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Brazilian Journal of Otorhinolaryngology 2008Idiopathic hypertrophy of the masseter muscle is a rare disorder of unknown cause. Some authors associate it with the habit of chewing gum, temporo-mandibular joint...
Idiopathic hypertrophy of the masseter muscle is a rare disorder of unknown cause. Some authors associate it with the habit of chewing gum, temporo-mandibular joint disorder, congenital and functional hypertrophies, and emotional disorders (stress and nervousness). Most patients complain of the cosmetic change caused by facial asymmetry, also called square face, however, symptoms such as trismus, protrusion and bruxism may also occur. The goals of the present investigation were: to report a case of idiopathic masseter hypertrophy, describe its symptoms and treatment. The patient reported bilateral bulging in the region of the mandible angle, of slow and progressive evolution. He did not complain of pain or discomfort, however there was bilateral otalgia, nighttime trismus and stress. In his physical exam we noticed bilateral masseter hypertrophy without local inflammatory alterations. We indicated surgical treatment with an extraoral approach. Complementary tests are indicated when there is diagnostic doubts. Treatment varies from conservative to surgical, and the later depends on surgeon skill and experience.
Topics: Diagnosis, Differential; Humans; Hypertrophy; Male; Masseter Muscle; Salivary Gland Neoplasms; Temporomandibular Joint Disorders; Young Adult
PubMed: 19082365
DOI: 10.1016/S1808-8694(15)31393-8 -
Spine Dec 2001This is a case report of a patient with hypertrophy of the posterior longitudinal ligament (HPLL) in the lumbar spine, with assessment of operative treatment and a... (Review)
Review
STUDY DESIGN
This is a case report of a patient with hypertrophy of the posterior longitudinal ligament (HPLL) in the lumbar spine, with assessment of operative treatment and a 10-year follow-up using magnetic resonance imaging.
OBJECTIVES
To report on the long-term outcome of a case of lumbar HPLL, to review the literature on case reports of HPLL, and to outline the pathology of HPLL in the lumbar spine.
SUMMARY OF BACKGROUND DATA
There have been several reports of HPLL in the cervical spine and thoracic spine. However, the authors found no reports of this condition in the lumbar spine and no reports of long-term follow-up. Two types of pathology are associated with HPLL: primary hypertrophy of the ligament and secondary hypertrophy associated with intervertebral disc herniation.
METHODS
A 10-year follow-up evaluation of a 56-year-old man with HPLL at L2 is reported. The patient was observed using serial physical examinations, radiographs, and MRIs over 10 years. Because he did not respond to conservative management, surgical treatment was applied. After complete decompression by hemilaminectomy and resection of hypertrophied ligament, the nerve roots were freed of constriction through the neural foramens at L2 and L3.
RESULTS
One year after the operation the patient was asymptomatic without evidence of recurrence of the disease.
CONCLUSIONS
HPLL is a very rare disease. This appears to be the first report of the disease in the lumbar spine.
Topics: Humans; Hypertrophy; Longitudinal Ligaments; Lumbar Vertebrae; Magnetic Resonance Imaging; Male; Middle Aged; Spinal Stenosis
PubMed: 11740375
DOI: 10.1097/00007632-200112150-00028 -
Clinics in Plastic Surgery Apr 2016Gigantomastia is a disabling condition for patients and presents unique challenges to plastic surgeons. Presentation can occur throughout different phases of life, and... (Review)
Review
Gigantomastia is a disabling condition for patients and presents unique challenges to plastic surgeons. Presentation can occur throughout different phases of life, and treatment often begins with nonoperative measures; however, the most effective way to relieve symptoms is surgical breast reduction. Because of the large amount of tissue removed, surgeons can encounter different intraoperative and postoperative complications. By understanding this disease process and these complications, surgeons can attempt to minimize their occurrences. The authors present an overview of the cause, preoperative evaluation, techniques, and outcomes. Additionally, they present outcomes data from their center on 40 patients.
Topics: Breast; Female; Humans; Hypertrophy; Mammaplasty
PubMed: 27012802
DOI: 10.1016/j.cps.2015.12.006 -
Cardiovascular Research Jan 1994The aim was to investigate why cardiac hypertrophy causes increased vulnerability to arrhythmias during myocardial ischaemia. (Comparative Study)
Comparative Study
OBJECTIVE
The aim was to investigate why cardiac hypertrophy causes increased vulnerability to arrhythmias during myocardial ischaemia.
