[Takotsubo syndrome and hyperthyroidism: a case report]. / Síndrome de Takotsubo e hipertiroidismo: a propósito de un caso.

Stress cardiomyopathy, or Takotsubo syndrome, is similar to that of an acute coronary syndrome, with electrocardiographic changes and an increase in troponin levels; however, coronary arteriography typically shows no obstructive lesions. One of the characteristic patterns are regional wall motion abnormalities identified by echocardiography. It has been described in association with thyroid disorders, although the causal mechanism is not clearly established. We present the case of a woman with acute chest pain and electrical and analytical changes. A severe ventricular dysfunction was observed but the coronary tree was free of lesions, all of which was compatible with a stress cardiomyopathy. Hyperthyroidism due to Graves' disease was observed as a trigger. The identification and management of clinical factors that might predispose patients to Takotsubo syndrome or impact on subsequent clinical outcome is mandatory.

[Author Correction: Takotsubo syndrome and hyperthyroidism: a case report]. / Corrección de autores: Síndrome de Takotsubo e hipertiroidismo: a propósito de un caso.

This corrects the authors listed in "Takotsubo syndrome and hyperthyroidism: a case report" published in volume 42(2) pages 215-220, doi: 10.23938/ASSN.0713.

Prognostic value of change in anti-thyroglobulin antibodies after thyroidectomy in patients with papillary thyroid carcinoma.

PURPOSE: Anti-thyroglobulin antibodies (TgAb) can be used as a surrogate tumor marker in the follow-up of papillary thyroid carcinoma (PTC). We try to determine if the change in TgAb levels in the first post-operative year is a good predictor of persistence/recurrence risk in TgAb-positive PTC patients. METHODS/PATIENTS: 105 patients with PTC who underwent thyroidectomy between 1988 and 2014 were enrolled. We calculated the percentage of change in TgAb levels with the first measurement at 1-2 months after surgery and the second one at 12-14 months. RESULTS: TgAb negativization was observed in 29 patients (27.6%), a decrease of more than 50% was observed in 57 patients (54.3%), less than 50% in 12 patients (11.4%) and in 7 patients (6.7%) the TgAb level had increased. The percentage of persistence/recurrence was 0, 8.8, 16.7 and 71.4% in each group, respectively (p < 0.001). In the multivariate analysis, only the percentage of change in TgAb showed a significant association with the risk of persistence/recurrence, regardless of other factors such as age, size and TNM stages. CONCLUSIONS: Changes in TgAb levels in the first year after surgery can predict the risk of persistence/recurrence of TgAb-positive PTC patients. Patients who achieved negativization of TgAb presented an excellent prognosis.

Erythrocyte anion exchanger activity and intracellular pH in essential hypertension.

The present study was designed to examine the activity of the sodium-independent chloride-bicarbonate anion exchanger and the sodium-proton exchanger in erythrocytes of 30 normotensive and 35 hypertensive subjects and its relation to the previously reported decrease in erythrocyte pH. Erythrocyte cytosolic pH was measured by the pH-sensitive fluorescent probe 2'-7'-bis(2-carboxyethyl)- 5(6)-carboxyfluorescein. The activity of the anion exchanger was determined by acidifying cell pH and measuring the initial rate of the net sodium-independent, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid-sensitive, bicarbonate influx driven by an outward proton gradient. The activity of the sodium-proton exchanger was determined by acidifying cell pH and measuring the initial rate of the net sodium-dependent proton efflux driven by an outward proton gradient. The activity of the anion exchanger was higher in hypertensive than control individuals (18,863 +/- 1081 vs 15,629 +/- 897 mmol/L cells per hour, P < .05). The activity of the sodium-proton exchanger was higher in hypertensive than control individuals (301 +/- 45 vs 162 +/- 23 mmol/L cells per hour, P < .005). Basal erythrocyte pH was lower in hypertensive than control individuals (7.27 +/- 0.02 vs 7.33 +/- 0.01, mean +/- SEM, P < .05). With the 100% confidence (lower) limit of the normotensive population as a cutoff point, a subgroup of 11 hypertensive patients had an abnormally low erythrocyte pH (< 7.19).(ABSTRACT TRUNCATED AT 250 WORDS)

Elevated levels of parathyroid hormone in essential hypertensive patients with increased erythrocyte potassium efflux.

