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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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FDG positron emission tomography (PET) may be useful to detect the condition early. Other imaging studies including MRI, CT scans, and X-rays may reveal inflammation and/or damaged cartilage facilitating diagnosis.
Biopsy of the cartilage tissue (for example, ear) may show tissue inflammation and destruction, and may help with the diagnosis. The Biopsy of cartilage in patients with relapsing polychondritis may demonstrate chondrolysis, chondritis, and perichondritis.
Perichondritis is inflammation of the perichondrium, a layer of connective tissue which surrounds cartilage. A common form, auricular perichondritis ("perichondritis auriculae") involves infection of the pinna due to infection of traumatic or surgical wound or the spread of inflammation into depth. It may lead to severe deformation of the pinna if not treated vigorously with IV antibiotics. The causative organism is usually "Pseudomonas aeruginosa". A rare form is laryngeal perichondritis ("perichondritis laryngis"). It develops suddenly due to an injury, virulent organisms or compromised immune status of the host, and also affects cartilage of the larynx. This may result in deformations and stenoses.
In chronic recurrent sialadenitis or chronic sclerosing sialadenitis, acute attacks are managed with conservative therapies such as hydration, analgesics (mainly NSAIDs), sialogogues to stimulate salivary secretion, and regular, gentle gland massage. If infection is present, appropriate cultures should be obtained, followed by empirical antibiotic therapy initially, for example amoxicillin/clavulanate or clindamycin which cover oral flora.
If there are attacks more than approximately 3 times per year or severe attacks, surgical excision of the affected gland should be considered.
For sinusitis lasting more than 12 weeks a CT scan is recommended. On a CT scan, acute sinus secretions have a radiodensity of 10 to 25 Hounsfield units (HU), but in a more chronic state they become thickened, with a radiodensity of 30 to 60 HU.
Nasal endoscopy and clinical symptoms are also used to make a positive diagnosis. A tissue sample for histology and cultures can also be collected and tested. Allergic fungal sinusitis (AFS) is often seen in people with asthma and nasal polyps. In rare cases, sinusoscopy may be made.
Nasal endoscopy involves inserting a flexible fiber-optic tube with a light and camera at its tip into the nose to examine the nasal passages and sinuses. This is generally a completely painless (although uncomfortable) procedure which takes between five and ten minutes to complete.
There are no definitive diagnostic tests for CP/CPPS. This is a poorly understood disorder, even though it accounts for 90–95% of prostatitis diagnoses. It is found in men of any age, with the peak incidence in men aged 35–45 years. CP/CPPS may be inflammatory (Category Ⅲa) or non-inflammatory (Category Ⅲb), based on levels of pus cells in expressed prostatic secretions (EPS), but these subcategories are of limited use clinically. In the inflammatory form, urine, semen, and other fluids from the prostate contain pus cells (dead white blood cells or WBCs), whereas in the non-inflammatory form no pus cells are present. Recent studies have questioned the distinction between categories Ⅲa and Ⅲb, since both categories show evidence of inflammation if pus cells are ignored and other more subtle signs of inflammation, like cytokines, are measured.
In 2006, Chinese researchers found that men with categories Ⅲa and Ⅲb both had significantly and similarly raised levels of anti-inflammatory cytokine TGFβ1 and pro-inflammatory cytokine IFN-γ in their EPS when compared with controls; therefore measurement of these cytokines could be used to diagnose category Ⅲ prostatitis. A 2010 study found that nerve growth factor could also be used as a biomarker of the condition.
For CP/CPPS patients, analysis of urine and expressed prostatic secretions for leukocytes is debatable, especially due to the fact that the differentiation between patients with inflammatory and non-inflammatory subgroups of CP/CPPS is not useful. Serum PSA tests, routine imaging of the prostate, and tests for Chlamydia trachomatis and Ureaplasma provide no benefit for the patient.
Extraprostatic abdominal/pelvic tenderness is present in >50% of patients with chronic pelvic pain syndrome but only 7% of controls.
Healthy men have slightly more bacteria in their semen than men with CPPS. The high prevalence of WBCs and positive bacterial cultures in the asymptomatic control population raises questions about the clinical usefulness of the standard 4-glass test as a diagnostic tool in men with CP/CPPS. The use of the four-glass test by American urologists is now rare, with only 4% using it regularly.
Men with CP/CPPS are more likely than the general population to suffer from Chronic Fatigue Syndrome (CFS), and Irritable Bowel Syndrome (IBS).
Experimental tests that could be useful in the future include tests to measure semen and prostate fluid cytokine levels. Various studies have shown increases in markers for inflammation such as elevated levels of cytokines, myeloperoxidase, and chemokines.
Some conditions have similar symptoms to chronic prostatitis: Bladder neck hypertrophy and urethral stricture may both cause similar symptoms through urinary reflux ("inter alia"), and can be excluded through flexible cytoscopy and urodynamic tests.