METHODS
The electrophysiological basis for this increased vulnerability was studied in isolated perfused guinea pig hearts obtained 50 and 150 d after aortic constriction, and in sham operated controls. Cellular electrophysiology, conduction, and refractory periods were examined during control perfusion and during low flow (coronary flow reduced to 10% of control) and zero flow ischaemia. ECGs in patients with left ventricular hypertrophy and in controls matched for age and heart rate were also studied.
RESULTS
Aortic constriction increased heart weight:body weight ratio by 33% at 50 d and by 69% at 150 d. Action potentials were unchanged in hypertrophied hearts. Significant conduction delay occurred in 150 d hypertrophied hearts [conduction time index 23(SEM 4) ms v 18(3) ms, p < 0.001; QRS width 40(1) ms v 35(1) ms, p < 0.01], but not in 50 d hypertrophied hearts. Conduction delay was also present in humans with left ventricular hypertrophy [QRS width 96(13) ms v 87(8) ms, p < 0.01]. Although the QTc interval was increased in humans, at 422(23) ms v 411(17) ms in controls, p < 0.05, this could be explained by the increased QRS duration. During ischaemia, ventricular arrhythmias tended to occur earlier in hypertrophied hearts. Hypertrophy was also associated with a greater increase in conduction delay. Ischaemia reduced action potential duration and refractory periods; the reduction in action potential duration was attenuated by hypertrophy (p < 0.01), although the reverse was apparent during low flow ischaemia at 50 d.
CONCLUSIONS
Delayed conduction is an important feature of severe cardiac hypertrophy in guinea pigs and man. Hypertrophy is associated with accentuated conduction delay and altered repolarisation during ischaemia.
Topics: Animals; Cardiomegaly; Electrocardiography; Electrophysiology; Guinea Pigs; Heart Conduction System; Humans; Hypertrophy, Left Ventricular; Myocardial Ischemia; Myocardial Reperfusion Injury
PubMed: 8068073
DOI: 10.1093/cvr/28.1.47 -
Development (Cambridge, England) Sep 2011An important unresolved question in skeletal muscle plasticity is whether satellite cells are necessary for muscle fiber hypertrophy. To address this issue, a novel...
An important unresolved question in skeletal muscle plasticity is whether satellite cells are necessary for muscle fiber hypertrophy. To address this issue, a novel mouse strain (Pax7-DTA) was created which enabled the conditional ablation of >90% of satellite cells in mature skeletal muscle following tamoxifen administration. To test the hypothesis that satellite cells are necessary for skeletal muscle hypertrophy, the plantaris muscle of adult Pax7-DTA mice was subjected to mechanical overload by surgical removal of the synergist muscle. Following two weeks of overload, satellite cell-depleted muscle showed the same increases in muscle mass (approximately twofold) and fiber cross-sectional area with hypertrophy as observed in the vehicle-treated group. The typical increase in myonuclei with hypertrophy was absent in satellite cell-depleted fibers, resulting in expansion of the myonuclear domain. Consistent with lack of nuclear addition to enlarged fibers, long-term BrdU labeling showed a significant reduction in the number of BrdU-positive myonuclei in satellite cell-depleted muscle compared with vehicle-treated muscle. Single fiber functional analyses showed no difference in specific force, Ca(2+) sensitivity, rate of cross-bridge cycling and cooperativity between hypertrophied fibers from vehicle and tamoxifen-treated groups. Although a small component of the hypertrophic response, both fiber hyperplasia and regeneration were significantly blunted following satellite cell depletion, indicating a distinct requirement for satellite cells during these processes. These results provide convincing evidence that skeletal muscle fibers are capable of mounting a robust hypertrophic response to mechanical overload that is not dependent on satellite cells.
Topics: Animals; Blotting, Western; Female; Flow Cytometry; Hypertrophy; Mice; Muscle Fibers, Skeletal; Muscle, Skeletal; Polymerase Chain Reaction; Satellite Cells, Skeletal Muscle; Tamoxifen
PubMed: 21828094
DOI: 10.1242/dev.068858 -
Archives of Cardiovascular Diseases 2023Left ventricular hypertrophy is often associated with hypertension, which is not necessarily the cause of hypertrophy. Non-hypertension-related aetiologies often have a...
