Cases reported "potassium deficiency"

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1/11. Influence of severe potassium depletion and subsequent repletion with potassium on muscle electrolytes, metabolites and amino acids in man.

    1. Two women with severe hypokalaemic alkalosis were investigated by means of muscle biopsy before and at the end of 2 and 3 weeks respectively of intense therapy with potassium chloride. 2. The muscle biopsy material was analysed for water, electrolytes, adenine nucleotides, phosphocreatine, free creatine, pyruvate, lactate, glycogen and free amino acids. The extra- and intra-cellular distribution of water, electrolytes and amino acids was calculated by the chloride method. 3. Both patients showed a marked loss of intracellular potassium and an increase in intracellular sodium concentration. The muscle magnesium content was also slightly decreased. After repletion with potassium chloride, muscle sodium and potassium became normal. 4. The contents of creatine phosphate, ATP, ADP, AMP, lactate and pyruvate were within normal limits, but the phosphocreatine/total creatine ratio was reduced. After repletion, a small change in the apparent creatine-phosphokinase equilibrium had occurred, suggesting a minor increase in intracellular pH. 5. The concentrations of the basic amino acids, lysine, arginine and ornithine were increased far above normal. The intracellular accumulation of arginine was much higher than the increase in lysine concentration and histidine concentration was normal. This differs from findings in potassium-depleted rats, where the intracellular lysine concentration is much higher than arginine concentration and histidine is high as well. After potassium repletion the intracellular concentration of ornithine, lysine and arginine became normal in one case and decreased considerable in the other. An increased intracellular concentration of glutamate and glutamine was also observed after potassium repletion. ( info)

2/11. Thyrotoxic periodic paralysis: an unusual presentation of weakness.

    Thyrotoxic periodic paralysis is a rare endocrine disorder seen predominantly in men of Asian origin. The case is reported of a patient who presented to the accident and emergency department with sudden onset of weakness of his lower limbs. Hypokalaemia was identified and treated with resolution of symptoms. Additional tests identified the patient as being thyrotoxic. He was treated with oral antithyroid drugs. It is important to consider the diagnosis of thyrotoxic periodic paralysis in patients presenting with acute onset of weakness. The report discusses the epidemiology, presentation, treatment, and complications of this condition. ( info)

3/11. A primary sjogren's syndrome patient with distal renal tubular acidosis, who presented with symptoms of hypokalemic periodic paralysis: Report of a case study and review of the literature.

    Although renal tubular acidosis (RTA), secondary to autoimmune interstitial nephritis, develops in a large proportion of patients with sjogren's syndrome (SS), most of the subjects are asymptomatic. Here, we shall present a 39-year-old female patient who came to us with hypokalemic periodic paralysis (HPP), and who was later diagnosed with distal RTA. The patient, who had xerostomia and xerophthalmia for a long period of time, was diagnosed with primary SS from serologic and histologic findings. The patient recovered by being prescribed potassium replacement therapy. Although renal biopsy was not performed, corticosteroids were administered because HPP indicated severe interstitial nephritis. HPP did not reoccur during a 2-year follow-up period. We also review cases with SS-related distal RTA and HPP. ( info)

4/11. Acute muscle weakness owing to severe hypokalaemia resulting from dietary insufficiency: case report.

    Acute muscle weakness with severe hypokalaemia is not uncommon in adults but is rare in children. An 11-month-old girl presented with hypokalaemic paralysis following a 1-month insufficiency of dietary potassium. ( info)

5/11. Hypomagnesemia-induced cardiomyopathy.

    Magnesium is the fourth most abundant cation in the body and the second most plentiful intracellularly. Magnesium is crucial to mitochondrial integrity, oxidative phosphorylation, protein synthesis, nucleic acid stability, membrane permeability, and neuro-muscular excitability. In addition, magnesium deficiency induces other electrolyte disturbances including hypocalcemia, hypokalemia, and hypophosphatemia. Because it is not routinely measured, many physicians fail to remember the significance of this element. Reported here is a patient with bulimia who presented with a magnesium deficiency which resulted in her refractory and eventually fatal cardiomyopathy. The cardiac pathophysiology of hypomagnesemia, hypokalemia, hypocalcemia and hypophosphatemia is reviewed and correlated with the clinical and pathological findings. ( info)

6/11. Rapid regression of renal medullary granular change during reversal of potassium depletion nephropathy.

