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Anal sex cause anal sphincter atrophy

Anal sex cause anal sphincter atrophy

Advanced Search Abstract Objectives. SSc is a connective tissue, multisystem disorder of unknown aetiology. The exact pathophysiology of GIT involvement is not known, but it is related to both neurogenic and myogenic abnormalities as well as possible vascular and ischaemic changes. We aimed to investigate anal sphincter structure in patients with SSc.

Patients underwent anorectal manometry and endoanal US. There was no significant difference in atrophy scores [Sx: Internal anal sphincter , Atrophy , Faecal incontinence , Systemic sclerosis , Endoanal ultrasound , Anorectal involvement Introduction SSc is a connective tissue disorder of unknown aetiology characterized by excess collagen deposition, chronic inflammation and vascular changes that affect multiple organs [ 1 ].

The exact pathophysiology of GIT involvement is not known, but it is related to both neurogenic and myogenic abnormalities as well as possible vascular and ischaemic changes [ 3—5 ]. Histologically, the main changes seen in the GIT are smooth muscle atrophy and varying degrees of fibrosis as the disease progresses [ 6 ].

Oesophageal involvement is most common and upper gastrointestinal GI symptoms are frequently reported [ 7 , 8 ]. Lower GI involvement can lead not only to constipation and evacuation difficulty but also diarrhoea and faecal incontinence. In healthy subjects, faecal continence is maintained by the coordinated function of pelvic floor, rectum and the anal sphincters. The striated external anal sphincter EAS makes a small contribution towards the resting anal pressure, but is primarily responsible for the voluntary contraction of the anal sphincter [ 11 ].

Disruption or weakness of the IAS typically leads to passive faecal incontinence, whereas that of the EAS leads to urge faecal incontinence [ 12 , 13 ]. The IAS, being a smooth muscle, is more likely to be affected in SSc [ 14 ] and it has been suggested that the changes are similar to those seen in the lower oesophageal sphincter LOS.

The existing literature, none of which includes more than 18 patients with SSc, suggests that the IAS is thinned and hyperechoic on US in the majority of patients with SSc and faecal incontinence [ 15—17 ], although some patients may have a thickened hypoechoic sphincter, most likely secondary to collagen deposition [ 16 ]. Whether these differences relate to disease subtype or duration has not been addressed. Even less is known about patients with SSc and no faecal incontinence. If the pattern is similar to that seen in oesophageal involvement, we would expect to see structural and functional changes even in the absence of symptoms.

This study aimed to quantify the sonographic changes in the anal sphincters of patients with SSc with and without faecal incontinence. We hypothesized that defects in the sphincter mechanism would be less common in incontinent SSc patients than in incontinent controls ICs without SSc. We further hypothesized that atrophic sphincter changes would occur more often in symptomatic Sx than asymptomatic ASx SSc patients.

Methods Patients Forty-four patients with SSc, 24 Sx with anorectal symptoms and 20 ASx without anorectal symptoms patients, were recruited to the study. Twenty patients, age and sex matched to the Sx SSc patients, referred to our GI physiology unit for investigations of faecal incontinence, were used as ICs. All patients gave informed consent to participate in the study, which was approved by the University College Hospital research ethics committee.

Incontinence was assessed by using the Wexner incontinence score, a validated questionnaire assessing incontinence based on frequency and stool consistency.

Questionnaires SSc patients were asked to complete the following questionnaires on the day of their assessments. Scleroderma GI tract 1. Short form SF general health questionnaire: Anorectal manometry No bowel preparation was given before testing. An eight-channel radial water-perfused manometry system with a perfusion rate of 0. A latex-free balloon with ml capacity was attached at the end of the manometry catheters Ardmore Healthcare Limited, Amersham, UK, external diameter 3.

With the subject in the left lateral position, the station pull-through technique was employed to assess anal canal length, anal resting pressure and anal squeeze pressure. Conventional anal endosonography was performed according to a standard technique [ 18 ]. Images of the anal sphincters were taken at proximal, mid- and distal canal levels. Images were acquired by a trained radiographer and assessed independently by two experts.

The anal sphincter complex was examined and the integrity and atrophy of the internal and external sphincters were described as follows, and scored 1—3 for analysis purposes [ 19 ]. Statistics Statistical analysis was performed using GraphPad Prism. As some of the values measured were non-normally distributed, results are expressed as median and interquartile range. The non-parametric Mann—Whitney and Kruskal—Wallis tests were used for comparisons of two and three groups, respectively.

Results Patients Forty-four SSc patients were studied. Twenty-four patients were Sx, reporting faecal incontinence, and 20 patients were ASx. Sex- and age-matched patients with incontinence were used as controls. Table 1 summarizes the demographics and incontinence scores of the three patient groups.

The median disease duration was 5. There was no significant difference in the percentage of oesophageal symptoms between Sx and ASx SSc patients. Unfortunately, oesophageal manometry results were available for only two patients, and therefore we could not assess for correlation between abnormal oesophageal and anorectal manometry.

Parity was higher in the IC group. Table 2 summarizes the quality-of-life questionnaire scores in SSc patients. Table 1 Demographic characteristics of three patient groups and disease characteristics of the SSc patients Patient characteristics.

