Filter by keywords:



Filtering documents. Please wait...

1/31. Familial hypokalemic periodic paralysis and wolff-parkinson-white syndrome in pregnancy.

    PURPOSE: To describe the anesthetic and obstetrical management of a pregnant patient with co-existing Familial hypokalemic periodic paralysis (FHPP) and wolff-parkinson-white syndrome (WPW). CLINICAL FEATURES: A 29 yr-old primigravida with FHPP and WPW presented to the antenatal clinic at 18 wk gestation, for consideration of her anesthetic and obstetrical management during labour and delivery. A plan was constructed to avoid the known precipitating factors of FHPP including carbohydrate loading, cold, mental stress and exercise, which could lead to acute attacks of weakness. She presented for induction of labour at 41 wk and three days. An epidural catheter was sited early in labour. The second stage was limited to less than one hour. She had a rotational forceps delivery for which the epidural was extended to provide anesthesia. A healthy male baby was delivered. The patient made an uncomplicated recovery and was discharged home on the second postnatal day. The peripartum potassium was kept within the normal range with intravenous as well as oral potassium supplementation. No arrhythmias were reported. CONCLUSION: Assessment of the patient at an early stage in her pregnancy allowed for a multidisciplinary approach to this patient and her medical problems. A plan was made to avoid known precipitating factors during labour, delivery and the postnatal period well in advance of her date of confinement, leading to a successful outcome for mother and child.
- - - - - - - - - -
ranking = 1
keywords = potassium
(Clic here for more details about this article)

2/31. Hypokalemic thyrotoxic paralysis: a rare cause of tetraparesis with acute onset in Europeans.

    We describe a 21-year-old Italian male affected by hypokalemic tetraparesis with acute onset. In the emergency ward, the patient was agitated, with tachycardia (140/min) and systolic hypertension (180/70 mm Hg). He was not able to flex the lower extremities against a light resistance and furthermore, he was hypotonic and without tendon reflexes. One hour later he developed strength deficit of the upper extremities as well. Biochemical analyses revealed severe hypopotassemia (2.1 meg/l). After administration of 140 meq potassium phosphate, the patient began to improve, and 12 h after the onset he was able to walk normally. Successive investigations documented an undiagnosed case of Graves' disease. Thyrotoxic hypokalemic paralysis has been observed almost only in Asians, however, with this case and others reported, we believe that it should be considered as a cause of muscular paralysis also in Caucasians.
- - - - - - - - - -
ranking = 0.5
keywords = potassium
(Clic here for more details about this article)

3/31. Hypokalaemic periodic paralysis associated with controlled thyrotoxicosis.

    Familial hypokalaemic periodic paralysis is an autosomal dominant muscle disease which has been linked to point mutations in the skeletal muscle L-type calcium channel alpha 1 subunit (alpha 1 s). It consists of muscular weakness episodes due to hypokalaemia caused by intracellular shifting of potassium. We describe the case of a young man of Kurdish origin, with a history of Graves' disease, who was admitted to the emergency room with hypotonic tetraplegia associated with severe hypokalaemia.
- - - - - - - - - -
ranking = 0.5
keywords = potassium
(Clic here for more details about this article)

4/31. propranolol rapidly reverses paralysis, hypokalemia, and hypophosphatemia in thyrotoxic periodic paralysis.

    hypokalemia and hypophosphatemia are commonly encountered during paralysis in patients with thyrotoxic periodic paralysis (TPP) and may contribute to neuromuscular manifestations. potassium and phosphate supplements have been recommended to hasten recovery and prevent cardiopulmonary complications. However, this recommendation has not yet proven efficacious. Hyperadrenergic activity has been implicated in the pathogenesis of TPP. We tested whether nonselective beta-blockers could terminate neuromuscular symptoms rapidly while reducing an intracellular shift of potassium and phosphate. We describe two patients who had an acute attack of TPP with characteristic hypokalemia and hypophosphatemia associated with low urinary potassium and phosphate excretion. After oral propranolol, 3 mg/kg, serum potassium and phosphate concentrations increased promptly in 2 hours in both patients, and there was complete amelioration of paralysis. No rebound hyperkalemia or hyperphosphatemia was detected. Given their efficacy in this pilot study, they should be considered as a first-line therapy for TPP.
- - - - - - - - - -
ranking = 1.5
keywords = potassium
(Clic here for more details about this article)

5/31. Thyrotoxic periodic paralysis in a Caucasian man in treatment for Graves' disease.

