1/31. Hypomagnesaemia.In the management of electrolyte abnormalities along with hypokalaemia and hypocalcaemia, etc, presence of hypomsgenesaemia should be thought of even when serum magnesium is within normal limit as magneium is a predominantly intracellulr ion. Two cases of hypomagnesaemia as one of the factors of electrolyte distrubances are communicated in this write-up.- - - - - - - - - - ranking = 1keywords = long (Clic here for more details about this article) |
2/31. Long QT interval resembling long qt syndrome in a newborn with electrolyte dysbalance.The Q-T interval by electrocardiogram may be prolonged as a congenital or acquired condition. The congenital form, long qt syndrome (LQTS) is an electrical disorder associated with a high mortality rate. However, in newborns, electrolyte abnormalities are one of the most common causes of a long Q-T interval. We describe a newborn with a prolonged Q-T interval (0.55 secs) and abnormal T waves resembling LQTS. In this case, the patient had an electrolyte disturbance which was effectively treated. This case emphasizes the importance of investigating and distinguishing between the congenital and acquired forms of prolonged Q-T intervals.- - - - - - - - - - ranking = 9keywords = long (Clic here for more details about this article) |
3/31. Aminoglycoside-induced reversible tubular dysfunction.Nonoliguric renal insufficiency is a well-known nephrotoxic consequence of aminoglycosides, although reversible tubular damage in the absence of any change in the renal function has been occasionally found. Reported herein are 2 representative cases of a reversible tubular damage due to prolonged aminoglycoside administration: a patient with a Fanconi-like syndrome of proximal tubular dysfunction and a patient with a syndrome of hypokalemic metabolic alkalosis associated with hypomagnesemia.- - - - - - - - - - ranking = 1keywords = long (Clic here for more details about this article) |
4/31. Woman with postpartum ventricular tachycardia and hypomagnesemia.A 28-year-old Japanese woman who had received continuous intravenous infusion of magnesium sulfate from 24 weeks of pregnancy until delivery underwent cesarean section at 30 weeks and gave birth to twins. serum magnesium sharply declined to a subnormal level of 1.5 mg/dL on postpartum day 4. The patient exhibited sinus bradycardia (48 b.p.m.) with intermittent supraventricular contraction on postpartum day 2, intermittent ventricular bigeminy on postpartum day 3, and frequent selfterminated polymorphic ventricular tachycardia on postpartum day 4. The electrocardiogram (ECG) disclosed that the patient had prolonged QTc of 0.45-0.67. Correction of serum magnesium improved ECG findings promptly, resulting in the disappearance of arrhythmias. Hypomagnesemia due to postpartum diuresis may have played a role causing ventricular tachyarrhythmia in this patient.- - - - - - - - - - ranking = 1keywords = long (Clic here for more details about this article) |
5/31. Acquired long qt syndrome and monomorphic ventricular tachycardia after alternative treatment with cesium chloride for brain cancer.Individuals searching for symptomatic relief or a potential cure are increasingly seeking and using nontraditional therapies for their various diseases. Little is known about the potential adverse effects that patients may encounter while undergoing these alternative treatments. cesium chloride is an unregulated agent that has been reported to have antineoplastic properties. cesium chloride is advertised as an alternative agent for many different types of cancers and can be purchased easily on the internet. Recently, QT prolongation and polymorphic ventricular tachycardia were reported in several patients taking cesium chloride as alternative treatment for cancer. We report acquired QT prolongation and sustained monomorphic ventricular tachycardia in a patient who self-initiated and completed a course of cesium chloride as adjunctive treatment for brain cancer.- - - - - - - - - - ranking = 6keywords = long (Clic here for more details about this article) |
6/31. Torsade de pointes and long qt syndrome following major blood transfusion.We report a rare complication following transfusion of a large volume of blood in an adult patient. An electrophysiological disturbance of the cardiac cycle with prolongation of the QT interval developed, which was followed by recurrent episodes of torsade de pointes, a unique form of ventricular tachycardia. The most likely cause of this acquired long qt syndrome was hypomagnesaemia secondary to massive blood transfusion. Treatment with a magnesium infusion restored the QT interval to normal and temporary ventricular pacing prevented further ventricular arrhythmias.- - - - - - - - - - ranking = 6keywords = long (Clic here for more details about this article) |
