Hyperkalemic periodic paralysis aggravated by voltage - gate sodium channel blocker antiepileptic drug?

Hyperkalemic periodic paralysis (hyperkalemic PP) is a rare muscle disease that has onset in infancy or early childhood and is manifested by transient episodes of paralysis. In this case we presented a young male adult with attacks of weakness, after commencement of the antiepileptic drug - Carbamazepine. We hypothesize that Carbamazepine, as voltage-gate sodium channel blocker, aggravated the symptoms of hyperkalemic PP, as sodium channelopathies, in this young-male-patient, trough influence on membrane depolarization.

Biotic patterns of heart rate variation in depressed and psychotic subjects.

This article presents novel quantitative methods to study R to R interval (RRI) series that identify their characteristic pattern of organization, Bios, and their variation in psychiatric illness. In this study twenty-four hour series of RRI were extracted from Holter recordings of healthy subjects (N = 74) and small groups of patients with affective depression or psychosis. These data were analyzed with recurrence and statistical methods. In all subjects, RRI series showed complexes (clusters of recurrences), such as those observed with mathematically-generated biotic series but not in chaotic or random series. RRI series from healthy persons showed diversification (increase in variance with the duration of the series analyzed), novelty (less recurrence isometry than copies randomized by shuffling), causal order (more consecutive isometry than shuffled copies), and asymmetric statistical distribution. These imprints of creative processes are characteristic of mathematical Bios, and are absent in chaos. Bios can be distinguished from random walk series by the nonrandom pattern of the series of differences between heartbeats, as well as by measures of consecutive isometry and of partial autocorrelation. These defining characteristics of Bios are significant signs of health. In comparison with healthy controls, psychiatric patient groups showed more isometry and more consecutive isometry than healthy subjects. Psychiatric patients also showed no diversification. This study highlights the process that produces heart rate variation as being non-stationary and creative (bios, not equilibrium or chaos) and causal (not stochastically generated by the coexistence of multiple factors). These results thus are significant regarding psychiatric health.

The biotic pattern of heartbeat intervals.

The observed pattern of variation in heart rate indicates biotic patterns that change in time as portrayed by the variable morphology of recurrence plots (temporal complexity) as well as by diversification and novelty.

Bios data analyzer.

The Bios Data Analyzer (BDA) is a set of computer programs (CD-ROM, in Sabelli et al., Bios. A Study of Creation, 2005) for new time series analyses that detects and measures creative phenomena, namely diversification, novelty, complexes, nonrandom complexity. We define a process as creative when its time series displays these properties. They are found in heartbeat interval series, the exemplar of bios .just as turbulence is the exemplar of chaos, in many other empirical series (galactic distributions, meteorological, economic and physiological series), in biotic series generated mathematically by the bipolar feedback, and in stochastic noise, but not in chaotic attractors. Differencing, consecutive recurrence and partial autocorrelation indicate nonrandom causation, thereby distinguishing chaos and bios from random and random walk. Embedding plots distinguish causal creative processes (e.g. bios) that include both simple and complex components of variation from stochastic processes (e.g. Brownian noise) that include only complex components, and from chaotic processes that decay from order to randomness as the number of dimensions is increased. Varying bin and dimensionality show that entropy measures symmetry and variety, and that complexity is associated with asymmetry. Trigonometric transformations measure coexisting opposites in time series and demonstrate bipolar, partial, and uncorrelated opposites in empirical processes and bios, supporting the hypothesis that bios is generated by bipolar feedback, a concept which is at variance with standard concepts of polar and complementary opposites.

Effect of high NaCl diet on spontaneous hypertension in a genetic rat model with reduced nephron number.

OBJECTIVE: An inherited reduction in nephron number has been implicated in the development of salt-sensitive hypertension and end stage renal disease. The Munich Wistar Frömter (MWF) rat represents a genetic model with a 30-50% reduction of nephrons compared with normal rats. MWF rats develop spontaneous hypertension and increased urinary albumin excretion (UAE). We addressed the question whether the inherited defect in this model leads to salt-sensitive hypertension. METHODS: At the age of 6 weeks, we started male and female MWF/Fub rats and salt-resistant Lewis (Lew) reference rats on either a normal NaCl (0.2%) or a high NaCl (8%) diet (n = 8, each group). Systolic blood pressure (SBP) and UAE were measured at 14 weeks. RESULTS: Under a normal diet, MWF/Fub rats demonstrated significantly elevated SBP compared to Lew rats both in male (165 +/- 2 versus 133 +/- 3 mmHg, P < 0.0001) and female (156 +/- 3 versus 134 +/- 3 mmHg, P < 0.0001) rats. After high NaCl treatment, SBP was significantly higher in both male and female MWF/Fub rats (+55 mmHg and +36 mmHg, P < 0.0001, respectively) compared with MWF/ Fub under a normal diet UAE was also significantly higher in male and female MWF/Fub rats after high NaCl excess (P < 0.0005, respectively). In contrast, both SBP and UAE remained unchanged in response to high NaCl in Lew rats. CONCLUSIONS: Our findings demonstrate that both the hypertension and UAE are sensitive to high NaCl loading in female and male MWF/Fub rats. Thus, an inborn nephron deficit may lead to salt-sensitive hypertension and renal dysfunction.