BACKGROUND
Left ventricular hypertrophy is often associated with hypertension, which is not necessarily the cause of hypertrophy. Non-hypertension-related aetiologies often have a strong impact on patient management, and therefore require a thorough and careful workup. When considering all left ventricular hypertrophies, even the mild ones, the number of patients who need a workup increases drastically. This raises the need for a tool to evaluate the pretest probability of the origin of left ventricular hypertrophy.
AIM
To predict the hypertensive origin of left ventricular hypertrophy using machine learning on first-line clinical, laboratory and echocardiographic variables.
METHODS
We used a retrospective single-centre population of 591 patients with left ventricular hypertrophy, starting at 12mm maximal left ventricular wall thickness. After splitting data in a training and testing set, we trained three different algorithms: decision tree; random forest; and support vector machine. Model performances were validated on the testing set.
RESULTS
All models exhibited good areas under receiver operating characteristic curves: 0.82 (95% confidence interval: 0.77-0.88) for the decision tree; 0.90 (95% confidence interval 0.85-0.94) for the random forest; and 0.90 (95% confidence interval: 0.85-0.94) for the support vector machine. After threshold selection, the last model had the best balance between its specificity of 0.96 (95% confidence interval: 0.91-0.99) and its sensitivity of 0.31 (95% confidence interval: 0.17-0.44). All algorithms relied on similar most influential predictor variables. Online calculators were developed and made publicly available.
CONCLUSIONS
Machine learning models were able to determine the hypertensive origin of left ventricular hypertrophy with good performances. Implementation in clinical practice could reduce the number of aetiological workups needed in patients presenting with left ventricular hypertrophy.
Topics: Humans; Hypertrophy, Left Ventricular; Retrospective Studies; Echocardiography; Hypertension; Algorithms; Machine Learning
PubMed: 37474391
DOI: 10.1016/j.acvd.2023.06.005 -
Cardiovascular Clinics 1990Left ventricular hypertrophy imposes a definite risk of increased cardiovascular morbidity and mortality. This increased risk is independent of other risks (including... (Review)
Review
Left ventricular hypertrophy imposes a definite risk of increased cardiovascular morbidity and mortality. This increased risk is independent of other risks (including that of hypertension). The precise mechanism or mechanisms that account for this risk are not known, although several possible factors have been identified. A variety of antihypertensive agents have been shown to decrease the mass of hypertrophied left ventricle, although some may also diminish the mass of the normal ventricle. No study to date has demonstrated improvement in the risk from LVH with so-called reversal of LVH with pharmacologic agents.
Topics: Cardiomegaly; Coronary Disease; Humans; Male; Risk Factors
PubMed: 2140072
DOI: No ID Found -
Annales de Chirurgie Plastique Et... Jul 2020Clitoral hypertrophy is a rare genital malformation that can be congenital or acquired. In congenital forms, the most common cause is adrenal hyperplasia. The acquired...
Clitoral hypertrophy is a rare genital malformation that can be congenital or acquired. In congenital forms, the most common cause is adrenal hyperplasia. The acquired forms are caused by endocrinological diseases, benign tumours or cysts. Idiopathic clitoral hypertrophies can be detected after the elimination of secondary causes. A complete assessment is needed to treat the origin of clitoridomegaly. The hypertrophy is often increased or unmasked during sexual arousal with the appearance of a true vulvar appendage in erection. It is often accompanied by a hypertrophy of the clitoral hood and can cause psychological suffering with an impact on the quality of sexual life. When the cause of clitoral hypertrophy is diagnosed, treated or stabilized, the plastic surgeon may be called upon for surgical correction. Reconstructive surgery in this area has evolved considerably since the historical clitoral amputations which led to the current technique of partial resection with sparing the dorsal neurovascular pedicle of the clitoris as described by Professor Paniel. We propose a modified conservative technique to treat clitoral hypertrophy and the clitoral hood and present two clinical cases: ventral reduction clitoridoplasty with preservation of the neurovascular pedicle associated with a chevron plasty of the clitoral hood and a lipofilling of the labia majora. The postoperative follow-up is simple with reports of great satisfaction from patients regarding their quality of life.