    Thyrotoxic periodic paralysis (TPP) is the main secondary form of hypokalemic periodic paralysis and is mostly associated with Graves' disease. Initially diagnosed in Asian countries, TPP has been sporadically reported in different populations of the western world. Increased Na /K( )-ATPase activity seems to be responsible for the marked hypokalemia observed during the transient paralysis attacks. We report on a 35-year-old Italian man without history of hypokalemic periodic paralysis and hyperthyroidism, in treatment for Graves' disease, who suffered episodes of flaccid paralysis even with normal thyroid hormone levels. An insulin-glucose provocation test confirmed our diagnosis. Oral and parenteral potassium reverse the symptoms. Monitoring of thyroid function is also important to prevent further attacks.
- - - - - - - - - -
ranking = 0.5
keywords = potassium
(Clic here for more details about this article)

6/31. Two novel mutations of thiazide-sensitive Na-Cl cotrans porter (TSC) gene in two sporadic Japanese patients with gitelman syndrome.

    gitelman syndrome is a renal disorder characterized by hypokalemia, hypomagnesemia, metabolic alkalosis and hypocalciuria due to the defective tubular reabsorption of magnesium and potassium. This disease is caused by mutations of thiazide-sensitive Na-Cl cotransporter (TSC) gene. gitelman syndrome is usually distinguished from bartter syndrome by the presence of both hypomagnesemia and hypocalciuria. However, a phenotypic overlap is sometimes observed. We encountered two sporadic Japanese patients with gitelman syndrome and analyzed their TSC gene. These patients were diagnosed as gitelman syndrome by the typical clinical findings and biochemical abnormalities, such as mild muscular weakness, periodic paralysis, tetany, metabolic alkalosis, hypomagnesemia and hypocalciuria. In patient 1, a novel two base deletion (del TG at nucleotide 731 and 732) in exon 5 and a two base deletion (del TT at nucleotide 2543 and 2544) in exon 21 previously reported in a Japanese patient were identified. The patient 2 had a missense mutation (L623P), that was also identified in Japanese patients, and a novel in-frame 18 base insertion in exon 6 as a heterozygous state. family analysis of two patients confirmed an autosomal recessive inheritance. In conclusion, we add two new mutations of the TSC gene in Japanese patients with gitelman syndrome. Because the differential diagnosis between bartter syndrome and gitelman syndrome is sometimes difficult, molecular analysis would be a useful diagnostic tool, particularly in unusual cases with phenotypic overlapping.
- - - - - - - - - -
ranking = 0.5
keywords = potassium
(Clic here for more details about this article)

7/31. acetazolamide-induced muscle weakness in hypokalemic periodic paralysis.

    A 46-year-old man with hypokalemic periodic paralysis (HypoPP) and diabetes mellitus (DM) had worsened muscle weakness after acetazolamide (ACZ) treatment. During the paralytic episode, serum potassium levels were reduced, and serum chloride and insulin levels were increased. The data suggested proximal renal tubular acidosis due to ACZ. We determined arterial-venous concentrations of potassium, insulin and glucose across the forearm. Venous potassium levels were markedly reduced. ACZ is thought to potentiate potassium uptake into muscles. Hyperinsulinemia and DM could contribute to ACZ-induced exacerbation in our patient. We should pay more attention to ACZ-treated HypoPP patients with hyperinsulinemia and DM.
- - - - - - - - - -
ranking = 2
keywords = potassium
(Clic here for more details about this article)

8/31. Severe hypokalaemia in a Chinese male.