[Renal tubular function in children with hypercalciuria]. / Funkcije tubula bubrega kod dece s hiperkalciurijom.

INTRODUCTION: Renal stone disease is commonly due to hypercalciuria [1, 2], which may be assessed either from a 24-hour urinary collection or from the fasting first morning urine. Hypercalciuria during childhood has been defined by a 24-hour calcium excretion greater than 3.5 mg/kg per day and/or calcium to creatinine ratio greater than 0.20 [3]. The alteration in the calcium transporting systems plays a pathogenetic role in promoting hypercalciuria [4, 5]. Since calcium reabsorption along the nephron is intimately related to that of other electrolytes and substances, it can be hypothesized that patients with hypercalciuria may have other renal tubular defects. The aim of the study was to investigate proximal tubular function (tubular reabsorption of sodium, potassium, phosphate and glucose) and distal tubular function (urinary concentrating capacity and acidifying capacity) in children with hypercalciuria. PATIENTS AND METHODS: Two groups of children were studied: hypercalciuric group included 23 children with hypercalciuria (10 males, aged 11.9 +/- 4.1 years), of whom 6 with nephrolithiasis, and control group included 42 healthy children (20 males, aged 11.2 +/- 3.8 years). All subjects had normal serum values for calcium, sodium, potassium, phosphate and glucose, as well as normal renal function. The urinary excretion of calcium, sodium, potassium, phosphate, glucose and creatinine was measured in a 24-hour urine specimen by standard laboratory methods. Urine osmolality and urinary specific gravity were measured following 12-hour water-deprivation test. A short ammonium chloride loading test was performed in 3 patients with urinary pH above 5.5. The fractional excretion of sodium, tubular phosphate reabsorption and renal threshold phosphate concentration were calculated according to standard formula. Statistical analysis was performed using the t-test and analysis of variance (ANOVA). Kruskal-Wallis method was used to compare urinary phosphate excretion between two groups. RESULTS: Table 1 summarizes urinary excretion of electrolytes in children with hypercalciuria compared with healthy controls. We found that urinary sodium excretion was significantly increased in patients with hypercalciuria when compared with controls (p < 0.05). Urinary phosphate excretion was significantly higher in patients with hypercalciuria in comparison to controls, and this was accompanied by a significant lowering of the tubular phosphate reabsorptive threshold (p < 0.05). Urinary potassium excretion tended to be lower, although not significantly, in the hypercalciuric children than in normal subjects. Table 2 shows the mean values +/- standard deviation of urinary specific gravity, urinary osmolality and urinary pH. Urinary specific gravity mean value was significantly lower in patients with hypercalciuria in comparison to controls (p < 0.05). Urinary pH was found below 5.5 in all patients. Glycosuria was detected in 3 patients (13.3%). As shown in Graph. 1, a significant correlation between the urinary excretion of calcium and sodium was demonstrated in both groups of children (r = 0.29; p < 0.01). DISCUSSION: The present study shows that children with hypercalciuria have significantly higher urinary sodium and urinary phosphate excretion in comparison to controls, while urinary potassium excretion is normal in both groups of children. According to some recent reports [6-9], these findings may indicated defects of the renal tubular transport of sodium and phosphate which may be interpreted as a cause or a consequence of the alteration of the calcium transporting system. Defects in both proximal and distal renal tubular functions have been demonstrated in patients with nephrolithiasis, particularly those with hypercalciuria. Proximal renal tubular defects include defects in sodium, fluid, phosphate and glucose reabsorption, which were evident also in our patients. (ABSTRACT TRUNCATED)

[Sodium excretion in children with lithogenic disorders]. / Izlucivanje natrijuma kod dece s litogenim poremecajima.