Sialadenitis (sialoadenitis) is inflammation of a salivary gland. It may be subdivided temporally into acute, chronic and recurrent forms.
Health care providers distinguish bacterial and viral sinusitis by watchful waiting. If a person has had sinusitis for fewer than 10 days without the symptoms becoming worse, then the infection is presumed to be viral. When symptoms last more than 10 days or get worse in that time, then the infection is considered bacterial sinusitis. Imaging by either X-ray, CT or MRI is generally not recommended unless complications develop. Pain caused by sinusitis is sometimes confused for pain caused by pulpitis (toothache) of the maxillary teeth, and vice versa. Classically, the increased pain when tilting the head forwards separates sinusitis from pulpitis.
Chronic mucocutaneous candidiasis can be diagnosed in an affected individual via the following methods/tests:
In chronic bacterial prostatitis there are bacteria in the prostate, but there may be no symptoms or milder symptoms than occur with acute prostatitis. The prostate infection is diagnosed by culturing urine as well as prostate fluid (expressed prostatic secretions or EPS) which are obtained by the doctor performing a rectal exam and putting pressure on the prostate. If no fluid is recovered after this prostatic massage, a post massage urine should also contain any prostatic bacteria.
Prostate specific antigen levels may be elevated, although there is no malignancy. Semen analysis is a useful diagnostic tool. Semen cultures are also performed. Antibiotic sensitivity testing is also done to select the appropriate antibiotic. Other useful markers of infection are seminal elastase and seminal cytokines.
Treatment options include antibiotic therapy (not a permanent solution), endodontic (root canal) therapy, or extraction.
Periapical periodontitis of some form is a very common condition. The prevalence of periapical periodontitis is generally reported to vary according to age group, e.g. 33% in those aged 20–30, 40% in 30- to 40-year-olds, 48% in 40- to 50-year-olds, 57% in 50- to 60-year-olds and 62% in those over the age of 60. Most epidemiologic data has been generated in European countries, especially Scandinavia. Millions of root canal treatments are carried out in the United States each year, although the total number of root canal treatments is an imperfect indicator of the prevalence of periapical periodontitis, since not always is it performed due to the presence of periapacial periodontitis, and not all cases of asymptomatic periodontitis will be treated in this manner, either due to lack of patient attendance or watchful waiting.
Management of chronic granulomatous disease revolves around two goals: 1) diagnose the disease early so that antibiotic prophylaxis can be given to keep an infection from occurring, and 2) educate the patient about his or her condition so that prompt treatment can be given if an infection occurs.
Chronic granulomatous disease is the name for a genetically heterogeneous group of immunodeficiencies. The core defect is a failure of phagocytic cells to kill organisms that they have engulfed because of defects in a system of enzymes that produce free radicals and other toxic small molecules. There are several types, including:
- X-linked chronic granulomatous disease (CGD)
- autosomal recessive cytochrome b-negative CGD
- autosomal recessive cytochrome b-positive CGD type I
- autosomal recessive cytochrome b-positive CGD type II
- atypical granulomatous disease
Management for an individual with chronic mucocutaneous candidiasis consists of the following(relapse occurs once treatment is ceased, in many cases):
Nasal vestibulitis is the diffuse dermatitis of nasal vestibule. It is often caused by "Staphylococcus aureus." It may be secondary to chronic rhinorrhea, nose picking or viral infections. In acute vestibulitis, the skin is red, swollen and tender. In chronic vestibulitis, induration of vestibular skin and crusting is seen. It is treated by cleaning the nasal vestibule of all crusts with a cotton applicator soaked in hydrogen peroxide. Antibiotic steroid ointment is sometimes helpful. Chronic fissures are treated by cautery.
Systemic antibiotics such as amoxicillin or metronidazole are sometimes used in addition to debridement based treatments.
"Systemic antimicrobials in conjunction with scaling and root planing (SRP), can offer an additional benefit over SRP alone in the treatment of periodontitis, in terms of clinical attachment loss (CAL) and probing pocket depth (PPD) change, and reduced risk of additional CAL loss. However, differences in study methodology and lack of data precluded an adequate and complete pooling of data for a more comprehensive analyses. It was difficult to establish definitive conclusions, although patients with deep pockets, progressive or 'active' disease, or specific microbiological profile, can benefit more from this adjunctive therapy."
There is only very weak evidence linking to coronary heart disease.
There is little evidence linking progression of periodontal disease to low birth weight or preterm birth:
"In these women with periodontitis and within this study's limitations, disease progression was not associated with an increased risk for delivering a pre-term or a low birthweight infant."
