1/26. Primary hypomagnesemia caused by isolated magnesium malabsorption: atypical case in adult.Isolated magnesium malabsorption is a rare disorder, which bas been described in no more than 30 patients worldwide. patients with this disorder typically present with convulsion and diarrhea in early infancy. Hypomagnesemia and hypocalcemia were found in a 35-year-old man with muscle cramps, who bad been diagnosed as primary hypoparathyroidism. Oral magnesium therapy corrected the low serum calcium, magnesium and parathyroid hormone levels. We report an atypical case of isolated magnesium malabsorption in an adult.- - - - - - - - - - ranking = 1keywords = muscle cramp, cramp, muscle (Clic here for more details about this article) |
2/26. Transient posterior encephalopathy induced by chemotherapy in children.The cases of three children, 16, 12, and 12 years of age, who suffered sudden confusional state and cortical blindness lasting 12 to 30 minutes while under treatment with high-dose methotrexate, cyclophosphamide, and dactinomycin for a lower limb osteosarcoma are reported. Transient neuropsychologic deficits arose after the acute phase of treatment: left hemispatial neglect and constructive apraxia (Patient 1); constructive apraxia (Patient 2); and constructive apraxia and alexia without aphasia (Patient 3). The three patients recovered completely from all their deficits within the time frame of 3 hours to 2 weeks. Arterial hypertension and hypomagnesemia were found during the acute phase in all patients. In patients 2 and 3, magnetic resonance imaging revealed increased parieto-occipital T(2) signal involving gray and white matter. In patients 1 and 2, HmPAO-SPECT revealed parieto-occipital hypoperfusion that resolved a few days later. The alterations detected by neuroimaging were concurrent with the appearance and disappearance of the clinical symptoms. Such transient acute episodes have been named occipital-parietal encephalopathy. On the basis of our clinical, laboratory, and neuroimaging findings, an explanation for the origin of this syndrome, a migrainelike mechanism, triggered by chemotherapy-induced hypomagnesemia, is proposed.- - - - - - - - - - ranking = 2.5100416917334E-5keywords = limb (Clic here for more details about this article) |
3/26. Latent tetany and anxiety, marginal magnesium deficit, and normocalcemia.The identification of marginal magnesium deficit, such as we have detected in a patient with anxiety, depression, and psychomatic complaints, is a difficult diagnostic problem. electromyography of a limb, rendered acutely ischemic either just before or after hyperventilation, can elicit latent tetany in this condition, as well as in calcium deficiency. We have demonstrated iterative electrical activity in our patient, whose magnesium deficit is attributable to renal wasting of magnesium. We have elicited similar patterns in several other patients, who had marginally low serum magnesium and who also exhibited weakness, anxiety, and psychosomatic disorders. This preliminary report suggests the need for further consideration of the possibility that chronic magnesium-deficit may contribute to the syndrome of latent tetany, psychosomatic complaints, and weakness.- - - - - - - - - - ranking = 2.5100416917334E-5keywords = limb (Clic here for more details about this article) |
4/26. The refeeding syndrome and hypophosphatemia.The refeeding syndrome is an underappreciated entity characterized by acute electrolyte derangements--notably hypophosphatemia--that occur during nutritional repletion of patients with significant suboptimal caloric intake. Adverse effects of hypophosphatemia include cardiac failure, muscle weakness, immune dysfunction, and death. hypokalemia and hypomagnesemia commonly complicate refeeding syndrome as well; however, this report briefly reviews the clinical manifestations of refeeding-induced hypophosphatemia.- - - - - - - - - - ranking = 0.00012905403438703keywords = muscle (Clic here for more details about this article) |
5/26. Renal sodium handling study in an atypical case of Bartter's syndrome associated with mitochondriopathy and sensorineural blindness.Bartter's syndrome is a disorder that has been linked to mutations in one of three ion transporter proteins: NKCC2 (type I), ROMK (type II) and CCLNKB (type III), which affects a final common pathway that participates in ion transport by thick ascending limb cells. We present an atypical case of mitochondriopathy combined with tubule functional disturbances compatible with Bartter's syndrome and definitive sensorineural blindness. Our patient had a peculiar clinical presentation with signs of salt and volume depletion, low blood pressure and secondary hyperaldosteronism, associated with hypokalemic metabolic alkalosis, hypocalcemia and severe hypomagnesemia, uncommon in genetic forms of Bartter's syndrome. The enhanced absolute and fractional sodium excretion in our patient compared to volunteers was accompanied by increased post-proximal sodium rejection, suggesting a striking ion transport dysfunction in these nephron segments. These findings lead to the Bartter's syndrome diagnosis, accompanied by a suppose mitochondrial tick ascending loop of henle epithelium dysfunction that may reflect the high energy supplied by mitochondria electron transport chain, required for this nephron segment to maintain normal ion transport.