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At least 145 records · Page 8Linked to original sources
PubMed1978

Symposium on colon and anorectal surgery. Pruritus ani: a practical approach.

Pruritus ani is a symptom of diverse cause and varied presentation which will respond in most cases to measures directed at keeping the anal area clean and dry. The role of the surgeon is to evaluate the patient to determine the status of the problem and to rule out threatening conditions, to educate the patient in his responsibility for continuing care and prevention, and to prescribe initial therapy to relieve symptoms. Follow-up evaluation is necessary to intensify treatment for the unresponsive patient, to diagnose further or identify the candidate for surgery, and to refer the patient with uncontrolled pruritus exhibiting a dermatosis for dermatological diagnosis and therapy. The crux of this practical management rests in the control of perianal moisure, the elimination of which gives an enfilading effect to therapy.

Female↗
PubMed1994

Hemorrhoids, fissures, and pruritus ani.

The diagnosis and management of hemorrhoids, fissures, and pruritus ani probably accounts for more than 81% of the complaints centered on this part of the human anatomy. This brief treatise offers a safe and practical approach to the management of these three diseases.

Fissure in Ano↗
PubMed1987

Pruritus ani.

Management of pruritus ani rests on a few basic principles. The first and foremost is to listen to the patient and accept how uncomfortable and even disabling this common disorder can be. Such causes as parasites, diarrhea, trauma, hemorrhoids, and fistulas must be accurately diagnosed and treated. Contributing factors, such as poor hygiene or, paradoxically, too vigorous cleansing, must be corrected. Certain foods, such as spices and citrus fruits, need to be eliminated from the diet. Use of all over-the-counter preparations, cleaning pads, and solutions except water must be stopped. Finally, a mild steroid cream should be prescribed on a temporary basis, and the patient should be reexamined in two to three weeks. In the vast majority of cases, the physician will have a very happy and appreciative patient.

Humans↗
PubMedDate not supplied

Pruritus ani.

In the anal region, pruritus may be both idiopathic (mainly of psychological/psychiatric origin) and secondary to an underlying disorder or related to local causes (mainly of dermatologic interest). Persistent pruritus ani is, in particular, a challenging experience for the dermatologist.

Diagnosis, Differential↗
PubMed1999

Pruritus ani.

The possible dermatological and proctologic causes, of Pruritus Ani that often, due to its persistence and for its consequent lesions of scratching, becomes a real disease, are analysed. Particular attention is given to therapeutical treatment, describing which hygienic-dietetic rules must be followed and which treatments can be utilised, if the cause of the symptom is known and if it is possible to remove it or not. Moreover, personal experience on 312 patients examined in twelve years is reported.

Adult↗
PubMed2004

Pruritus ani.

BACKGROUND: Pruritus ani is a common presenting problem in general practice, one that is particularly distressing to patients. However, there is little available research on which to base management OBJECTIVE: This article discusses the causes and management of this distressing symptom based on thecurrent available evidence. DISCUSSION: Perianal itch probably arises from localised inflammation. This may be the result of anorectal disease, skin disorders, excessive cleaning, application of local irritants or other causes. In children, perianal itch may be caused by intestinal hermetic Infection such as pinworm. Whatever the initial cause, the problem may at times become chronic, with scratching inflaming the area and more itching resulting. Avoiding trauma from excess washing, toilet paper and topical agents is important. Treatments likely to be effective are emollients such as sorbolene, a short course of topical hydrocortisone cream and capsaicin cream.

Adult↗
PubMedDate not supplied

A new concept of the anatomy of the anal sphincter mechanism and the physiology of defecation. XXIII. An injection technique for the treatment of idiopathic pruritus ani.

An injection technique for the treatment of idiopathic pruritus ani is presented. The technique was performed on 67 patients after failure of other methods to achieve permanent cure. The technique comprises injection of 5% solution of phenol in almond oil in the subcutaneous tissue of the rectal neck aiming at destruction of the "epithelial debris" which exists in this area and is considered the primary cause in idiopathic pruritus. Cure was obtained in 62 patients (92.5%). The remaining five patients underwent recurrence after a period of remission, and were cured after a second injection. The advantages of the present technique over others in common use are discussed.

Adult↗
PubMed1985

Pruritus ani: could it be malignant?

The management of extramammary perianal Paget's disease should include a careful search for an associated carcinoma in the pelvic viscera by means of proctoscopy and x-ray. Such local malignancies as Bowen's disease, which may be pigmented and multifocal in this region, and invasive squamous cell carcinoma may first manifest themselves as pruritus ani.