There is recently emerged evidence linking chronic periodontitis with head and neck squamous cell carcinoma: "Patients with periodontitis were more likely to have poorly differentiated oral cavity SCC than those without periodontitis (32.8% versus 11.5%; P = 0.038)".
There is evidence to suggest that periodontal disease may play a role in the pathogenesis of Alzheimer's Disease.
Epididymitis can be classified as acute, subacute, and chronic, depending on the duration of symptoms.
The diagnosis of chronic pancreatitis is based on tests on pancreatic structure and function. Serum amylase and lipase may be moderately elevated in cases of chronic pancreatitis, amylase and lipase are nearly always found elevated in the acute condition. A secretin stimulation test is considered the best test for diagnosis of chronic pancreatitis. Other tests used to determine chronic pancreatitis are serum trypsinogen, computed tomography, ultrasound and biopsy.
When chronic pancreatitis is caused by genetic factors, elevations in ESR, IgG4, rheumatoid factor, ANA and anti-smooth muscle antibody may be detected.
Diagnosis is readily made by the cotton-swab test, in which pressure is applied in a circular fashion around the vulvar vestibule to assess complaints of pain. Laboratory tests are used to exclude bacterial or viral infection, and a careful examination of the vulvo/vaginal area is conducted to assess whether any atrophy is present.
Diagnosis is typically based on symptoms. Conditions that may result in similar symptoms include testicular torsion, inguinal hernia, and testicular cancer. Ultrasound can be useful if the diagnosis is unclear.
Epididymitis usually has a gradual onset. Typical findings are redness, warmth and swelling of the scrotum, with tenderness behind the testicle, away from the middle (this is the normal position of the epididymis relative to the testicle). The cremasteric reflex (elevation of the testicle in response to stroking the upper inner thigh) remains normal. This is a useful sign to distinguish it from testicular torsion. If there is pain relieved by elevation of the testicle, this is called Prehn's sign, which is, however, non-specific and is not useful for diagnosis.
Before the advent of sophisticated medical imaging techniques, surgical exploration was the standard of care. Today, Doppler ultrasound is a common test: it can demonstrate areas of blood flow and can distinguish clearly between epididymitis and torsion. However, inasmuch as torsion and other sources of testicular pain can consistently be determined by palpation alone, some studies have suggested that the only real benefit of an ultrasound, which is a fairly expensive procedure (~US$300 to US$800 in 2013), is to assure the patient that he does not have testicular cancer. Nuclear testicular blood flow testing is rarely used.
Additional tests may be necessary to identify underlying causes. In younger children, a urinary tract anomaly is frequently found. In sexually active men, tests for sexually transmitted diseases may be done. These may include microscopy and culture of a first void urine sample, Gram stain and culture of fluid or a swab from the urethra, nucleic acid amplification tests (to amplify and detect microbial DNA or other nucleic acids) or tests for syphilis and HIV.
Antibiotic therapy has to overcome the blood/prostate barrier that prevents many antibiotics from reaching levels that are higher than minimum inhibitory concentration. A blood-prostate barrier restricts cell and molecular movement across the rat ventral prostate epithelium. Treatment requires prolonged courses (4–8 weeks) of antibiotics that penetrate the prostate well. The fluoroquinolones, tetracyclines and macrolides have the best penetration. There have been contradictory findings regarding the penetrability of nitrofurantoin , quinolones (ciprofloxacin, levofloxacin), sulfas (Bactrim, Septra), doxycycline and macrolides (erythromycin, clarithromycin). This is particularly true for gram-positive infections.
In a review of multiple studies, Levofloxacin (Levaquin) was found to reach prostatic fluid concentrations 5.5 times higher than Ciprofloxacin, indicating a greater ability to penetrate the prostate.
Persistent infections may be helped in 80% of patients by the use of alpha blockers (tamsulosin (Flomax), alfuzosin), or long term low dose antibiotic therapy. Recurrent infections may be caused by inefficient urination (benign prostatic hypertrophy, neurogenic bladder), prostatic stones or a structural abnormality that acts as a reservoir for infection.
In theory, the ability of some strains of bacteria to form biofilms might be one factor amongst others to facilitate development of chronic bacterial prostatitis.
Escherichia coli extract and cranberry have a potentially preventive effect on the development of chronic bacterial prostatitis, while combining antibiotics with saw palmetto, lactobacillus sporogens and arbutin may lead to better treatment outcomes.
Bacteriophages hold promise as another potential treatment for chronic bacterial prostatatis.
The addition of prostate massage to courses of antibiotics was previously proposed as being beneficial and prostate massage may mechanically break up the biofilm and enhance the drainage of the prostate gland. However, in more recent trials, this was not shown to improve outcome compared to antibiotics alone.
The diagnosis of this syndrome can be done via the test "Branchiootorenal syndrome via the SIX5 Gene" whose purpose is mutation confirmation and risk assessment (screening).