Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There were 50 patients with acute epididymitis who were evaluated prospectively by history, examination and microbiologic studies, including cultures for aerobes, anaerobes, Neisseria gonorrhoeae, Chlamydia trachomatis and Ureaplasma urealyticum. Escherichia coli was the predominant pathogen isolated from the urine of men more than 35 years old, while Chlamydia trachomatis and Neisseria gonorrhoeae were the predominant pathogens isolated from the urethra of men less than 35 years old. The etiologic role of Escherichia coli and Chlamydia trachomatis was confirmed by isolation from epididymal aspirates from a high proportion of men with positive urine or urethral cultures for these agents. Chlamydia trachomatis epididymitis accounted for two-thirds of idiopathic epididymitis in young men and often was associated with oligospermia. Of 9 female sexual partners of men with Chlamydia trachomatis infection 6 had antibody to Chlamydia trachomatis, of whom 2 had positive cervical cultures for this organism and 2 others had non-gonococcal pelvic inflammatory disease. Antibiotic therapy with tetracycline was effective for the treatment of men with Chlamydia trachomatis epididymitis and should be offered to the female sex partners.
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PMID:Etiology, manifestations and therapy of acute epididymitis: prospective study of 50 cases. 37 66

Epididymal disease is in our experience responsible for about 40 per cent of male infertility situations. The diagnosis of epididymal oligospermia can be suspected by the presence of firm normal volume testicles, by the absence of any elevation of FSH, and eventually, by a (slightly) hardened epididymis at palpation. The definite diagnosis however will only be established by quantitative reading of the testicular biopsy. Besides in oligospermic patients clinical information isolates an eventual new group where healthy epididymis could interfere with sperm quality by its malposition.
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PMID:Oligospermia associated with normal testicular function and epididymal lesions or malpositions. 134 38

Of the 595 infertile African males studied, 192 (30.8%) were azoospermic and 413 (69.40%) had oligospermia. Azoospermia was caused by obstruction to the vas and/or epididymis in 44% of cases and testicular lesions in the remaining 56% of cases, whilst the oligospermia was probably caused by obstruction in 4.7% of cases and testicular lesions in 85.3%. Bilateral testicular biopsies were performed on 302 patients. A variety of pathological conditions were observed; the most prevalent was hypospermatogenesis, in 12% of cases. A significant portion (37.2%) of patients without testicular biopsies had clinically detectable testicular or epididymal abnormalities. There was a higher incidence (12%) of inflammatory testicular or prostatic conditions in this study as compared with those found in Europeans, suggesting that inflammatory conditions contribute more to male infertility in Africa. Only a single case of chromosomal abnormality was detected.
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PMID:Etiological factors of male infertility in Africa. 135 43

Samples of sperm have been obtained from 95 who consulted us for infertility. In each case seminal plasma was examined for levels of alpha-1,4-glucosidase and L-carnitine. Our results have led us to fix the threshold value of 42.6 mlU per ejaculate for alpha-1,4-glucosidase and 960 nanomoles of L-carnitine below those levels that we thought occur where the origin of the oligospermia is obstructive (series 1 patients). In series 2 patients the cause of the oligospermia purely being secretory, there is normal epididymal function and therefore the excretory doubts are proven. It is not impossible to have both pathologies because we have found this in men of the intermediate groups C and D. We have found that there is a correlation between the presence of epididymal pathology and a drop in epididymal markers which can be found in severe oligospermia (which can be epididymal in origin and not testicular). Also when there is non abnormalities in the spermogram. This last situation can occur in "invisible" abnormalities of spermaturation in the epidymus.
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PMID:[The value of the level of alpha-1,4-glucosidase and seminal l-carnitine in patients with oligoasthenospermia]. 182 86

Rats were exposed to 0, 0.1, 1, and 12 ppm of hexafluoroacetone (HFA) for 6 h/day, 5 days/week for 90 days. The exposed rats were killed after 30 or 90 days exposure, and 28 or 84 days post-exposure (PE). There were no exposure-related pathological lesions in the rats exposed to 0.1 or 1.0 HFA for 90 days. After 30 days exposure to 12 ppm HFA, rats showed lower body weight gain, testicular atrophy, and oligospermia or aspermia in the epididymal tubules. At 30 days exposure, the atrophic testes had marked depletion of round spermatids in spermatogenic stages I-VIII and elongated spermatids in spermatogenic stages IX-XIV, but mature spermatids appeared only slightly decreased. Numerous spermatocytes in meiotic division in spermatogenic stage XIV were necrotic. At 90 days exposure, the testes showed severe atrophy with almost all seminiferous tubules affected and both immature and mature spermatids had disappeared from the seminiferous tubules. The epididymal tubules were devoid of spermatozoa. After 28 days PE, regeneration of atrophic testes was evident but varied markedly among the exposed rats. The number of seminiferous tubules producing elongated and mature spermatids was significantly lower than that of normal testes. Many seminiferous tubules had not regained normal spermatogenesis and the epididymal tubules showed marked oligospermia. After 84 days PE, normal spermatogenesis was still only partially restored to the atrophic testes, with many of the regenerating tubules still devoid of normal spermatogenesis.
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PMID:Testicular toxicity of rats exposed to hexafluoroacetone (HFA) for 90 days. 204 29

