluate the role of renal prostaglandin biosynthesis in demeclocycline-induced polyuria. Three groups of animals were evaluated. Group 1 animals received only the diluents used for both demeclocycline and indomethacin. Group 2 received demeclocycline (20 mg/kg/day) and the indomethacin diluent. Group 3 received both demeclocycline and indomethacin (10 mg/kg/day). After eight days of demeclocycline administration, urine flow rate increased in the group 2 animals from 15.1 +/- 2.1 to 31.1 +/- 5.1 ml/day. Indomethacin failed to alter the magnitude of demeclocycline-induced polyuria despite a 60% reduction in urine prostaglandin E excretion rats. These studies demonstrate that the concentrating defect induced by demeclocycline can occur independent of alterations in praostaglandin biosynthesis and suggest that a change in renal prostaglandin biosynthesis is not an etiologic factor in demeclocycline-induced polyuria.

Animals↗
PubMed1981

Serious hyponatremia in patients with cancer: management with demeclocycline.

Seventeen patients with cancer or aplastic anemia received demeclocycline as treatment for hyponatremia. Prior to demeclocycline therapy no patients showed clinical signs of fluid overload or saline depletion. In all patients inappropriately concentrated urine (mean urine osmolality = 548 mOSM/kg H2O) or increased urine content of sodium (mean urine sodium = 91 mEq/L) were documented prior to demeclocycline therapy. No patient had developed hyponatremia in association with antineoplastic drug therapy. The average serum sodium (NaS) at the time of initiation of therapy was 121 mEq/L. NaS increased in all patients despite the simultaneous administration of generous volumes of fluid. NaS exceeded 130 mEq/L and average of 3.5 days following institution of demeclocycline. Patients lost an average of 2.3 kg during demeclocycline. The toxicity noted following demeclocycline was azotemia and increased serum creatinine. Eight patients developed serum urea nitrogen (SUN) in excess of 25 mg/dl; average maximum creatinine in these eight patients was 1.9 mg/dl. Average peak creatinine in eight patients who did not develop azotemia was 0.87 mg/dl. Azotemia seemed to be correlated with simultaneous administration of other nephrotoxic agents and with administration of higher doses (1200 mg/day) of demeclocycline.

Creatinine↗
PubMed1998

Perioperative vasopressin secretion treated by demeclocycline.

The purpose of this study was to evaluate the perioperative effects of demeclocycline on vasopressin (VP) in patients undergoing surgery, specifically coronary artery bypass grafting (CABG). This was a prospective, double-blind placebo-controlled clinical study using human subjects in a 575-bed tertiary care teaching community hospital. Thirty patients (20 males and 10 females) undergoing elective CABG over a 6-month period were randomized preoperatively to receive either demeclocycline or a placebo. Each patient received either a total of 1200 mg daily of demeclocycline or a placebo beginning 5 days preoperatively and continuing through postoperative day 2. Urine and serum osmolality, electrolytes, and VP levels were measured daily. Perioperative VP levels were significantly higher (P = 0.05) in the demeclocycline group despite decreased VP activity. The postoperative serum sodium and osmolality remained normal in the demeclocycline group and significantly decreased in the placebo group (P < 0.01). The urine osmolality increased significantly in the placebo group (P = 0.04) on postoperative day 1. We conclude that perioperative administration of demeclocycline reliably inhibits the effects of increased VP secretion commonly seen in patients undergoing CABG procedures. Applying these findings to surgical patients who are at increased risk of complicated fluid and electrolyte problems requires further study.

Adult↗
PubMed1999

[Effects of demeclocycline on psychiatric polydipsia in schizophrenic patients].

Excess intake of water by schizophrenic patients is referred to as psychiatric polydipsia. This symptom causes incontinence, vomiting and hyponatremia, and may sometimes lead to death. We have no effective therapeutic methods other than administrating sodium chloride solution and diuretics, or restricting the intake itself. A case was reported stating that demeclocycline, used in case where there is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), was effective for the treatment of psychiatric polydipsia. We administered demeclocycline to 8 schizophrenic patients with psychiatric polydipsia, and noticed improvement in incontinence, vomiting and hyponatremia. There was also a decrease of polydipsic behavior. Demeclocycline inhibits the antidiuretic effect of vasopressin on the distal renal tubule. Considering the function of demeclocycline and the relevance of vasopressin to the central nervous system, it has been suggested that demeclocycline has effects on the central nerve through vasopressin or cyclic AMP.

