Troponin I serum concentration: a new marker of left ventricular hypertrophy in patients with essential hypertension.

BACKGROUND: Troponin I, a specific cardiac muscle protein, has proven to be very helpful in detecting myocardial damage in ischemic heart disease. In order to assess if this laboratory test may also characterize some hypertensive subjects with proven cardiac damage, we compared troponin I serum concentrations of a group of patients affected by systemic hypertension and left ventricular hypertrophy (LVH) with troponin I serum concentrations of hypertensive patients without LVH and with normal controls. METHODS: Of 100 hypertensive patients consecutively enrolled in the study, 27 had an increased left ventricular mass by M-mode/two-dimensional echocardiographic examination. Of these, 4 were excluded for significant Holter ST-segment modification. Troponin I was measured in the remaining 23, in 23 age- and sex-matched hypertensive patients with normal left ventricular mass and in 23 normal controls. RESULTS: Troponin I serum concentration was higher than the upper limit of the normal values (0.5 ng/mi) in 12 of the 23 hypertensives with LVH. On the contrary, all hypertensives without LVH and all normal controls had troponin I serum concentration below the upper limit of the normal values. Consequently, the mean troponin I serum value was significantly higher in the group of hypertensive patients with LVH than in the group of patients without LVH (0.88 +/- 0.93 vs 0.27 +/- 0.08 ng/ml, p = 0.002) and in normal controls (0.88 +/- 0.93 vs 0.22 +/- 0.04 ng/ml, p = 0.0001). CONCLUSIONS: Our data indicate that a significant proportion of patients affected by essential hypertension with LVH have slightly elevated troponin I serum concentrations. This test seems to identify two subgroups of hypertensive subjects with LVH, and, considering that troponin I is a marker of myocardial damage, higher serum values probably indicate a more important cardiac involvement in the setting of a hypertensive disease.

Hepatocellular carcinoma complicating liver cirrhosis in type IIIa glycogen storage disease.

Type III glycogen storage disease (GSD III) is an autosomal recessive disorder characterized by the accumulation of abnormal glycogen in the liver and, in most patients, in the muscle. Although liver fibrosis is a well-known consequence of GSD III, until now only eight cases of liver cirrhosis and two cases of hepatocellular carcinoma have been described in patients affected by this disease. In this case report, the authors describe the clinical history of a patient affected by GSD III who developed severe liver disease during her adult life, progressing from fibrosis to cirrhosis and finally to hepatocellular carcinoma. Until now, the hepatic involvement in GSD III has been considered by most authors as mild and almost always self-limiting. This report, together with the previously published cases, clearly indicates that severe and progressive liver disease may complicate this metabolic disorder. These observations advise a careful hepatologic follow-up of patients affected by GSD III.