Andropause: endocrinology, erectile dysfunction, and prostate pathophysiology

This review summarizes major biological aspects of andrology of andropause, deficiency in androgens/growth hormones, and molecular parameters; erectile dysfunction (ED), the use of malleable, mechanical, inflatable devices as well as the application of Viagra (Sildenafil), alprotadil (Caverject), Yohimbine, and other drugs not yet approved by FDA, such as Papaverine, phentolamine (Vasomax), and apormorphine (Uprima); osteopenia/osteoporosis: testosterone/osteoporesis; supplementation during andropause: administration of andiogens, possible risk factors of androgens, calcium supplement and muscle mass; prostate pathophysiology: consequences of prostatectomy, prostate cancer, benign prostatic hyperplasia (BPH), hormone-dependent cancers; bladder and urethral dysfunction: neurological parameter, urodynamics technology; models on aging in male animals: comparative physiology of prostate of laboratory animals/farm animals; future research: functional anatomy of male reproductive organs, pharmacokinetics of osteoporosis, endocrinology/neuroendocrinology/chromosome anomalies supplementation during andropause, experimental animal models and future multicenter multidisciplinary research.     

Andropause: a misnomer for a true clinical entity

PURPOSE: A progressive decrease in androgen production is common in males after middle age. The resulting clinical picture has been erroneously named male menopause or andropause. A more appropriate designation is androgen decline in the aging male (ADAM). The syndrome is characterized by alterations in the physical and intellectual domains that correlate with and can be corrected by manipulation of the androgen milieu. We review the epidemiological aspects of aging and endocrinological manifestations of ADAM, and provide recommendations for treatment and monitoring of these patients. MATERIALS AND METHODS: We performed MEDLINE, Pubmed, Current Contents and Pharmaceutical Abstracts searches of relevant peer reviewed publications on andropause, male climacteric, adult hypogonadism and aging. In addition, conference proceedings were researched to provide a more complete review of the literature. Information was scrutinized and collated, and contributory data were reviewed and summarized. RESULTS: ADAM is a clinical entity characterized biochemically by a decrease not only in serum androgen, but also in other hormones, such as growth hormone, melatonin and dehydroepiandrosterone. Clinical manifestations include fatigue, depression, decreased libido, erectile dysfunction, and alterations in mood and cognition. CONCLUSIONS: The onset of ADAM is unpredictable and its manifestations are subtle and variable, which has led to a paucity of interest in its diagnosis and treatment. Urological practice commonly includes a large proportion of men older than 50 years. Therefore, it is important for urologists to recognize the manifestations of and be familiar with evaluations necessary to document ADAM as well as its treatment and monitoring.     

Cirrhotic glomerulonephritis: incidence, morphology, clinical features, and pathogenesis

Glomerulonephritis is a little known manifestation of liver cirrhosis. Since the introduction of sophisticated immunologic staining methods, glomerular morphologic abnormalities have been noted in more than 50% of patients with cirrhosis at both necropsy and biopsy. The distinctive pathologic findings consist of glomerular mesangial IgA deposits usually accompanied by complement deposition. Increased serum IgA levels are found in over 90% of cirrhotic patients with glomerular IgA deposition. Cirrhotic glomerulonephritis is usually a clinically silent disease, however, the diagnosis can be suspected by finding proteinuria or abnormalities of the urine sediment. The pathogenesis may relate to defective hepatic processing and/or portacaval shunting of circulating immune complexes.     