Fructose levels and fructolysis index in human semen were analysed to assess a correlation, if any, between the levels of this glycolysable sugar and sperm concentration. Semen was collected from normospermic men and men with azoospermia or oligospermia. Seminal fructose levels were elevated in men with obstructive azoospermia and in men who remained azoospermic following vasoepididy mostomy done to correct epididymal blockage. Men with sperm concentration of less than 20 million/ml pre-operatively or following vasoepididy mostomy, showed significantly high levels of fructose and lower fructolysis index. Fructose levels in normospermic infertile men, as well as in men with normal sperm counts (more than 20 million/ml), were similar to that in men of proven fertility.
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PMID:Seminal fructose in normal and infertile men. 271 90

The aim of this study was to determine the eventual fertility of those patients following vasectomy reversal who have no pressure-induced secondary epididymal blockage. These patients underwent simple vasovasostomy because at the time of the reversal surgery there were sperm present in large numbers in the vas fluid. It was possible to obtain long-term follow-up on 326 early patients who underwent vasectomy reversal 8-10 years ago. Two hundred and eighty-two of those patients had sperm in the vas fluid. These patients were studied for pregnancy rate and post-operative semen parameters in relation to presence or absence of sperm in the vas fluid at the time of vasectomy reversal, duration of time since vasectomy, pre-operative serum antisperm antibody titers, the influence of varicocoele and quantitative evaluation of testicular biopsy. All of the 44 patients with no sperm in the vas fluid remained azoospermic following vasovasostomy. Of the 282 patients with sperm in the vas fluid, 228 (81%) eventually impregnated their wives. Twenty-four patients with sperm in the vas fluid (9%) were azoospermic and did not impregnate their wives. Of the 258 patients who had sperm patency, the pregnancy rate was 88%. The number of mature spermatids per tubule in the testis correlated closely with the post-operative sperm count in patent cases. Quantitative evaluation of the testicular biopsy revealed normal spermatogenesis, even in patients with azoospermia or severe oligospermia post-operatively. Technical failures were due to blockage either at the vasovasostomy site, or epididymal blockage unrecognized at the time of vasovasostomy.2+perm count had a minimal impact on the
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PMID:Pregnancy after vasovasostomy for vasectomy reversal: a study of factors affecting long-term return of fertility in 282 patients followed for 10 years. 271 9

Sixty male leprosy patients (mean age 27.2 +/- 5.04 years) selected at random, were studied for gonadal involvement with the mean duration of illness 4.17 +/- 3.27 years. Only lerpomatous and borderline leprosy cases developed testicular and epididymal changes. Testicular pain and/or swelling (lepromatous 62.5%, borderline 30%) was the main presenting feature. Altered sexual function was observed in 34(56.6%) cases, and 11 patients revealed altered sexual hair pattern. Gynecomastia was seen in 9 cases. Reduced testicular size along with its soft feeling was present in 25% of cases while no testicular sensation was felt in 8 (13.3%) cases, and impaired testicular sensation in 9 (15%) of them. Spermogram revealed azoospermia in 19 (35%) and oligospermia in 16 (26.6%) cases. Histo-pathology revealed evidences of leprous pathology irrespective of testicular size, semen picture and clinical manifestations. There was marked variation in histopathological findings in testes and hence it was difficult to categorise them into vascular, interstitial and obliterative phase.
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PMID:Male gonads in leprosy--a clinico-pathological study. 320 78

Only when a patient presents a situation of azoospermia with normal hormonal assays the attention is focussed on the epididymis and in all other cases testicular damage is automatically suspected. However, there are many instances where oligospermia cannot be explained and where the testicular biopsy shows vigourous spermatogenesis. Detection of difficulties in epididymal transit is a new differential diagnosis of oligoasthenospermia. The delicate structure of the epididymis can be destroyed by infections that in extreme cases do cause complete obstructions but much more frequently lead to sub-total blocks. The diagnosis is made by comparing ejaculates with testicular biopsies and their very meticulous quantitative reading. A good selection of cases can lead to microsurgical repair of epididymal damage and significant improvement of sperm quality.
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PMID:[Epididymal oligospermia]. 325 4

Four patients with persistent oligospermia and necrospermia were found to have severely degenerated sperm in the ejaculate. However, in those examined, testicular sperm were ultrastructurally normal, indicating that sperm degeneration and death was occurring during epididymal passage or storage or both or upon mixing with the seminal plasma at ejaculation. Seminal plasma was found to be nontoxic to normal donor sperm. In three patients, frequent ejaculation (two ejaculates per day for 4 or 5 days) was used to deplete epididymal sperm reserves and reduce the period spent in the epididymis. This resulted in a threefold to sevenfold increase in percentage of motile sperm in the ejaculate and a similar increase in sperm motility index. The authors propose the term "epididymal necrospermia" to describe this previously undefined type of male infertility.
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PMID:Human male infertility caused by degeneration and death of sperm in the epididymis. 337 83


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