PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 9716292

Prostatitis: US perspective.

A J Schaeffer
View original source ↗Export metadata ↓

Abstract

The diagnosis and management of prostatitis syndromes is a challenge to the clinician. Careful history and examination of the prostate fluid and quantitative segmented bacteriologic cultures will lead to proper categorization into the recognized forms of the prostatitis syndrome. Antimicrobial therapy is effective in the majority of men with acute and chronic bacterial prostatitis (CBP). Fluoroquinolone agents appear to have an increasingly important role in this regard, although a randomized, prospective, double-blind study is still lacking. Alpha-1-selective blocking agents may relieve symptomatology of chronic pelvis pain syndrome (CPPS). Other non-prostatic sources of voiding symptoms should be sought and ruled out, especially malignancy or inflammatory disorders.

Explore related subjects

Acute DiseaseAdolescentAdultAgedChronic DiseaseDiagnostic Techniques, UrologicalHumansMaleMiddle AgedPelvic PainProstatitisJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A J Schaeffer. 1998. Prostatitis: US perspective.. https://doi.org/10.1016/s0924-8579(98)00029-6

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2000

Nerve growth factor antibody exacerbates neuropathological signs of experimental allergic encephalomyelitis in adult lewis rats.

In this study, experimental allergic encephalomyelitis (EAE) rats and rats exhibiting EAE expressing high circulating anti-nerve growth factor antibody were daily monitored for clinical signs and chronic relapses. Eighty-five days after EAE induction, blood, spinal cord and brain stem were used for histological examination, nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) evaluation. The results showed that NGF-deprived rats display more severe clinical signs of disease. These effects were associated with a significant reduction of NGF in the brain stem and spinal cord but not of BDNF, which decreased only in spinal cord. These observations provide additional support to the hypothesis of a protective NGF role in rats exhibiting EAE.

Acute Disease↗
PubMed2000

Body iron stores and early neurologic deterioration in acute cerebral infarction.

BACKGROUND: Iron-dependent free radicals formation has been related to greater damage in cerebral ischemia. The authors analyzed whether increased body iron stores were associated with early neurologic worsening and excitatory amino acid release in patients with acute ischemic stroke. METHODS: Ferritin, total iron, and glutamate concentrations in plasma and CSF were measured on admission in 100 consecutive patients with a cerebral infarction of <24 hours' duration. The authors diagnosed progressing stroke when the Canadian Stroke Scale score decreased one or more points between admission and 48 hours. Cranial CT was performed on admission and repeated on days 4 to 7 of hospitalization. RESULTS: Ferritin concentrations in plasma (median 391, range 119 to 500 versus 148, 21 to 399 ng/mL) and in CSF (17.4, 6.8 to 82, versus 4.8, 0.6 to 14 ng/mL) were significantly higher in the 45 patients with subsequent progressing stroke than in those with nonprogressing stroke (p < 0.001). There was a positive correlation between ferritin and glutamate concentrations in plasma (r = 0.81, p < 0.001) and CSF (r = 0.64, p < 0.001). Plasma ferritin concentrations >275 ng/mL in plasma (OR, 33.5; 95% CI, 4.7 to 235) and >11 ng/mL in CSF (OR, 11.4; 95% CI, 3. 1 to 41) were independently and significantly related to early neurologic worsening. The effect was reduced by >60% after controlling for glutamate concentrations, but remained significant. CONCLUSIONS: High plasma and CSF ferritin concentrations within the first 24 hours from the onset of ischemic stroke are associated with early neurologic deterioration. Increased body iron stores may contribute to stroke progression by enhancing the cytotoxic mechanisms in cerebral ischemia.

Acute Disease↗
PubMed2000

Trisomy 10 in acute myeloid leukemia: three new cases.

Trisomy 10 is a rare nonrandom cytogenetic abnormality found in association with acute myeloid leukemia (AML). The hematological and clinical features associated with this finding have not yet been clearly defined. A literature review revealed 13 cases of trisomy 10 in AML, some reported as a minority component of a more comprehensive AML study and therefore lacking a full description of both clinical and hematological features. We present a summary of these reports and add three new cases to the literature.

Acute Disease↗