男性更年期综合征

男性更年期的提出是根据 5 0岁以上的部分男性可以出现与女性更年期综合征相似的临床症状。这个概念问世 5 5年以来 ,陆续出现了众多的相关概念来描述男性生命过程中的这一特殊时期 ,并对这些概念及其含义争论不休。目前 ,男性更年期综合征、迟发性性腺功能低下和中老年男性雄激素部分缺乏综合征 3者都在临床和研究中广泛使用 ,曾经用来笼统地代表男性生命过程中的这一种特殊现象 ,但是从严格意义上讲 ,它们彼此之间存在着差异。研究者出于不同的研究目的 ,在设计试验或总结相关资料时可能会选择某些概念 ,在使用相关概念前务必要明确自己的真实意图和研究对象的具体特点 ,准确地选择概念 ,不可混淆彼此的区别     

Postoperative acute refractory right ventricular failure: incidence, pathogenesis, management and prognosis

Isolated acute refractory right ventricular failure is extremely uncommon. There are greater prospects of seeing a right dominant biventricular failure, as the two ventricular chambers are contiguous. The overall clinical spectrum is determined by the relative ischemic involvement of the right or left ventricle. The postoperative acute refractory right ventricular failure that develops after cardiotomy, heart transplant, or during a left ventricular assist device support, may have somewhat dissimilar elements of origin, but the resultant clinical picture and the management are essentially similar. In this collective review, the authors have summarized the incidence, pathogenesis, management and prognosis of postoperative acute refractory right ventricular failure, in adult cardiac surgical practice. The incidence of post-cardiotomy acute refractory right ventricular failure ranges from 0.04 to 0.1%. Acute refractory right ventricular failure has also been reported in 2-3% patients after a heart transplant and in almost 20-30% patients who receive a left ventricular assist device support. The main contributor to this problem is a disproportionate ischemic involvement of the right ventricle. Other pertinent contributors to this problem are pulmonary hypertension and an altered interventricular balance. The latter component is predominant in recipients of a left ventricular assist device support. Postoperative acute refractory right ventricular failure has been successfully managed with conventional pulmonary vasodilators, mechanical support with a pulmonary artery balloon pump, a right ventricular assist device, or cavopulmonary diversion. Unfortunately, the reported initial salvage rate is only 25-30%. This problem is often underestimated. Support measures are often started late or terminated prematurely. These factors have contributed to a poor initial salvage rate in this group of patients.     

Ureteral carcinoma in situ after successful intravesical therapy for superficial bladder tumors: incidence, possible pathogenesis and management

A total of 66 patients with multifocal, progressive, flat carcinoma in situ of the bladder responded completely to intravesical bacillus Calmette-Guerin therapy for more than 1 year. Of the patients 19 (29 per cent) had clinical evidence of distal ureteral carcinoma in situ between 13 and 30 months (median 15 months) after bacillus Calmette-Guerin treatment. After evaluation of a positive urinary cytology study failed to reveal recurrent urothelial tumor of the bladder or prostatic urethral mucosa 6 patients underwent distal ureterectomy, 2 underwent nephroureterectomy, and 11 were managed by ureteroscopic resection and fulguration. In patients with carcinoma in situ of the bladder treated successfully with topical therapy the ureters represent a potential site of in situ carcinoma.     

Frostbite: pathogenesis and treatment

Frostbite, once almost exclusively a military problem, is becoming more prevalent among the general population and should now be considered to be within the scope of the civilian physician's practice. Studies into the epidemiology of civilian frostbite have identified several risk factors that may aid the clinician in the diagnosis and management of cold injuries. Research into the pathophysiology has revealed marked similarities in inflammatory processes to those seen in thermal burns and ischemia/reperfusion injury. Evidence of the role of thromboxanes and prostaglandins has resulted in more active approaches to the medical treatment of frostbite wounds. Although the surgical management of frostbite involves delayed debridement 1 to 3 months after demarcation, recent improvements in radiologic assessment of tissue viability have led to the possibility of earlier surgical intervention. In addition, several adjunctive therapies, including vasodilators, thrombolysis, hyperbaric oxygen, and sympathectomy, are discussed.     