INTRODUCTION: The causes of nephrolithisis are multifactorial and have not yet been enough investigated [1]. Hypercalciuria is the most common cause of metabolic nephrolithiasis [2-4]. Close relationship between urinary calcium and urinary sodium has been a subject of reported observations in the past, showing that high urinary sodium is associated with high urinary calcium [5-7]. Hyperoxaluria, hyperuricosuria and cystinuria are also metabolic disorders that can lead to nephrolithiasis. Recent studies have indicated that urinary elimination of cystine is influenced by urinary sodium excretion. Based on these observations it has been hypothesised that patients with high urinary sodium excretion are at high risk of urinary stone disease. The purpose of the study was to investigate sodium excretion in a 24-hour urine and first morning urine collected from children with lithogenic metabolic abnormalities (hypercalciuria, hyperoxaluria, hyperuricosuria, cystinuria), both with nephrolithiasis and without it, in order to determine its significance in urinary calculi formation. PATIENTS AND METHODS: Urinary sodium excretion was investigated in 2 groups of children: patients with lithogenic metabolic abnormalities, but without urinary stone disease (L group) and patients with nephrolithiasis (C group). Both groups were divided into 2 subgroups: patients with hypercalciuria and without it. There were 22 patients in group L (mean age 11.97 +/- 4.13 years), of whom 17 formed a hypercalciuric subgroup and 5 formed a non-hypercalciuric subgroup (3 patients with hyperuricosuria and 2 patients with hyperoxaluria). Group C consisted of 21 patients with nephrolithiasis (mean age 12.67 +/- 3.44 years), of whom 6 formed a hypercalciuric subgroup and 15 formed a non-hypercalciuric group (2 patients with cystinuria and 13 patients without lithogenic metabolic abnormalities). Control group consisted of 42 healthy age-matched children. All subjects had a normal renal function. A detailed history and clinical examination were done, and ultrasonography was performed in all patients. A 24-hour urine, first morning urine and serum specimen were analysed for sodium, potassium, calcium, uric acid, urea and creatinine. Fractional excretion of sodium, as well as urinary sodium to creatinin ratio and urinary sodium to potassium ratio, were calculated from the findings. Sodium and potassium levels were determined by flame photometry, calcium was measured by atomic absorption technique (Beckman Atomic Spectrophotometer, Synchron CX-5 model, USA), uric acid by carbonate method and creatinine by Jaffe technique. Cystine and dibasic amino acids were quantified by ion chromatography. Urinary oxalate excretion was determined by enzyme spectrophotometry. Hypercalciuria was defined by 24-hour calcium excretion greater than 3.5 mg/kg per day and/or calcium to creatinine ratio greater than 0.20 [8]. Uric acid excretion was expressed as uric acid excretion factored for glomerular filtration, according to Stapleton's and Nash's formula [9]. Normal values were lower than 0.57 mg/dl of glomerular filtration rate in 24-hour samples. Mean values were statistically analyzed by Pearson's linear correlation and analysis of variance (ANOVA). RESULTS: Urinary sodium concentration values including urinary sodium to potassium ratios, are shown in Table 1. We found that urinary sodium excretion was significantly increased in patients of both L and C groups when compared with controls (p < 0.05). Further analysis of the subgroups showed that urinary sodium excretion was significantly higher only in patients with hypercalciuria of both L and C groups in comparison to controls (p < 0.05) (Table 2). A significant positive correlation was found between 24-hour urinary sodium to creatinine ratio and urinary calcium to creatinine ratio (r = 0.31; p < 0.001) (Graph 1), as well as between urinary sodium to potassium ratio in 24-hour and first morning urine (r = 0.69; p < 0.001) (Graph 2). (A

[Recurrences of viral hepatitis A]. / Relapsi u toku virusnog hepatitisa A.

The aim of the study was to examine the frequency, severity, persistence and etiology of relapses occurring during the hepatitis A viral infection. Therefore, a prospective study of 910 patients suffering from hepatitis A (HA) was carried out. The clinical examination and determination of glutamyl pyruvic transaminase (GPT) in the serum every 7-14 days till recovery (usually during 6--8 months) were performed. HAV infection was confirmed by detecting anti-HAV IgM in the blood of all the examined by radioimmunoassay. In 876 (93.3%) patients HA had typical clinical features and a monophasic course. All cases made a rapid clinical recovery and liver function tests improved strikingly between 1 and 4 months after the onset of illness. However, in 34 (3.7%) of 910 patients, after an asymptomatic interval of 4--8 weeks, relapsing hepatitis occurred. Mild clinical symptoms: fatigue, myalgia, nausea, epigastric discomfort accompanied by the elevated levels of GPT in the serum were noticed in 11 patients, while 3 of them redeveloped jaundice. In 23 remaining patients relapses of hepatitis were asymptomatic, except for the reappearance of icterus in six cases. The only way to establish the exacerbation of the disease was through the pathological findings of GPT in the serum, which increased 10--60 times above the upper limit of the normal value. While 25 patients had one relapse, in 9 there were two or more relapses, so that hepatitis had a biphasic or polyphasic course. The second relapse was registered 3--6 weeks after the first one disappeared. Through biochemical tests the average values of the GPT were established: 1566 U/L in the acute stage, 107 U/L during the early stage of convalescence and 1016 U/L during the first relapse of hepatitis. After the first relapse and during remission, in 9 patients the average values of GPT in the serum were 84 U/L, while during the second relapse 518 U/L. Clinical signs of relapsing hepatitis disappeared approximately in 4 days, but liver function tests decreased slowly and persisted elevated between 5 and 12 months. A possibility of establishing the etiology of relapsing hepatitis, which has yet remained unknown, is discussed. Anti-HAV IgM were present in all 34 patients during the initial and relapsing phase of hepatitis and in 26 cases in the latter phase of convalescence between 9 and 11 months after the beginning of the disease. Serological tests excluded infection with hepatitis B, cytomegalovirus and Epstein-Barr virus. With a great probability other infections and toxic agents damaging the liver could have been excluded.(ABSTRACT TRUNCATED AT 400 WORDS)