Anti-Bacterial Agents↗
PubMed1988

The use of demeclocycline in the treatment of patients with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome).

Eight patients (7 men and 1 woman, mean age 43.1 +/- 8.9 years) with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome) underwent treatment with demeclocycline in an effort to normalize serum sodium levels and thereby protect the PIP patients against complications including hyponatremic seizures and coma. There tended to be an improvement (p = .080) in early morning serum sodium following treatment with demeclocycline (baseline 132.6 +/- SD 3.3 and treatment serum sodium 134.8 +/- SD 3.3 mEq/1). At the same time, there was an increase (p = .043) in urinary specific gravity following treatment with demeclocycline (baseline 1.0047 +/- SD .0029 and treatment urinary specific gravity 1.0063 +/- SD .0026). Clinical indications for and potential mechanisms of action of demeclocycline treatment in the PIP syndrome are discussed.

Adult↗
PubMed1975

Demeclocycline treatment in the syndrome of inappropriate antidiuretic hormone secretion.

We have studied the effects of demeclocycline on the water metabolism of a patient with the syndrome of inappropriate antidiuretic hormone (ADH) secretion who presented with a serum sodium concentration of 110 meq/litre. Free water clearance was studied before, during, and after treatment with demeclocycline. This study shows that demeclocycline (900 mg/day) can at least partially inhibit the action of ADH in the setting of tumor-induced ADH secretion, with the production of a reversible, partial nephrogenic diabetes insipidus, and with few or no side effects. Demeclocycline may be useful in the treatment of chronic inappropriate ADH secretion.

Carcinoma, Small Cell↗
PubMed1977

Renal failure associated with demeclocycline in cirrhosis.

Three patients with cirrhosis, ascites, and dilutional hyponatremia were treated with demeclocycline in an attempt to correct the abnormal water retention. Demeclocycline administration (600 to 900 mg/day for 8 to 9 days) resulted in [a] increased blood urea nitrogen and plasma creatinine concentrations; [b] reduction of the inulin clearance by between 63% to 78% and of paraaminophippurate clearance by 36% to 77%; and [c] an impairment of the renal concentrating ability. Urine osmolality decreased to hypotonic levels, but polyuria did not appear, probably because it was prevented by the reduction of the glomerular filtration rate. Renal failure was reversible on withdrawal of demeclocycline. No other causes than demeclocycline administration could be found to explain the reduction of the glomerular filtration rate and the estimated renal plasma flow.

Blood Urea Nitrogen↗
PubMed1980

Plasma demeclocycline levels and nephrotoxicity. Correlation in hyponatremic cirrhotic patients.

In five hyponatremic, cirrhotic patients, demeclocycline hydrochloride was used to inhibit the hydroosmotic effect of vasopressin. In four, renal impairment developed during the 7 to 20 days of demeclocycline hydrochloride (900 to 1,200 mg/day) administration. In these four patients, creatinine clearance fell (72 to 20 mL/min, P less than .01) as BUN (12 to 47 mg/dl, P less than .02) and serum creatinine (0.9 to 4.2 mg/dl, P less than .01) levels rose. The azotemic effect of the drug could not be accounted for consistently by volume depletion secondary to its natriuretic effect. However, a close correlation between plasma demeclocycline levels and its azotemic effect was observed. We conclude that a nephrotoxic effect of demeclocycline severly limits its usefulness in treating hyponatremia in the cirrhotic patient.

Adult↗
PubMed1994

Prophylaxis of carbamazepine-induced hyponatremia by demeclocycline in six patients.