Anus Neoplasms↗
PubMed1987

Pruritus ani. Classification and management.

Pruritus ani is a common dermatologic complaint that can be frustrating to treat. Effective therapy depends upon recognition of a variety of etiologic factors that may contribute to the symptom.

Humans↗
PubMed1999

Quantitative study of the effects of denervation and castration on the levator ani muscle of the rat.

The levator ani muscle (LA) of the rat is highly androgen-sensitive and, like all skeletal muscles, deteriorates structurally and functionally when denervated. In order to elucidate the interplay of neural and endocrine influences, the separate and combined effects of denervation and castration on myofiber cross-sectional area and nuclear populations were quantitatively studied. In one group of 4-month-old male rats (A), the LA was denervated. Another group (B) was surgically castrated and a third group (C) was both denervated and castrated. The control rats (D) remained both gonad- and nerve-intact. After two months, the LA was obtained for myofiber and nuclear enumeration, cross-sectional area and satellite cell frequency determination. In the denervated muscle of gonad-intact rats (Group A), myofiber cross-sectional area was markedly diminished (265.84+/-11.38 microm2; compared with controls [Group D]: 1519.98+/-79.41 microm2; P < 0.05). Satellite cell nuclei, as a percentage of total sublaminar nuclei (i.e., satellite cell ratio), increased significantly (4.26%, from a control value of 1.91%). Castration alone (Group B) resulted in pronounced myofiber atrophy (mean cross-sectional area: 754.03+/-89.63 microm2) but had no significant effect on satellite cell ratio (2.36%). The combination of castration and denervation (Group C) elicited the same degree of myofiber atrophy as denervation alone (Group A) but had no significant impact on satellite cell ratio. Instead, the nuclear count per myofiber declined to about a third of the control level (300.5+/-38.49 compared with 861.7+/-24.8; P < 0.05). The results indicate that the atrophic effects of denervation and castration on the LA are non-synergistic and mechanistically similar. They also show that the inability of satellite cells to respond mitotically to the withdrawal of neural input under disandrogenized conditions is a factor in the myonuclear depletion of the denervated muscle of castrated rats.

Anal Canal↗
PubMed2001

Testosterone mediates satellite cell activation in denervated rat levator ani muscle.

Denervation stimulates quiescent satellite cells in skeletal muscle to reenter the cell cycle. In the androgen-sensitive rat levator ani muscle (LA), this mitotic response to loss of neural input fails to occur in castrated animals. To elucidate the role of androgens in denervation-induced satellite cell proliferation, the denervated LA of castrated rats (Group A) was compared with that of animals infixed with testosterone implants after castration (Group B). Mean myofiber cross-sectional areas (Group A: 362.95 microm(2) +/- 27.74; Group B: 403.13 microm(2) +/- 53.87) and linear nuclear densities (Group A: 74.07 mm(-1) +/- 17.58; Group B: 104.13 mm(-1) +/- 4.06) were similar (P > 0.05) in both groups. The androgen-deprived myofibers of Group A, however, had a significantly lower nuclear content (271.0 +/- 74.91 vs. 1,285.80 +/- 81.74 in Group B; P < 0.05) on account of their considerably shorter mean length (3.44 mm +/- 0.29 vs. 12.31 mm +/- 0.92 in Group B; P < 0.05). The proportional representation of satellite cells in hormone-replaced, denervated muscle was more than twice that in the untreated group (Group B: 5.15 +/- 0.83% vs. Group A: 2.28 +/- 0.23%; P < 0.05). In absolute terms, the satellite cell number in Group B was approximately an order of magnitude greater than in Group A (408.4 x 10(3) vs. 38.08 x 10(3)). The results confirm the absence of testosterone as the factor responsible for the inability of satellite cells in the LA of castrated rats to respond mitotically to the withdrawal of neural input after denervation.

Anal Canal↗
PubMed2005

A proposed mechanism for intermediate atresia ani (AA), based on a porcine case of AA and hypospadias.

