[Adjuvant therapy in colonic carcinoma].
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Biomedical subjects
Publications and source records attributed to H Frenzel.
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UNLABELLED: Both arterial hypertension and aortic stenosis lead to pressure overload of the left ventricle. As intramyocardial vasculature is confronted with pressure overload in hypertension but not in aortic stenosis, structural differences are to be expected in both forms of left ventricular hypertrophy. With the aid of morphometry, we investigated human myocardium from autopsied hearts from six patients with arterial hypertension and 10 controls, as well as myectomy specimens from cardiac surgery from 14 patients with aortic stenosis. Mean left ventricular myocytic diameter was significantly (P less than 0.05) increased compared with controls (12.4 +/- 1.5 microns) during hypertension (+27%) as well as aortic stenosis (+65%) (P less than 0.05). This was combined with a greater volume density of perimyocytic fibrosis (controls = 0.8 +/- 0.4 V upsilon %) during hypertension (+250%) and aortic stenosis (+587%) (P less than 0.05). Walls of intramyocardial arterioles (external diameter 20-40 and 40-80 microns) were thickened to 32% and 44% (P less than 0.05) during hypertension, but not during aortic stenosis. Compared with controls, perivascular fibrosis of these arterioles was increased by +215% and 61% (P less than 0.05), respectively, during hypertension, but not during aortic stenosis. CONCLUSIONS: Myocytic hypertrophy and increased perimyocytic fibrosis accompany intraventricular pressure overload (hypertension and aortic stenosis) in human hearts. Myocardial structure as a result of arterial hypertension, but not aortic stenosis, is also characterized by intramyocardial arteriole wall-thickening and increased perivascular fibrosis. Thus, distinct structural reaction patterns are noted in the cardiac hypertrophy associated with hypertension and aortic stenosis.
A reduced maximal coronary vasodilatator capacity is reported in patients with hypertensive heart disease, suggesting structural abnormalities of intramyocardial arterioles. Right septal endomyocardial catheter biopsies (EMCB) of 30 patients with arterial hypertension and of 10 heart donors were investigated morphometrically. In hypertension, the mean external diameter (21.9 +/- 3.0 vs. 17.4 +/- 2.9 microns, p less than or equal to 0.01) of arterioles and the mean arterial wall area (284 +/- 80 vs. 167 +/- 69 microns2, p less than or equal to 0.05) were increased as compared with heart donors. Perivascular fibrosis was markedly increased (260 +/- 183 vs. 41 +/- 30 microns2, p less than or equal to 0.05) as well as volume density of fibrosis (3.0 +/- 1.7 vs. 0.9 +/- 0.8 Vv%, p less than or equal to 0.01) in hypertensive heart disease. There was no significant correlation between echocardiographically determined left ventricular mass index (115 +/- 25 g/m2 for men and 104 +/- 12 g/m2 for women) and mean arteriolar wall area (r = +0.17) or volume density of fibrosis (r = +0.2) in hypertensive heart disease. Our investigations show that in patients with arterial hypertension there is a thickening of intramyocardial arteriolar walls and an increase in fibrosis. Intramyocardial vascular alterations seem to manifest in hypertension independent from left ventricular hypertrophy.
Abnormal, dysplastic intramyocardial arteries were reported in autopsied hearts of hypertrophic cardiomyopathy. To elucidate their significance, the operatively-excised myectomy specimens of 24 patients with hypertrophic-obstructive cardiomyopathy (HOCM), of 18 patients with valvular aortic stenosis and of 10 postmortem normal hearts were investigated. Eight patients with HOCM had dysplastic intramyocardial arteries (greater than 100 microns external diameter) as well as dysplastic arterioles (less than 100 microns external diameter). The value of the scores for the thickness and fibroelastosis of the media was nearly doubled, the tunica intima was frequently thickened, and the lumen was relatively reduced in dysplastic vessels. Neither in controls nor in aortic stenosis dysplastic arteries were found. Volume density of patchy fibrosis (scars) was increased in patients with dysplastic arterial vessels (HOCM II) (7.2 +/- 4.4 Vv%) (p less than or equal to 0.05) as compared with HOCM without dysplastic vessels (HOCM I) (0.8 +/- 2.3 Vv%), with aortic stenosis (0.9 +/- 1.6 Vv%) or with controls (0 Vv%), Patients with HOCM II were significantly (p less than or equal to 0.05) younger (30 +/- 13 years) than those with HOCM I (53 +/- 12 years), aortic stenosis (56 +/- 12 years), or controls (63 +/- 21 years). The anterior septum was significantly thicker in HOCM II (29 +/- 7 mm) than in HOCM I (22 +/- 4 mm), in aortic stenosis (19 +/- 3 mm), or in controls (12 +/- 2 mm). Syncopes were complained by about 75% (6/8) of patients in HOCM II, by 54% (9/16) in HOCM I, and by 44% (8/18) in aortic stenosis (not significant).(ABSTRACT TRUNCATED AT 250 WORDS)
In approximately 10% of all cases of endobrachesophagus a malignant degeneration occurs. A frequent endoscopic and bioptic control of the endobrachesophagus is the prognostic decision in order for a developing adenocarcinom to be identified in the early stages. Our casuistry demonstrates the problematic nature of the diagnostic and therapy of a multifocal adenocarcinom in an endobrachesophagus.