    A 34-year-old Chinese man developed acute, severe, generalized muscle weakness while mountain climbing. In the Emergency Department that morning, the most striking abnormalities were flaccid paralysis of both upper and lower limbs and a plasma potassium (K ) concentration (P(K)) of 1.7 mmol/l. To explain the basis for this constellation of findings, an imaginary consultation was sought with Professor McCance, the legendary integrative physiologist. Using both a deductive and a quantitative analysis, he illustrated that a simple story of an acute shift of K into cells was not sufficient to explain the patient's hypokalaemia. The clue he used to suspect a large total body deficit of K was a higher than expected rate of K( ) excretion on the initial spot urine (higher than expected ratio of K : creatinine in the urine). This interpretation was supported by the fact that the patient needed a large supplement of K( ) to raise his P(K) to just under 3 mmol/l. It was only after more detailed studies based on urine chemistry that an accurate diagnosis and effective treatment could be instituted. The final question was why one of the hallmarks of the diagnosis of hyperaldosteronism (hypertension) was absent, yet hypokalaemia was so severe.
- - - - - - - - - -
ranking = 0.5
keywords = potassium
(Clic here for more details about this article)

9/31. A mutation in the KCNE3 potassium channel gene is associated with susceptibility to thyrotoxic hypokalemic periodic paralysis.

    Hypokalemic Periodic Paralyses comprise diverse diseases characterized by acute and reversible attacks of severe muscle weakness, associated with low serum potassium. The most common causes are Familial hypokalemic periodic paralysis (FHypoKPP), an autosomal dominant disease, and Thyrotoxic hypokalemic periodic paralysis (THypoKPP), secondary to thyrotoxicosis. Symptoms of paralysis are similar in both diseases, distinguished by thyrotoxicosis present in THypoKPP. FHypoKPP is caused by mutations in ionic channel genes calcium (CACN1AS), sodium (SCN4A) and potassium (KCNE3). Since both diseases are similar, we tested the hypothesis that THypoKPP could carry the same mutations described in FHypoKPP, being the paralysis a genetically conditioned complication of thyrotoxicosis. In 15 patients with THypoKPP, using target-exon PCR, CSGE screening, and direct sequencing, we excluded known mutations in CACN1AS and SCN4A genes. On the other hand, we were able to identify the R83H mutation in the KCNE3 gene in one sporadic case of THypoKPP, a man who had been asymptomatic until developing thyrotoxicosis caused by Graves' disease; we confirmed the disease-causing mutation in 2 of 3 descendants. R83H was recently found in two FHypoKPP unrelated families, in which the mutant decreased outward potassium flux, resulting in a more positive resting membrane potential. We, therefore, identified the first genetic defect in THypoKPP, a mutation in the KCNE3 gene.
- - - - - - - - - -
ranking = 3.5
keywords = potassium
(Clic here for more details about this article)

10/31. Manifestation of thyrotoxic periodic paralysis in two patients with adrenal adenomas and hyperandrogenaemia.

    Hypokalaemic periodic paralysis is a fairly common complication of hyperthyroidism in Asian populations, but a rare event in Caucasians. In the present work we describe 2 male Caucasian patients with thyrotoxic periodic paralysis (TPP) as initial clinical manifestation of Graves' disease. Further diagnostic procedures demonstrated unilateral adrenal adenoma and hyperandrogenaemia in both patients. To date, only few data are available concerning the hormonal status of Caucasian patients with TPP. The constellation of TPP and adrenal adenomas with increased levels of androgens has not been described previously. Since androgens are capable of inducing sodium-potassium ATPase, which is thought to be centrally involved in the pathogenesis of TPP, hyperandrogenaemia may have triggered the manifestation of paralytic attacks in our patients. It may be of interest to focus not only on thyroid dysbalances in patients with TTP but also to investigate other hormonal disturbances.
- - - - - - - - - -
ranking = 0.5
keywords = potassium
(Clic here for more details about this article)
| Next ->


Leave a message about 'Hypokalemic Periodic Paralysis'


We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.