BACKGROUND: Hyponatremia has been reported to occur in approximately 5% of carbamazepine-treated patients who otherwise do well on that agent. Demeclocycline has been used in the treatment of hyponatremia of various etiologies including one case of carbamazepine-induced hyponatremia. METHOD: We extended these observations by studying the effects of demeclocycline on carbamazepine-induced hyponatremia in six psychiatric inpatients. RESULTS: Once serum sodium concentrations had normalized after carbamazepine discontinuation, demeclocycline prevented further decreases in sodium levels upon rechallenge with carbamazepine in five of six patients. Gender, smoking, and neurologic compromise may have played a role in the development of carbamazepine-induced hyponatremia as well as response to this strategy, although our sample size is too small to make firm conclusions. CONCLUSION: Demeclocycline was successfully used in the prophylaxis of carbamazepine-induced hyponatremia and may be useful in cases that respond best to carbamazepine treatment.

Adult↗
PubMed1977

Demeclocycline. Treatment for syndrome of inappropriate antidiuretic hormone secretion.

The efficacy of demeclocycline hydrochloride in suppressing the tubular action of tumoral antidiuretic products was tested in seven patients with the syndrome of inappropriate antidiuretic hormone secretion. In all patients, demeclocycline hydrochloride (1,200 mg/day) induced production of hypotonic urine and corrected hyponatremia despite large fluid intakes. Comparison of the response to a standard water load before and during treatment showed a notable improvement in the response to water ingestion. Even though demeclocycline moderately impairs renal function, it appears to be the treatment of choice in the chronic form of the syndrome.

Administration, Oral↗
PubMed1989

Disposition kinetics and distribution of demeclocycline in various biological fluids in female goats.

A pharmacokinetic study of demeclocycline was carried out following intravenous administration at 5 mg/kg body weight in lactating goats. Demeclocycline appeared within 5 min in plasma, interstitial fluid (isf) and urine, while it appeared at 1 h in milk. Peak concentrations of 21.70 +/- 4.06, 2.67 +/- 0.23, 5.65 +/- 0.45 and 82.23 +/- 10.06 micrograms/ml were attained at 5 min and at 6, 8 and 8 h in plasma, isf, milk and urine respectively. A potentially therapeutic concentration of greater than or equal to 0.5 micrograms/ml was maintained from 5 min-36 h, 30 min-30 h, 1-36 h and 5 min-48 h in plasma, isf, milk and urine respectively. The drug was detectable in all the above biological fluids for at least 48 h. A low distribution half life (t1/2 alpha) of 0.44 +/- 0.04 h and a high elimination half life (t1/2 beta) of 19.24 +/- 1.22 h denote rapid distribution but very slow elimination of the drug in goats. A high tissue plasma concentration ratio [K12:(K21-beta)] of 5.12 +/- 0.97 during the elimination phase and a Vdarea of 1.59 +/- 0.18 L/kg indicate uniform distribution of demeclocycline in the tissues and body fluids of goats. The dosage regimen for maintaining minimum plasma concentration (Cp infinity min = MIC) of 0.5, 1.0 and 1.5 micrograms/ml at selected dosage intervals of 12 and 24 h was also calculated.

Animals↗
PubMed1978

Superiority of demeclocycline over lithium in the treatment of chronic syndrome of inappropriate secretion of antidiuretic hormone.

We evaluated demeclocycline and lithium therapy in 10 patients with the syndrome of inappropriate secretion of antidiuretic hormone. Despite severe water restriction, all patients had hyponatremia (mean +/- S.E.M. serum sodium of 122 +/- 1.1 meq per liter) and elevated urine osmolality (744 +/- 59 mOsm per kilogram) before treatment. Demeclocycline (600 to 1200 mg daily) restored serum sodium concentration to 139 +/- 1.1 meq per liter within five to 14 days, permitting unrestricted water intake in all patients. In three patients given lithium carbonate (900 mg daily) the serum sodium concentration, urine osmolality and urine volume were unchanged; since two patients had adverse central-nervous-system symptoms during lithium therapy, further study of this agent was abandoned. A patient with an unusual 22-year history of the syndrome was unresponsive to lithium, whereas long-term treatment with demeclocyline was markedly effective. Demeclocycline is superior to lithium in the treatment of the syndrome and may obviate the need for severe water restriction.

Adult↗
PubMed1978

Demeclocycline in the treatment of the syndrome of inappropriate antidiuretic hormone release: with measurement of plasma ADH.