Previous observations suggest that Ca(2+)-dependent K+ efflux is increased in erythrocytes from spontaneously hypertensive rats. On the other hand, it has been reported that hyperparathyroidism induces an increase in Ca(2+)-dependent K+ efflux of human erythrocytes. To investigate whether Ca(2+)-dependent K+ efflux is altered in essential hypertension quinine-sensitive K+ efflux was measured in erythrocytes from 20 normotensive controls and 30 nontreated essential hypertensives. The quinine-sensitive K+ efflux was similar for hypertensive patients (593 +/- 20 mmol/L cells/h) as compared with normotensive controls (532 +/- 34 mmol/L cells/h). Ten hypertensives exhibited values of quinine-sensitive K+ efflux above an upper normal limit of 650 mmol/L cells/h. As compared with controls those patients presented elevated plasma levels of parathyroid hormone (P less than .05). In addition, a positive correlation was found between parathyroid hormone and quinine-sensitive K+ efflux in the above ten hypertensives (R = 0.85, P less than .001). These results suggest that an excess of parathyroid hormone may be involved in the increase of Ca(2+)-dependent K+ efflux present in some essential hypertensive patients.

Rat atrial natriuretic peptide stimulates K+ fluxes in human erythrocytes.

Ouabain- and bumetanide-resistant potassium fluxes were measured in human erythrocytes incubated in a medium containing calcium and a calcium ionophore. Pharmacological concentrations of rat atrial natriuretic peptide stimulated these fluxes. Although human erythrocytes lack atrial natriuretic peptide receptors, our results suggest that the hormone can modify transmembrane K+ movements.

[Atheroembolic disease. Presentation of a case of multisystemic involvement and review of the literature]. / Enfermedad ateroembólica. Presentación de un caso de afectación multisistémica y revisión de la literatura.

The atheroembolic disease is an entity characterized by obstruction of multiple small arteries by cholesterol crystals. The incidence rises steeply with advancing age and following an invasive procedure involving arteries in patients with atherosclerosis. Actually it has a growing interest due to the increased frequency and to the lack of appropriate therapy. In this paper we report a clinical case of multiple system disease secondary to anticoagulant therapy in a 69 years old patient. We review the pathogenesis, clinical features, laboratory dates and pathology of the disease.

Measurement of foveal thickness by optical coherence tomography in adult haemodialysis patients with diabetic nephropathy.

BACKGROUND: Several studies have demonstrated the efficacy of hemodialysis (HD) on macular edema in diabetic patients. OBJECTIVE: To study the effects of a HD session on foveal thickness by optical coherence tomography (OCT) in adult patients with type 2 diabetes mellitus with chronic renal failure (CRF) secondary to stage 5 diabetic nephropathy in HD. PATIENTS AND METHODS: We studied 25 eyes of 14 patients who underwent analytical studies and pre-HD and post-HD OCT. RESULTS: As a group, the foveal thickness did not change after one session of HD in the 25 eyes studied (245.28 ± 52.21 µ versus 240.40 ± 40.25 µ) (p = 0.428) (2% reduction) or correlated with any clinical or laboratory parameters analyzed.When comparing the subgroup of 13 eyes in which the foveal thickness did not change or decreased compared to the subgroup of 12 eyes in which the foveal thickness increased we found that in the first subgroup the bath temperature was significantly higher (37.00 ± 0.00 versus 36.29 ° C, p = 0.008) and the conductivity was significantly lower (14.00 ± 0.00 versus 14.29 ± 0.10 mS / cm, p = 0.030). CONCLUSION: HD may modify the foveal retinal thickness as a function of changing parameters such as bath temperature and conductivity.

Increased duration of simulated childbirth injuries results in increased time to recovery.