7/31. Delayed onset of ataxia in a patient with short bowel syndrome: a case of vitamin e deficiency.Chronic gastrointestinal disease can result in nutritional deficiencies that can have a direct effect on the neurologic system. Although acute abnormalities can be corrected, symptoms are rarely reversible. Recognizing the appropriate abnormality is a crucial part of long-term treatment strategies in this population. Because motor and cerebellar symptoms can contribute to poor feeding, aggressive supplementation should begin as soon as symptoms are recognized. We present a patient with delayed onset and progressive hypovitaminosis E and briefly review diagnostic and therapeutic options.- - - - - - - - - - ranking = 1keywords = long (Clic here for more details about this article) |
8/31. Familial hypomagnesemia with hypercalciuria and nephrocalcinosis associated with CLDN16 mutations.Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC), an autosomal recessive renal tubular disorder, is characterized by the impaired tubular reabsorption of magnesium and calcium in the thick ascending limb of the loop of henle and an eventual progression to end-stage renal disease. Recent studies have reported that this disease is caused by mutations in the CLDN16 gene, which encodes the tight junction protein, paracellin-1. Paracellin-1 belongs to the claudin family and regulates the paracellular transport of magnesium and calcium. Here, we report on two Korean siblings with typical clinical features of FHHNC in association with compound heterozygous mutations, G233C and 800delG, in CLDN16. Their parents were asymptomatic heterozygous carriers of the single mutations. This is the first report of FHHNC in korea, and the mutations reported are novel.- - - - - - - - - - ranking = 1keywords = long (Clic here for more details about this article) |
9/31. Gitelman-like syndrome after cisplatin therapy: a case report and literature review.BACKGROUND: cisplatin is a well-known nephrotoxic antineoplastic drug. Chronic hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria is one of the rare complications associated with its use. CASE PRESENTATION: A 42-year-old woman presented with a 20 year-history of hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria after cisplatin-based chemotherapy for ovarian cancer. This patient has had chronic muscle aches and fatigue and has had episodic seizure-like activity and periodic paralysis. Only thirteen other patients with similar electrolyte abnormalities have been described in the literature. This case has the longest follow-up. CONCLUSION: cisplatin can cause permanent nephrotoxicity, including Gitelman-like syndrome. This drug should be considered among the possible causes of chronic unexplained electrolyte disorders.- - - - - - - - - - ranking = 1keywords = long (Clic here for more details about this article) |
10/31. central nervous system magnesium deficiency.The central nervous system concentration of magnesium (Mg ) appears to have a critical level below which neurologic dysfunction occurs. Observations presented suggest that the interchange of the Mg ion between the cerebrospinal fluid, extracellular fluid, and bone is more rapid and dynamic than is usually believed. This is especially so when the hypertrophied parathyroid gland is associated with significant skeletal depletion of Mg as judged by history rather than serum level. Magnesium, much like calcium, has a large presence in bone and has a negative feedback relationship with the parathyroid gland. A decline in central nervous system Mg may occur when the skeletal buffer system orchestrated largely by the parathyroid glands is activated by an increase in serum calcium. Observations in veterinary medicine and obstetrics suggest that the transfer of Mg from the extracellular fluid into bone during mineralization processes may be extensive. If the inhibition of the hypertrophied parathyroid gland is prolonged and the skeletal depletion of Mg extreme, serious neurologic symptoms, including seizures, coma, and death, may occur. noise, excitement, and bodily contact appear to precipitate neurologic symptoms in Mg ( )-deficient human subjects as it has been documented to occur in Mg ( )-deficient experimental animals. The similarity of the acute central nervous system demyelinating syndromes with reactive central nervous system Mg deficiency is reviewed.- - - - - - - - - - ranking = 1keywords = long (Clic here for more details about this article) |
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