A patient with the syndrome of inappropriate antidiuretic hormone release (SIADH) following head injury and meningitis was studied during treatment with demeclocycline, a drug known to produce a reversible nephrogenic diabetes insipidus. No changes were observed during six days of demeclocycline 1200 mg/24 hr but urine output increased significantly, with the production of a dilute urine, when the dose was increased to 2400 mg/24 hr. The patient lost weight, and all biochemical features of the syndrome were rapidly corrected despite an unchanged fluid intake and despite the persistence of high plasma levels of ADH. The rise in serum sodium was accompanied by mild sodium retention, as measured by external balance and exchangeable sodium. A complication of treatment was the development of acute renal failure possibly induced by a nephrotoxic effect of high circulating levels of demeclocyline. On stopping demeclocyline renal function returned to normal and, after some delay, SIADH returned, and was still present 9 months after initial presentation. This confirms earlier reports of the efficacy of demeclocycline in SIADH; but the authors advise caution against increasing the dose above 1200 mg/24 hr.

Demeclocycline↗
PubMed1979

Demeclocycline in the treatment of the syndrome of inappropriate secretion of antidiuretic hormone.

Fourteen patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have been treated with demethylchlortetracycline (demeclocycline) 1200 mg daily. In 12 patients the underlying lesion was malignant. The serum sodium returned to normal (greater than 135 mmol/l) in all patients after a mean of 8.6 days (SD +/- 5.3 days). Blood urea rose significantly from the pretreatment level of 4.2 +/- 2.3 mmol/l to 10.1 +/- 5.1 mmol/l at ten days (P less than 0.001). The average maximum blood urea was 13.4 +/- 6.8 mmol/l. In four patients the urea rose above 20 mmol/l, and in two of these demecyocycline was discontinued because of thie rise. The azotaemia could be attributed to a combination of increased urea producation and a mild specific drug-induced nephrotoxicity. Discontinuation of demeclocycline in six patients led to a fall in serum sodium, in one case precipitously, and return of the urea towards normal levels. Demeclocycline appears therefore to be an effective maintenance treatment of SIADH, and the azotaemia that occurs is reversible and probably dose dependent.

Adult↗
PubMed1978

Renal function during treatment of inappropriate secretion of antidiuretic hormone with demeclocycline.

Two patients with the syndrome of inappropriate secretion of antidiuretic hormone were studied in a metabolic ward during treatment with 1.2 g demeclocycline daily. In both patients, demeclocycline treatment led to increased renal water excretion with consequent correction of hyponatremia and hypo-osmolality. Three episodes of reversible deterioration in glomerular filtration rate developed in these patients. Each episode was accompanied by clinical evidence of extracellular fluid volume contraction, and on each occasion there was an inappropriate natriuresis with daily urinary sodium excretion remaining above 50 mEq. Although demeclocycline effectively reverses the electrolyte abnormalities of this syndrome, the potentially dangerous side effects that may develop exclude the routine usage of the drug.

Demeclocycline↗
PubMed1985

Demeclocycline improves hyponatremia in chronic schizophrenics.

Serum sodium concentration increased significantly in eight hyponatremic schizophrenic subjects treated with demeclocycline. The incidence of severe hyponatremic episodes was significantly reduced. The authors argue that mild impairments in urinary dilution contribute to water intoxication in most chronic psychotics who develop this syndrome. Demeclocycline may help these patients.

Adult↗
PubMed1989

Quantitative analysis of demeclocycline by high-performance liquid chromatography.

A high-performance liquid chromatographic (HPLC) method suitable for the quality control of demeclocycline is described. The stationary phase is a poly(styrene-divinylbenzene) copolymer, kept at 60 degrees C. The mobile phase comprises 2-methyl-2-propanol-0.2 M potassium phosphate buffer (pH 9.0)-0.02 M tetrabutylammonium hydrogen sulphate (pH 9.0)-0.01 M sodium edetate (pH 9.0)-water (8:10:15:10:57, m/v/v/v/v). The flow rate is 1 ml min-1 and detection is performed at 254 nm. Official standards are compared and results for the analysis of a number of commercial bulk samples and preparations are presented. 4-Epidemeclocycline and demethyltetracycline are the main impurities. 4-Epidemethyltetracycline and 2-acetyl-2-decarboxamido-demeclocycline can also be present.

Capsules↗