Topics: Clitoris; Female; Humans; Hypertrophy; Quality of Life; Plastic Surgery Procedures; Vulva
PubMed: 32482351
DOI: 10.1016/j.anplas.2019.10.002 -
Cardiologia (Rome, Italy) Dec 1993In the progression from myocardial hypertrophy to heart failure, abnormalities in the interstitial space of the heart seem to play a critical role. The formation of an... (Review)
Review
In the progression from myocardial hypertrophy to heart failure, abnormalities in the interstitial space of the heart seem to play a critical role. The formation of an extracellular oedema and the alterations in coronary subendocardial perfusion are associated with the development of interstitial fibrosis. Cardiac experimental studies documented the presence of augmented interstitial fluid volume and pressure and a subsequent remodelling of the fibrillar network of the extracellular space of the myocardium during the phases of the cardiovascular response to a sudden overload. Variations of the Starling's forces balance caused by enhanced endothelial permeability or due to an impairment of cardiac lymphatic drainage may contribute to the development of an acute heart failure. During stable hyperfunction, the organization of a chronic oedema should account for interstitial changes in the hypertrophic myocardium. Reactive fibrosis seems to be under hormonal control. The activation of the renin-angiotensin-aldosterone system is responsible for interfascicular and intercellular accumulation of fibrillar collagen within the cardiac interstitium. Perivascular fibrosis in the subendocardium may impair intramyocardial distribution of coronary flow. When an inadequate hypertrophy occurs, because of an elevation in ventricular wall stress, myocardial oxygen consumption rises and this may lead to the exhaustion of coronary blood flow reserve in the subendocardial layers. This underperfusion may be responsible for the development of myocardial ischemia. Coronary hemodynamic changes in the microcirculation as those prompted by interstitial alterations may contribute to the onset of myocyte necrosis and to the formation of restorative fibrosis. The progressive mechanical overload of the spared hypertrophied myocytes could explain the initiation of a positive feedback mechanism which perpetuates endomyocardial perfusion impairment, interstitial oedema and remodelling, finally, causing myocyte deaths and fibrous tissue proliferation. These structural alterations and their pathophysiological counterparts appear to be closely related to the evolution from compensatory hypertrophy to chronic myocardial failure in hypertrophic heart disease.
Topics: Acute Disease; Cardiomegaly; Chronic Disease; Endomyocardial Fibrosis; Heart Failure; Humans; Myocardium
PubMed: 8020050
DOI: No ID Found -
Diseases of Aquatic Organisms Dec 2022Histopathological analysis of soft-shell clams Mya arenaria collected from 2 northwest Russian locations disclosed high prevalence of 2 pathological gill conditions. One...
Histopathological analysis of soft-shell clams Mya arenaria collected from 2 northwest Russian locations disclosed high prevalence of 2 pathological gill conditions. One involved the occurrence of more or less extended gill areas in which the branchial filaments showed hyperchromatic (basophilic) epithelium with some hypertrophied nuclei, which were considered presumptive signs of viral infection. Another pathological condition involved abnormal proliferation of the branchial epithelium, which lost the main differential features of the normal branchial epithelium (ciliated and simple cell layer structure), becoming non-ciliated, pseudostratified or stratified hyperchromatic epithelium with abundant mitotic figures and frequent apoptotic cells. The most complex cases involved loss of the normal branchial filament architecture, which was replaced with tumour-like growths consisting of branching, convoluted epithelial projections with a connective stroma. Images suggesting migration (invasion) of cells from the abnormally proliferating epithelium to the subjacent connective tissue, which would involve malignancy, were observed in one individual. The occurrence of both pathological conditions in clams from both locations and their co-occurrence in one clam suggest the possibility of a common, possibly viral, aetiology. Furthermore, the high prevalence of the abnormal proliferative disorder in non-polluted areas suggests an infectious aetiology. Additional studies are needed to assess a viral aetiology for the nuclear hypertrophy and/or the abnormal epithelial proliferation as well as the malignancy of the latter condition.
Topics: Animals; Cell Proliferation; Gills; Hypertrophy; Mya; Russia
PubMed: 36519685
DOI: 10.3354/dao03711