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 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There have been few major complications of percutaneous nephrostolithotomy (PNL) reported. We recently experienced cardiac arrest during PNL under epidural anesthesia. The patient was a 52 year old man weighing 64 kg who had been suffering from right renal pelvic stone for years. He was scheduled for PLN under epidural anesthesia. Analgesia was obtained to the level of Th6. The operation proceeded uneventfully for about 60 min. By this time, he suddenly complained nausea, and hypotension with bradycardia occurred. Blood pressure and pulse rate returned immediately to the normal level by IV atropine and ephedrine. But after three minutes, blood pressure and pulse rate went down again. This hypotension with bradycardia was unresponsive to epinephrine, calcium chloride and sodium bicarbonate. This was followed by asystole. Resuscitation was successful with the addition of epinephrine, calcium chloride, and sodium bicarbonate about 15 min after cardiac massage had started. The patient was, on the fifth postoperative day, with no evidence of impairment of renal, cardiac and respiratory functions but a slight impairment of neurologic function. Several possible causes for this cardiac arrest and anesthetic management of percutaneous nephrostolithotomy are discussed.
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PMID:[Sudden cardiac arrest during percutaneous nephrostolithotomy (PNL) under epidural anesthesia]. 232 60

Carbetimer (carboxyimamidate) is a low molecular weight derivative of ethylene/maleic anhydride polymer. This compound has demonstrated antitumor activity against several animal models with a daily x 5 schedule appearing most effective. A phase I clinical study of the daily x 5 schedule repeated every 28 days was therefore performed. Forty-one evaluable patients received 66 evaluable cycles of Carbetimer at daily doses ranging from 100-11,000 mg/m2. Hypercalcemia was the dose limiting toxicity with both patients at the 11,000 mg/m2 daily dose level and one patient who received 6 cycles of drug at the 4200 mg/m2 dose level developing severe hypercalcemia not explained by the underlying malignancy. Mild nausea, concentration and rate dependent arm pain at the site of infusion, proteinuria, and coagulopathy were also seen. Calcium balance studies revealed hypercalciuria, suggesting increased mobilization of calcium rather than renal retention. In vitro coagulation studies revealed concentration dependent prolongation of the partial thromboplastin time and thrombin time. No complete or partial responses were seen. However mixed response or biochemical response (reduction in serum lactic dehydrogenase) were seen in 5 patients with melanoma or renal cancer. Due to unacceptable toxicity at the 11,000 mg/m2 daily dose level, Carbetimer 8500 mg/m2 is the recommended dose for a 5-day treatment schedule every 28 days. Special attention should be directed toward possible activity against melanoma and renal cancer.
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PMID:Phase I trial of a 5-day course of carbetimer. 238 16

The pathophysiology and treatment of acute subarachnoid hemorrhage (SAH) are reviewed. SAH occurs when blood is released into the subarachnoid space, which surrounds the brain and spinal cord. Symptoms of SAH include severe headache, nausea, vomiting, neck pain, nuchal rigidity, and photophobia. The initial hemorrhage is fatal in 20-30% of patients. Complications of SAH include rebleeding, hydrocephalus, delayed cerebral ischemia associated with cerebral vasospasm, and seizures. The likelihood of rebleeding is increased by measures that rapidly lower intracranial pressure. The risk of developing hydrocephalus is associated with the volume of blood within the subarachnoid space and ventricular system. Cerebral vasospasm develops in 20-40% of patients, and up to 50% of affected patients die or suffer permanent neurological damage. Seizures occur in 5-15% of patients with SAH. Radiologic procedures form the foundation for the diagnosis of SAH. The most commonly used rating scale classifies the severity of SAH based on the clinical presentation of the patient. Surgery is the definitive treatment for the prevention of rebleeding. Hydrocephalus can only be treated surgically, most commonly by insertion of a drain. The only measures proved to be effective for treatment of delayed cerebral ischemia are volume expansion and the induction of hypertension. The calcium-channel blocker nimodipine was recently approved for treatment of arterial spasm in SAH. Intravenous nicardipine is also being studied for the same indication. These agents may improve clinical outcome substantially by limiting fixed neurological deficits. To prevent seizures, prophylactic antiepileptic therapy with phenytoin sodium is generally accepted. The SAH complications of rebleeding, hydrocephalus, delayed cerebral ischemia, and seizures are managed by surgical, drug, and fluid therapy.
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PMID:Pathophysiology and treatment of subarachnoid hemorrhage. 240 1