Ten patients (eight male/two female) with advanced dilated cardiomyopathy (NYHA III/IV) and a mean fractional shortening in two-dimensional echocardiogram of 20% (9 to 30%) and a mean sodium excretion of 21 mmol (8 to 40 mmol) per day, pretreated with digoxin, captopril and a mean frusemide-dose of 147 mg (80 to 500 mg) without an effective diuresis, were additional treated with 2.5 to 5 mg oral metolazone daily. All patients had a brisk diuresis within 24 hours and a mean weight loss of 8.9 kg (3 to 20 kg) until discharge. All patients improved considerably by additional metolazone-therapy. Seven patients developed a mild hyponatraemia (122 to 132 mmol/l), seven showed mild (greater than or equal to 3.2 mmol/l) and one had a serious hypokalaemia (2.8 mmol/l); spironolactone-pretreated patients developed no hypokalaemia. Notably none of the patients had serious blood pressure fluctuation or a deterioration of renal function. To avoid severe electrolyte-disturbances, additional metolazone-therapy should be practised in hospital, preferring low-dose metolazone and reducing frusemide-dose under careful biochemical monitoring after diuresis is started.
A 30-year-old woman presented with life-threatening ventricular tachycardia without overt heart disease. Ultrastructural investigation of endomyocardial biopsy disclosed abnormally structured and often enlarged mitochondria. Morphometry revealed the ratio of volume density of mitochondria to myofibrils to be markedly increased to 0.667 as compared with five controls (mean: 0.46; range: 0.445-0.479). Investigation of mitochondrial respiratory chain enzymes revealed a 90% reduction in activity of cytochrome c oxidase. Our data suggest that mitochondrial cardiomyopathy may induce malignant ventricular arrhythmias.
The prevalence of renal artery stenosis in diabetic patients is unknown, since no noninvasive and valid screening procedures are available. We have therefore evaluated 5194 consecutive autopsy protocols from patients who died between 1980 and 1988. In addition, all available clinical records for patients with renal artery stenosis (RAS) and a random sample were evaluated. It was found that 73% of patients with RAS were hypertensive, and 53% had diabetes, all but one being Type 2 (non-insulin-dependent). Renal artery stenosis was present in 225 (4.3%) of all patients [95% confidence interval (95% CI), 3.8-4.9], and was not reported in the patients' clinical records in 93% of cases. RAS was present in 8.3% of all diabetic patients (95% CI, 6.8-9.8%), the odds ratio being 3.5 (95% CI, 2.6-4.6). The frequency of renal artery stenosis in diabetic patients with hypertension was 10.1%. Bilateral renal artery stenosis was found in 43% of patients with RAS and diabetes, and in 30% of non-diabetic patients with RAS (P = 0.059). Our results indicate that renal artery stenosis often goes undetected before autopsy. The presence of non-insulin-dependent diabetes mellitus increases the risk of renal artery stenosis. The risk of bilateral renal artery stenosis is greater in diabetic patients. These results may be of significance with regard to the diagnostic evaluation and choice of antihypertensive treatment in hypertensive non-insulin-dependent diabetic patients.
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The pathological findings, including immunohistochemical and electron microscopical findings, in three infants who died unexpectedly of cardiac tumor or cardiomyopathy are reported. The first was a 13-month-old boy with tuberous sclerosis and multiple rhabdomyomas of the heart, who presented with a postpartal cardiac murmur and moderate cardiomegaly. The further history was unknown. The rhabdomyoma nodules were composed of spider cells containing small amounts of desmin and myosin as well as isolated myofibrils. Microscopically small glioma nodules contained high amounts of GFAP. The second case, a boy 4 months of age, died of a large benign fibrous histiocytoma of the heart after an uneventful history. Tumor cells contained alpha-1-anti-chymotrypsin and lysozyme. The third case, a girl 2 months of age, died unexpectedly of histiocytoid cardiomyopathy. The affected cells contained fat droplets, glycogen granules, many leptomer myofibrils and small amounts of myosin and desmin.
