This prospective study was designed to evaluate whether early changes in actin-free Gc-globulin levels were associated with complications and outcomes and to identify factors associated with persistent low actin-free Gc-globulin levels in acute liver failure (ALF). Thirty-two consecutive ALF patients admitted from October 2011 to December 2012 were followed up until death or complete recovery. All had serum actin-free Gc-globulin estimation at admission and at day three or expiry. Logistic regression analysis was performed to identify independent predictors of mortality. A receiver operating characteristic curve analysis was also performed. Nonsurvivors had significantly lower median actin-free Gc-globulin levels than survivors (87.32 vs 180 mg/L; P < 0.001). A receiver operating characteristic curve analysis revealed an area under curve (AUC) of 0.771 and showed that serum actin-free Gc-globulin level of ≤124 mg/L would predict mortality with 92% sensitivity and 71.4% specificity. Patients with lower serum actin-free Gc-globulin levels and decreasing trend in serum actin-free Gc-globulin levels were found to have more mortality and developed more complications. Logistic regression analysis showed that serum actin-free Gc-globulin, total leucocyte count and serum creatinine at admission were independent predictors of mortality. Incorporating these variables, a score predicting mortality risk at admission was derived. The scoring system was compared to MELD score and King's College Criteria as individual predictor of mortality. Serum actin-free Gc-globulin level at presentation is predictive of outcome and can be used for risk stratification. Its persistent low-level predicts mortality and is correlated with various complications.
Cirrhotic or hepatic myelopathy is a rare neurological complication of chronic liver disease usually seen in adults and presents as a progressive pure motor spastic paraparesis which is usually associated with overt liver failure and a surgical or spontaneous systemic portocaval shunt. We describe the development of progressive spastic paraparesis, in a patient with alcoholic cirrhosis with portal hypertension and portal colopathy who presented with the first episode of hepatic encephalopathy. The patient had not undergone any shunt procedure.
Any patient from a tuberculosis (TB) endemic area such as India with classical clinical features of fever, weight loss and lymphadenopathy, making a diagnosis of Kikuchi's disease (KD) prior to waiting for the 6-week culture is not appropriate. KD or histiocytic necrotising lymphadenitis is a rare self-limiting cervical lymphadenitis, often a diagnosis of exclusion. One needs to exclude TB, sarcodosis, lymphoma and autoimmune diseases to make such a diagnosis. The patient here with classical clinical presentation of TB with lymph node biopsy mimicking KD (biopsy and immunohistochemistry) posed a big diagnostic dilemma. However, culture of the biopsied lymphatic tissue was confirmed to be mycobacterium TB after the 6th week of incubation. The patient was treated with antitubercular drugs initially, and later, steroid was added in view of his persistent symptoms and he responded. One should wait for the tissue culture report to confirm or exclude the diagnosis of TB. Exclusion should not be based only on laboratory criteria. Histopathogically, TB can mimic any other granulomatous disorder.
| CASE REPORTA 57-year-old man, patient with an old anterior wall myocardial infarction and left ventricular ejection fraction of 0.3, developed episodes of paroxysmal palpitations over the last 6 months. These selflimited episodes were often accompanied by presyncope and severe light-headedness. A 24-hour Holter monitoring showed four salvos of short-lived broad QRS tachycardia. He was referred for an electrophysiologic study. | Electrophysiologic studyThe baseline tracing during sinus rhythm showed intervals within the normal range (PA = 32, AH = 78, HV = 55, QRS = 92 ms).During programmed ventricular stimulation, a wide complex nonsustained tachycardia (cycle length of 220 ms) was reproducibly induced with two extra stimuli delivered at the right ventricular apex. Five to ten seconds later, the broad QRS tachycardia transitioned to a slower narrow QRS complex tachycardia, with a cycle length of 335 ms (Figures 1 and 2A). During narrow QRS tachycardia, the sixth beat was a premature beat with left bundle branch-like morphology. What are the mechanisms of both tachycardias? 2 | COMMENTARY The narrow complex tachycardia cycle length diminished over the first 10 seconds, making it difficult to make any assumption regarding advancement of activation by the ventricular premature beat. The QRS complex during narrow QRS tachycardia shows left axis deviation.There was only intermittent ventriculoatrial conduction during the broad QRS tachycardia (Figure 2A), as evidenced by the initial 2 HA times being much shorter than the relatively constant HA time during narrow QRS tachycardia. The narrow QRS tachycardia showed a clear simultaneous atrial and ventricular activation, consistent with slow-fast atrioventricular nodal reentrant tachycardia (AVNRT); the unlikely differential diagnosis of an atrial tachycardia with a long atrioventricular interval.The broad QRS tachycardia without preceding His bundle potential and AV dissociation would invariably be ventricular tachycardia (VT). Very rarely, this could also be seen with a nodoventricular pathway reentry. Antidromic nodoventricular tachycardia circuit does not include the atrium; however, the retrograde arm is the AV node and His-Purkinje system. As shown in Figure 2B, there is ventricle-His bundle potential dissociation after the first two ventricular electrograms (constant VH interval), which makes antidromic nodoventricular pathway reentry untenable.
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