In this informal initial study, four female patients with intractable chronic abdominal pain, daily nausea, intermittent vomiting, and altered stool habits due to "functional" disease were investigated. A gonadotropin-releasing hormone (GnRH) analog agonist, leuprolide acetate (Lupron) [D-leu6, Desgly-NH2(10), Proethylamide9], was administered once daily (0.5 mg subcutaneously) for three months. At the end of the three-month period, three subjects were symptom-free and the fourth experienced only mild and intermittent pain. The leuprolide regimen was continued for an additional three months, and estrogen (0.625 mg orally) and calcium (1000 mg orally) were given daily to prevent osteoporosis. The patients remained symptom-free. A challenge with progesterone then induced recurrence of mild symptoms in each subject. Withdrawing leuprolide induced the baseline symptoms in all patients within three to five days. This regimen has now been continued for up to 15 months, and all four patients have remained generally symptom-free. Progesterone has also been given every three months to induce menses. A fifth patient, with Roux-en-Y syndrome, has also been treated with leuprolide. She is symptom-free after six months and has gained weight. In this initial observation period in patients with severe functional (neuromuscular) bowel disease, the GnRH analog agonist leuprolide controlled pain, nausea, and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Debilitating "functional" bowel disease controlled by leuprolide acetate, gonadotropin-releasing hormone (GnRH) analog. 249 61

In a multicentre open trial involving 229 investigators, cicletanine, a new antihypertensive agent, was administered orally in doses of 50 to 100 mg/day either alone (1,238 patients) or combined with another drug (430 patients). In this second group of patients with essential hypertension whose BP had not been normalized by a beta-blocker (n = 157), a calcium inhibitor (n = 67), an angiotensin-converting enzyme inhibitor (n = 134) or an alpha-blocker (n = 7), cicletanine normalized BP (less than 160/95 mmHg) in 48.8% of the patients and significantly lowered BP values which fell from 177.7 +/- 15.9/103.3 +/- 6.3 mmHg to 157.2 +/- 17.6/88.8 +/- 8.7 mmHg. The addition of cicletanine to treatments with beta-blockers, calcium inhibitors and angiotensin-converting enzyme inhibitors normalized BP in 48%, 52% and 47% of patients respectively. A significant reduction of symptoms was noted, notably as regards headache, dizziness, palpitations, lower limb oedema, asthenia, auditory disorders and dyspnoea. The side-effects reported (headache, dizziness, gastralgia, nausea, pruritus) were minor and non-specific; they accounted for the withdrawal of only 8 patients. The only significant, though moderate, biochemical variations observed were decreases in natremia and cholesterolaemia unconfirmed by qualitative analysis. Altogether, cicletanine proved to be effective and well tolerated when administered in combination with other antihypertensive drugs belonging to three main therapeutic classes.
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PMID:[Antihypertensive effectiveness and tolerance of cicletanine. Results obtained with bitherapy]. 257 67

Bulfield and others found X-linked muscular dystrophic (mdx) mouse by screening C57 BL/10 mice. The serum CK and PK are high in mdx mice, and they develop muscle degeneration 10-15 days after birth. The regeneration is vigorous in mdx mice and almost all the muscle fibers are replaced by regenerated fibers by 60 days after birth. Although mdx mice have been developed as a model for X-linked muscular dystrophy we have found that myotonic bursts are recorded when a glass microelectrode is inserted into the muscle fibers of hemidiaphragm preparations of mdx mice. Insertion myotonia is ceased by addition of the Na channel blocker tetrotoxin. Myotonia is not reduced, nor ceased by lowering the extracellular Ca to 1/15 of the volume of ordinary Tyrode's solution. Calcium antagonist, nicardipine at the dose of 10(-7), and 10(-6)M/L do not reduce myotonic bursts. Higher dose of nicardipine up to 2 x 10(-5)M/L abolished myotonic bursts. These results indicate that myotonic bursts are related to muscle membrane abnormalities, and each action potential occurs through Na channel, but not through Ca channel Higher dose of calcium antagonist can abolish myotonia by affecting Na channel in addition to their primary effects of Ca channel. The clinical effects of the Ca antagonist for myotonia was reported in one study. Since previous medications for myotonia including quinine HCl, procaine amide, diphenylhydantoin, and carbamazepine have some side effects such as tinnitus, headache, nausea, cardiac blocks, and bone marrow suppression, Ca antagonist may be used as a safe therapeutic drug for myotonia.
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PMID:[Intracellular recording of myotonia in mdx mouse and the effect of Ca antagonist in myotonia]. 279 3