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Severe anal bleeding together with increasing abdominal discomfort occurred in an 81-year-old woman previously hospitalized numerous times because of decompensated type II B diabetes. A suspected rectal cancer was excluded by biopsy from the lower to middle rectum, but the biopsy revealed histologically indurated and bleeding ulcerations. Typical nuclear inclusion bodies provided the diagnosis of virus-associated proctocolitis. Serological tests supported the diagnosis of infection with herpes simplex and cytomegalic virus. Laser coagulation stopped the bleeding. At the same time a Guillain-Barré syndrome was noted which improved after administration of cortisone and high parenteral doses of acyclovir.
Renal transplantation was performed in 2 patients with end-stage renal disease due to AA-type amyloidosis. One patient with amyloidosis of rheumatoid arthritis (RA) origin died twelve months after renal transplantation in cardiogenic shock. AA-amyloid deposits were demonstrated in the graft even though there were excellent function and no proteinuria. The second patient with amyloid nephropathy due to familial Mediterranean fever (FMF) showed no impairment of graft function 24 months after transplantation. These 2 cases are compared to an additional 31 cases of renal transplantation for amyloid nephropathy described in the literature. Proteinuria was reported in 32.3% and amyloid was detected in the functioning graft in 41.4%. The function was excellent even when small amyloid deposits were present in the graft. Renal transplantation is indicated in cases of amyloid nephropathy of the AA-type, provided life threatening amyloid involvement of other organs is not present.
Ten histological criteria were evaluated semiquantitatively in the liver biopsies of 60 patients with rheumatoid arthritis (RA) before initiation of methotrexate (MTX) and were compared with 40 biopsies taken during MTX treatment (mean cumulative dose 1.322 mg). Mesenchymal changes (Kupffer cell proliferation, portal tract infiltration) and parenchymal alterations (nuclear variability, ballooning, fatty infiltration) were very common without statistically significant difference between the 2 groups. Slight periportal and/or portal fibrosis was present in 25% of patients without statistical difference between groups. Central fibrosis occurred in 13.5-12.5%. We conclude that liver abnormalities in RA are not related to MTX treatment.
Metastatic lesions represent 1%-8% of all malignant tumours of the mouth and jaws, which are regarded as rare sites of metastases from different primary tumours. The vast majority of these lesions (90%) have been observed in the mandibula, and 5%-20% in the maxilla. Metastatic tumours in the oral soft tissue are very rare. The primary tumour that most commonly metastasizes to the mouth and jaws seems to be carcinoma of the lung, followed by breast cancer and renal cell carcinoma. The case of a 47-year-old woman with renal cell carcinoma and an intraoral soft tissue metastatic lesion is presented.
Liver histology demonstrated progressive cirrhosis in a 19-year-old girl with a subacute form of Wilson's disease. Despite D-penicillamine administration her liver functions rapidly deteriorated further. Orthotopic liver transplantation was performed. Postoperatively there were two mild rejection episodes, an organic psychiatric syndrome and generalized tremor. Copper metabolism and clinical symptoms became normal postoperatively. Five months after the transplantation she was in a good general condition, able to continue her education.
There is currently little information about the morphological changes of the myocardium accompanying the reversal of cardiac hypertrophy. In this study the hypothesis was tested that myocardial alterations induced by exercise will regress within a short interval after the end of training. Rat hearts were examined using morphometric and biochemical methods at the end of a 9-week period of endurance training and also 7, 10 and 14 days after its termination. At the end of the training period the heart weight had increased by 65% but the weight ratio of the right and left ventricular wall remained unchanged. A decline in the DNA content by 27% as well as a decrease in the volume density of the interstitial space by 14% and in the number of interstitial cell nuclei by 32% against controls, are explained by a 30% increase in the width of myofibres. The capillary density was reduced by 22% but the volume density of capillaries remained nearly constant as a result of widening of the capillary diameter by 27%. The surface density of capillaries was diminished by 10%. Ultrastructurally an increase in the ratio of mitochondrial to myofibrillar volume density was observed in the myocytes of hypertrophied hearts as compared to controls (0.54 and 0.63, respectively). Fourteen days after termination of training, 80% of the increment in heart weight had regressed. At this time the width of the myofibres and the volume density of the interstitial space had nearly normalized, while the capillary to fibre ratio had significantly increased. The ratio of mitochondrial and myofibrillar volume density became nearly normal, and a confluence of intermyofibrillar mitochondria resulted in significantly longer organelles. The increased DNA content 10 days after the training, as compared to controls, is attributable to the genesis of non-myocardial cells during the hypertrophic growth and their persistence during regression. The study has shown that cardiac hypertrophy induced by physical training nearly completely regresses within 14 days after termination of conditioning. The increased capillary to fibre ratio indicates neoformation of transversely oriented capillary branches in hypertrophy which particularly becomes apparent in two-dimensional estimation in the regression period. In comparison with myofibres, regression of capillaries seems to be delayed. The decline of heart weight and a significantly diminished RNA content during the regression of hypertrophy suggest that reduced synthesis is responsible for the decrease in heart weight.