Cryptorchidism: pathogenesis and histology

An impairment of the hypothalamopituitarygonadal axis was found to be the main cause of undescended testicles in 80 per cent of patients. Basing himself on personal observation, the author develops the theory that the mechanism of testicular descent is the stimulation by GnRH of the pituitary gland to release gonadotrophins, which in turn stimulate the interstitial cells to secrete testosterone. High local testosterone concentration fosters the development of the differentiating portion of the mesonephric duct into the epididymis. The epididymis induces descent by pushing rather than pulling the testis into the scrotal position. Any interference with this mechanism during the embryonal life leads to cryptorchid testes, which, in the vast majority of cases are localized at the external inguinal ring. The earlier the scrotal position is reached, the greater the chances of subsequent fertility.     

Hereditary carcinoma: pathogenesis and diagnosis

Effective prevention of cancer in patients with a hereditary disposition to malignant tumours was made possible by intensive prevention programs and molecular diagnosis. Taken hereditary non-polyposis colorectal cancer (HNPCC) as an example this article deals with the pathogenesis and molecular diagnosis in hereditary dispositions to cancer. HNPCC is inherited in an autosomal-dominant fashion and caused by germline mutations in genes responsible for detection an removal of DNA-basepair-mismatches (DNA-mismatch-repair-genes). The error rate in DNA replication is reduced thousandfold by these genes. A defective DNA-mismatch-repair results in tumours if the increased mutation rate causes alterations of tumour-suppressor- or oncogenes. HNPCC patients develop colorectal cancer but also tumours of the renal pelvis, the ureter, the small bowel, the endometrium and less often in other organs. The clinical presentation of these tumours may be characteristic, the clinical diagnosis may be guided by different clinical criteria catalogues. The suspicion is proven by the identification of a germline mutation in DNA-mismatch-repair-genes. This laborious diagnostic procedure is often preceded by prescreening procedures as the detection of microsatellite instability or immunohistochemical tests. Once the germline mutation is identified in a affected family member, the first degree relatives may be tested for this mutation. If they have inherited the mutation, they harbour a extremely high risk for developing cancer and therefore may be included in prevention programs. This so called predictive testing must be preceded by genetic counseling.     

Glucocorticoid-induced osteoporosis: pathogenesis and management

Glucocorticoid- (GC-) induced osteoporosis and an increased risk of fractures are one of the most serious problems for patient using long-term GC therapy, such as those with rheumatoid arthritis, autoimmune diseases, inflammatory bowel diseases, bronchial asthma, and chronic lung diseases. GCs are known to affect both bone formation and resorption. In rheumatoid arthritis, the etiology of bone loss is multifactorial, including local inflammation around joints, release of bone-absorbing cytokines, physical inactivity, and malnutrition, in addition to the use of GC. Two guidelines have been published, by the American College of Rheumatology Task Force in 1966 and by the UK Consensus Group in 1998. Both guidelines recommend that patients receiving GC therapy at doses of 7.5 mg/day of prednisolone or more for 6 months or longer should have their bone mineral density measured and begin preventive therapies. Calcium and vitamin D supplements, sex hormone replacement, and weight-bearing exercise are the first-line therapies. For patients who are unable to take sex hormone replacement therapy (HRT), bisphosphonates are recommended by both guidelines. In this article, we briefly summarize the pathogenesis of GC-induced osteoporosis and its prevention and treatment. Received: April 7, 2000     

Sprengel deformity: pathogenesis and management

Sprengel deformity (ie, congenital elevation of the scapula) is a rare clinical entity. However, it is the most common congenital anomaly of the shoulder. Sprengel deformity is caused by abnormal descent of the scapula during embryonic development. Sprengel deformity is associated with cosmetic deformity and decreased shoulder function. Diagnostic confusion with limited scoliosis can be dangerous to the patient because it may delay proper treatment of other abnormalities that may be present with even mild cases. Sprengel deformity is commonly linked to a variety of conditions, including Klippel-Feil syndrome, scoliosis, and rib anomalies. Nonsurgical management can be considered for mild cases. Surgical management is typically warranted for more severe cases, with the goal of improving cosmesis and function. Surgical techniques are centered on resection of the protruding portion of the scapula and inferior translation of the scapula. Recent long-term studies indicate that patients treated surgically maintain improved shoulder function and appearance.