Cardinal signs of red mold toxicosis in man and farm animals are vomiting, nausea, diarrhea, and food refusal. The red mold toxicosis has been suggested to be induced by trichothecenes, which are produced by Fusarium fungi. Fusarenon-X (F-X) is one of the trichothecene mycotoxins. The ip injection of F-X to rats causes an expansion of the small intestine and watery diarrhea. In this study, we measured the concentrations of protein, sodium, potassium, and calcium in the serum of rat treated with F-X for the sake of demonstrating the loss of serum protein and the decreases of serum sodium and calcium by F-X. Since it is well known that some diarrheal diseases are due to the increase of cyclic nucleotide level in the intestinal mucosa, we also measured cyclic AMP and cyclic GMP levels in the intestinal mucosa. It was demonstrated that F-X did not increase the cyclic AMP and cyclic GMP levels in the jejunal and the ileal mucosa at 8 and 24 hr after F-X treatment. The results obtained in this work suggest that F-X-induced diarrhea is not mediated by the cyclic nucleotide system.
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PMID:Studies on mechanisms of diarrhea induced by fusarenon-X, a trichothecene mycotoxin from Fusarium species: fusarenon-X-induced diarrhea is not mediated by cyclic nucleotides. 282 46

Safety, tolerance, and pharmacology of 9-beta-methylcarbacyclin calcium (ciprostene calcium) was investigated in healthy male volunteers. This stable prostacyclin analogue was infused intravenously into groups of 12, 11, and three volunteers for three, six, and eight hours, respectively, in doses up to 480 ng/kg/min. Based on the tolerance data obtained, a single-blind, placebo-controlled study was conducted. Seven subjects were infused for 8 hr/d for three days with ciprostene at a maximum dose of 160 ng/kg/min and seven subjects received placebo. One subject from each group did not complete the infusion schedule, and they were not included in the final analysis. During infusion of ciprostene, consistent changes in blood pressure and heart rate did not occur. Most frequent adverse drug reactions consisted of headache, restlessness, nausea, perspiration, flushing, and jaw pain. As compared with placebo, ADP-induced platelet aggregation was inhibited during the infusion period (P = .048). Significant (P = .04) elevations of platelet cyclic AMP were observed in subjects during infusion of ciprostene. Pre- versus postinfusion routine laboratory evaluations, fibrinogen concentration, antiplasmin activity, and plasminogen and template bleeding times remained unchanged. Placebo- and drug-treated subjects had a daily postinfusion shortening of euglobulin clot lysis time (ECLT). The preinfusion minus postinfusion ECLT for ciprostene subjects on days 2 and 3 (133 and 118 min, respectively) compared with placebo (239 and 217 min) suggest a trend to increased fibrinolytic activity. Based on the outcome of this trial, it is estimated that ciprostene is about 15 times less potent than prostacyclin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerance and pharmacology of ciprostene, a stable epoprostenol (prostacyclin) analogue in humans. 300 77

Forty-seven patients with chronic stable angina pectoris entered a thirteen-week open-label study with a transdermal therapeutic system of nitroglycerin in order to evaluate its clinical efficacy, safety, and patient acceptance. In 19 patients, a beta-blocker and in 17 patients a calcium-channel blocker were continued throughout the study period without alteration of their doses. The study consisted of a two-week run-in period and an eleven-week active drug period. Acute titration was done with nitroglycerin patches on the basis of weekly patient diaries on frequency of angina and sublingual nitroglycerin consumption. Overall, reductions in frequency of angina and in nitroglycerin consumption were statistically significant (p less than 0.05). Adverse reactions were common but tolerable. The reported side effects were headache in 32, skin rash in 18, dizziness in 10, palpitation and itching in 9 each, nausea in 7, flushing in 3, and vomiting in 1 patient. In conclusion, the present study demonstrates that individual dose titration with nitroglycerin patches for obtaining significant antianginal effect is essential. The present therapeutic system is convenient to use and well tolerated and had acceptable side effects in our study population.
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PMID:Clinical experience with a transdermal nitroglycerin system. 310 41

A 45-year-old female manifested lower abdominal fullness and symptoms of hypercalcemia with nausea, vomiting, and thirst. Physical examination showed a right ovarian mass and laboratory data demonstrated hypercalcemia (14.6 mg/dl). The radiographic findings confirmed a right ovarian tumor without any evidence of bone metastasis. Tests revealed that her PTH, nephrogenic urinary cyclic AMP, and 1-25 (OH)2 Vitamin D were not high but that her prostaglandin E2 (PGE2) was elevated. After correction of her calcium elevation with infusion and prednisolone, right oophorectomy with tumor excision was performed. A histological examination of the tumor revealed a mucinous cysto-adenocarcinoma. The postoperative course has been uneventful, with normal calcium and PGE2 values. This case illustrates that hypercalcemia associated with an ovarian carcinoma (Malignancy-associated hypercalcemia) can be mediated by the patient's PGE2 in part.
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PMID:[A case of hypercalcemia with ovarian carcinoma]. 323 Jun 42


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