BACKGROUND: Atresia Ani (AA) is one of the most common malformations of the lower gastrointestinal tract. It occurs in 1 in 1500 to 1 in 5000 human births. These patients suffer physically and psychologically from this disorder, and thus there is a research interest in the condition. There are 3 subcategories of AA: high, intermediate, and low. Each of these forms is likely related to separate etiological processes. METHODS: An anatomical study was performed on a porcine case of AA with a urorectal fistula and malformed urethra. RESULTS: This animal was found to have the intermediate form of AA. CONCLUSIONS: A new mechanism is hypothesized, distinct from that described for the high and low forms of AA. This proposed mechanism involves the persistence of the cloacal membrane. Evidence to support this hypothesis includes: location of the urorectal fistula in the region of the embryonic cloacal duct, the lack of anomalies usually seen in conjunction with AA associated with mutations of the Sonic Hedgehog gene, and the presence of a malformed urethra, which is significantly correlated to intermediate AA. This form of AA could be related to a failure of the cloacal membrane to break down at the appropriate time during urorectal separation.

Animals↗
PubMed2005

Reinnervation of the rat levator ani muscle after neonatal denervation.

After axonal injury on postnatal day 14 (P14), but not P21, motoneurons in the spinal nucleus of the bulbocavernosus (SNB) do not display their normal response to circulating testosterone levels. This could result from a permanent disruption of communication between motoneurons and their testosterone-sensitive target muscles. We assessed the extent of reinnervation of one of these target muscles, the levator ani (LA) muscle, 5 months after the pudendal nerve was cut either on P14 or P21. The number of motoneurons innervating the LA in control and nerve cut animals was determined using retrograde labeling procedures. Functional recovery of the LA muscle was determined via the testing of its in situ contractile properties. Compared to control muscles, reinnervated LA muscles were smaller, had fewer muscle fibers, generated a lower maximum tetanic tension, and were more fatigable. In spite of the fact that fewer motoneurons reinnervated the LA muscle after nerve cut on P14 than on P21, there were no differences in the weight or contractile properties of the LA muscle between these two groups. These data suggest that motoneurons that survived injury on P14 innervated more muscle fibers than normal and exhibited a similar ability to functionally reinnervate the target muscle as those motoneurons that survived injury on P21.

Age Factors↗
PubMed1982

Testosterone increases acetylcholine receptor number in the "levator ani" muscle of the rat.

The "levator ani" muscle of male rats provides a neuromuscular system in which both the muscle and its motoneurons have high levels of androgen receptors. Two weeks of castration caused a 48% loss of acetylcholine receptors in this muscle. One week of testosterone propionate injections initiated on week after castration increased receptor number by 27% over untreated castrate levels. These changes paralleled changes in muscle protein content. In contrast, castration and testosterone treatments of castrates had no effect on total. Triton X-100-extractable acetylcholinesterase activity. This system may provide a useful model of synaptic plasticity.

Acetylcholinesterase↗
PubMed1988

Synapse elimination occurs late in the hormone-sensitive levator ani muscle of the rat.

Using tetranitroblue tetrazolium (TNBT) to stain neuromuscular synapses, we compared the development of the adult pattern of innervation in two fast-twitch muscles in the rat: the androgen-sensitive levator ani (LA) and the extensor digitorum longus (EDL), which is not thought to be androgen sensitive. We found that about 18% of adult LA muscle fibers, but only about 2% of adult EDL fibers, are multiply innervated. Moreover, synapse elimination occurs substantially later in the LA compared with the EDL. At 2 weeks after birth, the EDL is already predominantly singly innervated, whereas the LA is still predominantly multiply innervated. The apparent delay in the normal time course of synapse elimination in the LA corresponds to a similar delay in other aspects of neuromuscular development (the time course of appearance of axonal retraction bulbs, the growth of fibers, and the development of adult motor terminal morphology). Finally, motor terminals change during synapse elimination from morphologies resembling growth cones to the adult form of neuromuscular synapses. Because the period of synapse elimination is significantly different for muscles that differ in their androgen sensitivity, hormonal sensitivity may represent an important property of motoneurons or muscle fibers influencing the normal time course of neuromuscular synapse elimination in rats. Thus, androgen might regulate the normal ontogenetic process of synapse elimination.

Aging↗
PubMed1989

Androgens modulate endplate size and ACh receptor density at synapses in rat levator ani muscle.

The dorsal bulbocavernosus or "levator ani" muscle of the rat is highly responsive to androgens. Both the muscle and the motoneurons which innervate it contain high concentrations of androgen receptors. The neuromuscular synapses in this muscle are also affected by changing androgen levels. In particular, the total number of ACh receptors (AChRs) in the muscle is lower in males that have been castrated, and it increases after treatment with the androgens, testosterone and 5 alpha-dihydrotestosterone. An examination of individual endplates using histochemistry and quantitative autoradiography suggested that the reduction in AChR number following castration is caused by reductions in both the size of endplates and in the density of AChRs at each synapse.

Aging↗