Stress urinary incontinence (SUI) development is strongly correlated with vaginal childbirth, particularly increased duration of the second stage of labor. However, the mechanisms of pelvic floor injury leading to SUI are largely unknown. The aim of this study was to determine the effects of increased duration of vaginal distension (VD) on voiding cystometry, leak point pressure testing, and histology. Sixty-nine virgin female rats underwent VD with an inflated balloon for either 1 or 4 h, while 33 age-matched rats were sham-VD controls. Conscious cystometry, leak point pressure testing, and histopathology were determined 4 days, 10 days, and 6 wk after VD. The increase in abdominal pressure to leakage (LPP) during leak point pressure testing was significantly decreased in both distension groups 4 days after distension, indicative of short-term decreased urethral resistance. Ten days after VD, LPP was significantly decreased in the 4-h but not the 1-h distension group, indicating that a longer recovery time is needed after longer distension duration. Six weeks after VD, LPP was not significantly different from sham-VD values, indicating a return toward normal urethral resistance. In contrast, 6 wk after VD of either duration, the distended rats had not undergone the same increase in voided volume as the sham-VD group, suggesting that some effects of VD do not resolve within 6 wk. Both VD groups demonstrated histopathological evidence of acute injuries and tissue remodeling. In conclusion, this experiment suggests pressure-induced hypoxia as a possible mechanism of injury in vaginal delivery.

[Effect of cyclic nucleotides on calcium dependent K+ channels, in human erythrocytes]. / Efectos de los nucleótidos cíclicos sobre los canales de K+ dependientes de calcio, en el eritrocito humano.

K+ efflux has been analyzed in human erythrocytes incubated in a K+ free medium containing ouabain, bumetanide, CaCl2, and the Ca2+ ionophore A23187. In these conditions, a K+ efflux, which is exponentially dependent on the concentration of A23187 present in the medium, has been observed. This flux is almost completely abolished by either quinine or EGTA, so that, the above K+ efflux has been considered Ca2+ dependent. The effects of cAMP, and cGMP, have been tested on this flux. Ca2+ dependent K+ efflux decreases in presence of millimolar concentrations of cAMP in the medium. The addition of methyl-isobutyl-xanthine to the incubation medium containing cAMP enhances the inhibitory effect of this compound. cGMP also inhibits the Ca2+ dependent K+ efflux. Our results suggest that cyclic nucleotides may modulate the activation of Ca2+ dependent K+ channels in human erythrocytes.

Renal siderosis in patients with heart-valve prostheses: clinical implications.

We have studied the clinical and morphological implications of renal siderosis, reviewing the autopsy protocols of 33 patients with valve prostheses in the heart. Seventeen patients had variable amounts of iron in the proximal tubules of the kidney. Renal siderosis was more frequent in women, in patients with longest time of evolution from the surgical procedure, and in patients with two valve prostheses. Histologically three degrees of renal siderosis may be defined: mild and moderate degrees of iron overload do not alter the kidney architecture, but kidneys, with severe siderosis show tubular atrophy and interstitial fibrosis. Episodes of acute renal failure (ARF) were more frequent in patients with more pronounced iron deposits, especially in the premortem stages. We conclude that renal siderosis may damage the proximal tubular epithelium of patients with valve prostheses in the heart; patients with renal overload of iron are more susceptible to episodes of ARF.

Loss of renal graft due to recurrent IgA nephropathy with rapidly progressive course: an unusual clinical evolution.

Recurrence of IgA nephropathy following renal transplantation has been described in 40-50% of patients, and it usually has a good outcome. We present the case of a 54-year-old man with IgA nephropathy who developed terminal renal failure in 1985, 3 years after the onset of the disease. In March 1986 he received a cadaveric renal allograft following treatment with ciclosporin and steroids. Eight months later he developed microhaematuria and proteinuria and 10 months later he developed acute nephritic syndrome and rapidly progressive renal failure. Renal biopsy disclosed an IgA nephropathy with epithelial crescents in 60% of glomeruli. Treatment with plasma exchange and cyclophosphamide was unsuccessful and the patient lost his graft and returned to regular haemodialysis 15 months after renal transplantation.