Disturbance of Consciousness Associated with Hypophosphatemia in a Chronically Alcoholic Patient.

Funabiki, Yasuko; Tatsukawa, Hirotaka; Ashida, Ko; Matsubara, Kazuo; Kubota, Yasushi; Uwatoko, Hirohisa; Kitamura, K

doi:10.2169/internalmedicine.37.958

Cited by 14 publications

(3 citation statements)

References 8 publications

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“…In addition, hypophosphatemia was observed in patients treated with sustained low-effi ciency dialysis (SLED) [5] , resulting in phosphate supplementation 3-4 days after SLED initiation [5,6] . Severe hypophosphatemia has been implicated as a cause of neurological abnormalities including, muscle pain, proximal muscle weakness, rhabdomyolysis, respiratory muscle paralysis, and encephalopathy [7] . Hypophosphatemia may lead to decreased myocardial performance [8] and depressed oxygen release from erythrocyte to peripheral tissue.…”

mentioning

confidence: 99%

Phosphate Kinetics during Different Dialysis Modalities

et al. 2005

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Background: An abnormal serum phosphate concentration is common in acute renal failure patients, with a reported incidence of 65–80%. Phosphate removal and kinetics during intermittent hemodialysis (IHD) have been investigated, but there is no information on its kinetics during slow low-efficiency dialysis (SLED) and continuous renal replacement therapy (CRRT). Methods: Eight IHD, 8 SLED, and 10 continuous venovenous hemofiltration (CVVH) patients with a residual renal clearance of <4.0 ml/min were studied during a single treatment to evaluate phosphate removal and kinetics. CVVH was studied the first 24 h after initiation. Dialysis/replacement fluid contained no phosphate. Kt/V, clearance of urea (Ku), inorganic phosphate (Kp) and solute removal was determined by direct dialysate quantification (DDQ). Results: Kp recorded with the three techniques were: IHD, 126.9 ± 18.4 ml/min; SLED, 58.0 ± 15.8 ml/min, and CVVH, 31.5 ± 6.0 ml/min. However, in shorter dialysis treatment the total removal of phosphate was significantly lower than in longer dialysis (IHD, 29.9 ± 7.7 mmol; SLED, 37.6 ± 9.6 mmol; CVVH, 66.7 ± 18.9 mmol, p = 0.001). The duration of treatment is the only factor determining phosphate removal (r = 0.7, p < 0.0001 by linear correlation model). Like IHD, phosphate kinetics during SLED could not be explained by the two-pool kinetic model, and the rebound of phosphate extended beyond 1 h after dialysis. Rebound, however, is less marked than in short dialysis. Conclusion: These results are reliable evidence about amount of phosphate removal and behavior of intradialytic phosphate kinetics in renal failure patients undergoing different dialysis modalities. These data will help clinicians plan phosphate supplementation and treatment intensity.

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Phosphate Kinetics during Different Dialysis Modalities

et al. 2005

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“…Although our patient suffered from substantially reduced serum phosphate the neurological deficits were not reversed by adequate substitution [4,6,15]. In addition, the MRI does not match the lesion patterns of symptomatic hypophosphataemia as reported by Weber et al [14].…”

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confidence: 55%

Use of high-dose cortisone in a patient with Marchiafava-Bignami disease

Gerlach¹,

Oehm²,

Wattchow³

et al. 2003

Journal of Neurology

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“…It is not well known the connection between hypophosphatemia and delirium tremens, (that is because serum inorganic phosphate test is not a routine examination). However, incidence of hypophosphatemia is 30-50% among hospitalized alcoholics (Funabiki et al, 1998). Hypocapnia is the most common cause of hypophosphatemia in hospitalized patients (Ratkovic-Gusic et al, 2004).…”

Section: Adp + P I = Atp + H 2 Omentioning

confidence: 99%

A Probable Etiology and Pathomechanism of Arousal and Anxiety on Cellular Level - Is It the Key for Recovering from Exaggerated Anxiety?

Sikter¹,

Guevara²

2011

Anxiety Disorders

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spiritual status and personality influence our breathing patterns (i.e. breathing rarely, frequently, irregularly) causing pH alteration in the organism. In this manner, the actual cytosolic pH of neurons affects arousal by modifying Ca 2+ conductance, establishing a particular feedback mechanism. The concentration of carbon dioxide can alter the whole organism at the same time because of its extremely high penetrance. If the the concentration thus altered endures for a long time (several hours to a week), the organism starts to "compensate". Stability of extra-and intracellular pH is of high priority. Renal function and various tissue buffer mechanisms (mostly) restore the pH in the intra-and extracellular space, but the concentration of other ions in the cytosol remains altered for longer. The development of the new ionmilieu needs 5-7 days (Gennari et al., 1972). The new ionmilieu of the cells differs from the physiological one (restoration of the original ionmilieu would take another 5-7 days at least). Then chronic hypocapnia or hypercapnia is followed by cascades that alter the whole ionmileu in the cells. They may even alter the neurotransmitter/endocrine status (Dodge et al., 1967; Bailey et al., 2003). Human is a species especially vulnerable to the long-term alteration of carbon dioxide levels. The explanation of this is the fact that humans become hypo-or hypercapnic not only by organic diseases, but by mental disorders as well, and-most importantly-because of learned behaviours. This latter can be dangerous, because it may result in diseases of civilization (Sikter et al., 2009). It is frequently asserted that it is the "stress of life" itself that causes diseases of civilization (induced by "stress-hormones") (Selye, 1956). This statement might be incorrect in that wild animals don't get diseases of civilization, (except if they are living near civilization) even though they are at least as much stressed as human beings are. Wild animals behave and react according to their instincts. According to our viewpoint, in this acute stress response the most important factors to consider are the strong catecholamine (e.g. noradrenaline) rush and acute hypocapnia. During this hyperarousal condition wild animals will fight or flee. This exertion results in increased carbon dioxide production and this in turn restores the biochemistry and physiology. Human hyperarousal stress response is biphasic, but it is also accompanied by hypocapnia. (See below.) In their response to stress human beings differ from wild animals in that their response to stress is more complex. They can mostly restrain their temper, thus often physical activity will not follow hyperarousal stress. Moreover, the enduring hypocapnia would result in ionmovements through membranes, causing metabolic, endocrine alterations, and illnesses because of the alteration of "milieu interieur". Namely, diseases of civilization are caused by the distress evoked by the lack of instinctive reaction to stress. Animals become anxious and depressed after chroni...

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Disturbance of Consciousness Associated with Hypophosphatemia in a Chronically Alcoholic Patient.

Cited by 14 publications

References 8 publications

Phosphate Kinetics during Different Dialysis Modalities

Phosphate Kinetics during Different Dialysis Modalities

Use of high-dose cortisone in a patient with Marchiafava-Bignami disease

A Probable Etiology and Pathomechanism of Arousal and Anxiety on Cellular Level - Is It the Key for Recovering from Exaggerated Anxiety?

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