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Anal sex cause anal sphincter atrophy

Advanced Search Abstract Objectives. SSc is a connective tissue, multisystem disorder of unknown aetiology. The exact pathophysiology of GIT involvement is not known, but it is related to both neurogenic and myogenic abnormalities as well as possible vascular and ischaemic changes. We aimed to investigate anal sphincter structure in patients with SSc. Patients underwent anorectal manometry and endoanal US. There was no significant difference in atrophy scores [Sx: Internal anal sphincter , Atrophy , Faecal incontinence , Systemic sclerosis , Endoanal ultrasound , Anorectal involvement Introduction SSc is a connective tissue disorder of unknown aetiology characterized by excess collagen deposition, chronic inflammation and vascular changes that affect multiple organs [ 1 ].

The exact pathophysiology of GIT involvement is not known, but it is related to both neurogenic and myogenic abnormalities as well as possible vascular and ischaemic changes [ 3—5 ].

Histologically, the main changes seen in the GIT are smooth muscle atrophy and varying degrees of fibrosis as the disease progresses [ 6 ]. Oesophageal involvement is most common and upper gastrointestinal GI symptoms are frequently reported [ 7 , 8 ]. Lower GI involvement can lead not only to constipation and evacuation difficulty but also diarrhoea and faecal incontinence.

In healthy subjects, faecal continence is maintained by the coordinated function of pelvic floor, rectum and the anal sphincters. The striated external anal sphincter EAS makes a small contribution towards the resting anal pressure, but is primarily responsible for the voluntary contraction of the anal sphincter [ 11 ]. Disruption or weakness of the IAS typically leads to passive faecal incontinence, whereas that of the EAS leads to urge faecal incontinence [ 12 , 13 ].

The IAS, being a smooth muscle, is more likely to be affected in SSc [ 14 ] and it has been suggested that the changes are similar to those seen in the lower oesophageal sphincter LOS. The existing literature, none of which includes more than 18 patients with SSc, suggests that the IAS is thinned and hyperechoic on US in the majority of patients with SSc and faecal incontinence [ 15—17 ], although some patients may have a thickened hypoechoic sphincter, most likely secondary to collagen deposition [ 16 ].

Whether these differences relate to disease subtype or duration has not been addressed. Even less is known about patients with SSc and no faecal incontinence. If the pattern is similar to that seen in oesophageal involvement, we would expect to see structural and functional changes even in the absence of symptoms. This study aimed to quantify the sonographic changes in the anal sphincters of patients with SSc with and without faecal incontinence. We hypothesized that defects in the sphincter mechanism would be less common in incontinent SSc patients than in incontinent controls ICs without SSc.

We further hypothesized that atrophic sphincter changes would occur more often in symptomatic Sx than asymptomatic ASx SSc patients. Methods Patients Forty-four patients with SSc, 24 Sx with anorectal symptoms and 20 ASx without anorectal symptoms patients, were recruited to the study.

Twenty patients, age and sex matched to the Sx SSc patients, referred to our GI physiology unit for investigations of faecal incontinence, were used as ICs. All patients gave informed consent to participate in the study, which was approved by the University College Hospital research ethics committee.

Incontinence was assessed by using the Wexner incontinence score, a validated questionnaire assessing incontinence based on frequency and stool consistency. Questionnaires SSc patients were asked to complete the following questionnaires on the day of their assessments. Scleroderma GI tract 1. Short form SF general health questionnaire: Anorectal manometry No bowel preparation was given before testing.

An eight-channel radial water-perfused manometry system with a perfusion rate of 0. A latex-free balloon with ml capacity was attached at the end of the manometry catheters Ardmore Healthcare Limited, Amersham, UK, external diameter 3.

With the subject in the left lateral position, the station pull-through technique was employed to assess anal canal length, anal resting pressure and anal squeeze pressure.

Conventional anal endosonography was performed according to a standard technique [ 18 ]. Images of the anal sphincters were taken at proximal, mid- and distal canal levels. Images were acquired by a trained radiographer and assessed independently by two experts.

The anal sphincter complex was examined and the integrity and atrophy of the internal and external sphincters were described as follows, and scored 1—3 for analysis purposes [ 19 ]. Statistics Statistical analysis was performed using GraphPad Prism.

As some of the values measured were non-normally distributed, results are expressed as median and interquartile range. The non-parametric Mann—Whitney and Kruskal—Wallis tests were used for comparisons of two and three groups, respectively.

Results Patients Forty-four SSc patients were studied. Twenty-four patients were Sx, reporting faecal incontinence, and 20 patients were ASx.

Sex- and age-matched patients with incontinence were used as controls. Table 1 summarizes the demographics and incontinence scores of the three patient groups.

The median disease duration was 5. There was no significant difference in the percentage of oesophageal symptoms between Sx and ASx SSc patients. Unfortunately, oesophageal manometry results were available for only two patients, and therefore we could not assess for correlation between abnormal oesophageal and anorectal manometry. Parity was higher in the IC group.

Table 2 summarizes the quality-of-life questionnaire scores in SSc patients. Table 1 Demographic characteristics of three patient groups and disease characteristics of the SSc patients Patient characteristics.

Anal sex cause anal sphincter atrophy

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4 Comments

  1. Parity was higher in the IC group. Endosonography has been proposed to predict the risk of recurrent bleeding after the endoscopic treatment of esophageal varices.

  2. Questionnaires SSc patients were asked to complete the following questionnaires on the day of their assessments. A latex-free balloon with ml capacity was attached at the end of the manometry catheters Ardmore Healthcare Limited, Amersham, UK, external diameter 3. There was no significant difference in the percentage of oesophageal symptoms between Sx and ASx SSc patients.

  3. Oesophageal involvement is most common and upper gastrointestinal GI symptoms are frequently reported [ 7 , 8 ]. SSc is a connective tissue, multisystem disorder of unknown aetiology.

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