- - - - - - - - - - ranking = 2.5100416917334E-5keywords = limb (Clic here for more details about this article) |
6/26. 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 = 2.5100416917334E-5keywords = limb (Clic here for more details about this article) |
7/26. Cetuximab therapy and symptomatic hypomagnesemia.We report that patients treated with cetuximab, a monoclonal antibody against the epithelial growth factor receptor (EGFR), occasionally develop a magnesium wasting syndrome with inappropriate urinary excretion. We first observed this phenomenon in a 34-year-old male patient with metastatic colorectal cancer who developed profound fatigue and symptomatic hypocalcemia and hypomagnesemia while on cetuximab plus irinotecan therapy. Other medications with the potential to cause magnesium wasting had not been administered. Intravenous magnesium supplementation was required for the duration of cetuximab therapy, but electrolyte abnormalities resolved after discontinuation of treatment. This case prompted review of serum chemistry reports for a consecutive case series of 154 colorectal cancer patients treated with cetuximab. Thirty-four patients (22%) had at least one serum magnesium measurement during cetuximab treatment, and six had grade 3 (< 0.9 mg/dL) and two had grade 4 (< 0.7 mg/dL) hypomagnesemia. Because EGFR is strongly expressed in the kidney, particularly in the ascending limb of the loop of henle where 70% of filtered magnesium is reabsorbed, EGFR blockade may interfere with magnesium transport. Because symptoms may be rapidly ameliorated with supplementation, we suggest that, when fatigue or hypocalcemia is encountered during cetuximab therapy, serum magnesium level be measured and repleted as necessary.- - - - - - - - - - ranking = 2.5100416917334E-5keywords = limb (Clic here for more details about this article) |
8/26. nausea, emesis, and muscle weakness in a pregnant adolescent.BACKGROUND: gitelman syndrome is a rare autosomal recessive disorder that presents in early adulthood with fatigue, muscle cramps and electrolyte abnormalities. CASE: A 17-year-old African-American woman presented at 17 weeks of pregnancy with nausea, emesis, profound lower extremity proximal muscle weakness, hypokalemia, and hypomagnesemia. After a thorough evaluation, Gitelman syndrome was diagnosed. The patient was maintained on high levels of potassium and magnesium supplementation throughout the rest of her pregnancy and delivered a healthy infant. CONCLUSION: In pregnancy, nausea and emesis is most commonly attributed to hyperemesis gravidarum. However, an atypical presentation of these symptoms and/or the coexistence of less common complaints warrant further investigation.- - - - - - - - - - ranking = 1.0006452701719keywords = muscle cramp, cramp, muscle (Clic here for more details about this article) |
9/26. Gitelman's syndrome with mental retardation.A 56-year-old mentally retarded Japanese woman (intelligence quotient: 49) was admitted to our hospital with the chief complaints of headache, dizziness, vomiting, and lower limb paralysis. Laboratory tests showed severe hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria. These findings suggested a diagnosis of Gitelman's syndrome (GS). We examined the thiazide-sensitive Na-Cl cotransporter (TSC) gene for the mutations that can be responsible for Gitelman's syndrome, and confirmed the diagnosis. After potassium and magnesium supplementation, her paralysis improved dramatically. The marriage of her parents was consanguineous. She had nine siblings (all with mental retardation), among whom five had died of unknown causes during childhood. Familial mental retardation has never been detected before in Gitelman's syndrome. Here we report a rare case of Gitelman's syndrome with familial mental retardation.- - - - - - - - - - ranking = 2.5100416917334E-5keywords = limb (Clic here for more details about this article) |
10/26. 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 = 0.00012905403438703keywords = muscle (Clic here for more details about this article) |
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