    Structural changes were studied on the kidney of a potassium-depleted man and on rat kidneys during potassium depletion and repletion. light and electron microscopy revealed rapid disappearance of intracytoplasmic granules in the renomedullary cells after potassium repletion in our patient as well as in rats. In potassium-depleted rats a series of ultrastructural changes, which were similar to those observed in the human kidney were seen with potassium repletion. Most of the granules were reduced in size and number, with loss of internal structure, shrinkage and condensation of their contents, and were almost totally eliminated by 72 h of potassium repletion. In some endothelial and interstitial cells, the granules were seen to be in the process of being extruded through an area of gap in the plasma membrane. The results indicate that most of the intracytoplasmic granules in the renal medulla rapidly disappeared by intracytoplasmic digestion and the rest of them were probably eliminated by exocytosis during reversal of potassium depletion nephropathy in man and rats. ( info)

7/11. Rapid progression of oxalosis-induced cardiomyopathy despite adequate haemodialysis.

    Crystals of calcium oxalate (CaC2O4) were found at autopsy in the heart of a patient who, over a period of 11 months, appeared to receive adequate haemodialysis and yet died of rapidly progressive heart failure. calcium oxalate crystals were not present in the kidneys which had been removed at the time of commencing haemodialysis. No secondary cause of oxalosis was evident. X-ray fluorescence analysis of the heart tissue revealed, as well as large amounts of calcium, excess strontium and markedly reduced amounts of potassium and rubidium. ( info)

8/11. Antacid-induced hypophosphatemia: an unusual cause of "pseudo-myopathy".

    A 69 year old man presented with painful proximal muscle weakness which clinically simulated polymyositis. Further evaluation revealed normal muscle enzymes and hypophosphatemia which resulted from unsuspected antacid abuse. "Pseudo-myopathy" is one example of the myriad of rheumatic diseases which may be mimicked by hypophosphatemia. ( info)

9/11. Improvement of growth hormone response to stimulation in primary aldosteronism with correction of potassium deficiency.

    Potassium depletion frequently occurs in primary aldosteronism and has been implicated as the cause of the impaired carbohydrate tolerance frequently associated with this syndrome. Glucose, insulin, and growth hormone regulation were studied in a 42-yr-old, male patient with an aldosterone-secreting adenoma when the patient was potassium-depleted and again after potassium repletion. Potassium repletion was documented by serial body potassium measurements, with an increase in body potassium from 2400 mEq to 2850 mEq after 400 mg spironolactone and 80 mEq supplemental potassium chloride were administered daily for 7 days. Potassium repletion resulted in improvement of the patient's glucose tolerance test, with a decrease in the peak glucose level from 184 mg/100ml to 130 mg/100ml and an increase in the peak insulin level from 46 muU/ml to 85 muU/ml. Intravenous administration of arginine resulted in a subnormal insulin response of 28 muU/ml in the base-line test and an increase to 59 muU/ml after potassium stores were repleted. growth hormone response to arginine infusion was also initially minimal at 12.5 ng/ml, increasing markedly to 26 ng/ml after potassium replenishment. insulin-induced hypoglycemia resulted in a depressed growth hormone response of 8 ng/ml when the patient was potassium-deficient, but a normal response of 30 ng/ml after potassium repletion. These observations demonstrate that impairment of both insulin and growth hormone responses to stimulation occur in primary aldosteronism with potassium depletion. These abnormalities may be reversed by potassium repletion. ( info)

10/11. Improvement in lacrimal and salivary secretions after alkali therapy in sjogren's syndrome with renal tubular acidosis.

    A patient with sjogren's syndrome developed renal tubular acidosis which led to systemic acidosis and potassium depletion. Treatment with Shohl's solution and potassium supplements was followed by subjective improvement in tear flow, salivary flow, and by disappearance of bronchitic symptoms. Detailed objective assessments were then made during the next year, twice on treatment and twice without. These confirmed the subjective impression of improvement. ( info)
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