Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031350 (pharyngitis)
 2,405 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Within 72 hours of visiting the Everglades National Park in south Florida, a 43-year-old man became ill with fever, malaise, myalgia, severe headache, pharyngitis, and enlarged, tender lymph nodes. Everglades (Venezuelan equine encephalomyelitis, subtype II) virus was isolated from a blood sample drawn from the patient five days after onset of symptoms.
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PMID:Everglades virus infection in man, 1975. 744 36

We describe a 60-year-old patient who presented with prolonged fever, weight loss, adenopathies and malaise. Two months later, an aphthous stomatitis and pharyngitis developed, together with ulcerations bilaterally in the groin. Two separate skin biopsies revealed the diagnosis of linear IgA dermatosis. This entity, which is well known to dermatologists but not to internists, should be added to the extensive list of disorders than can provoke the syndrome of fever of unknown origin.
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PMID:Linear IgA dermatosis: a new cause of fever of unknown origin. 854 92

A syndrome involving periodic fever, pharyngitis, adenitis and aphthous stomatitis is described in 8 children. Attacks are characterized by abrupt onset of fever and, in addition to the above symptoms, by malaise, headache and abdominal pain. Mild leukocytosis and elevation of the erythrocyte sedimentation rate are found in the laboratory. Patients exhibit normal growth and development and are otherwise healthy. PFAPA is clinically benign, with no long-term sequelae. Recognition and diagnosis of the syndrome eliminate the need for intensive work-up. The cause remains unknown. No evidence linking bacterial, viral, or fungal pathogens to this syndrome has been found. No patient has exhibited atypical lymphocytosis or neutropenia, and all patients had normal levels of immunoglobulin. All had received antibiotics early in the course of their illness but without effect. Cimetidine has been discussed in the literature as a possible treatment, but the results are controversial.
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PMID:[PFAPA syndrome: periodic fever, adenitis, pharyngitis and aphthous stomatitis]. 933 38

Erythromycin is a frequently used antibiotic in patients with atypical respiratory infection and/or an allergy to penicillin. We report the case of a young woman who developed severe cholestasis and jaundice following treatment with erythromycin stearate. Two years later her general practitioner prescribed erythromycin succinate for pharyngitis. She experienced a severe second episode of jaundice and malaise. Different esters of erythromycin have been introduced to reduce side effects such as allergic reactions to erythromycin. The findings in our patient underline the fact that hypersensitivity is caused by the erythromycin molecule, independent from the type of esterification. Because of these side effects newer makrolides should be given preference over erythromycin.
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PMID:Cholestasis and liver cell damage due to hypersensitivity to erythromycin stearate--recurrence following therapy with erythromycin succinate. 1008 Nov 26

We report 28 patients (20 male) with a syndrome characterized by abrupt onset of fever, malaise, aphthous stomatitis, tonsillitis, pharyngitis, and cervical adenopathy (PFAPA syndrome). Episodes of fever occurred at intervals of 5.1 +/- 1.3 weeks beginning at the age of 4.2 +/- 2.7 years. Fever, malaise, tonsillitis with negative throat cultures, and cervical adenopathy were reported in all 28 patients, aphthae in 19, headache in 5, abdominal pain in 5, and arthralgia in 3. Mild hepatosplenomegaly was observed in 6 patients. Mild leukocytosis, elevation of the erythrocyte sedimentation rate, and fibrinogen were found during attacks. These episodes of illness resolved spontaneously in 4.3 +/- 1.7 days. Serum IgD was found elevated (>100 U/mL) in 12 of the 18 patients tested (140.2 +/- 62.4 U/mL). Affected children grow normally, have no associated diseases, and have no long-term sequelae. Attacks were aborted by a single dose of oral prednisone (2 mg/kg) at the beginning of the attack in all 15 patients in whom this medication was prescribed. In 9 patients the syndrome has completely resolved (beginning at the age of 2.9 +/- 1.3 and lasting 8 +/- 2.5 years). In 3 other patients complete resolution of the attacks occurred after tonsillectomy was performed. PFAPA is sporadic, and no ethnic predilection was found. Increased awareness of the clinical syndrome has resulted in more frequent diagnosis and adequate treatment.
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PMID:Periodic fever, aphthous stomatitis, pharyngitis, and adenopathy syndrome: clinical characteristics and outcome. 1096 77

Although the anticonvulsant hypersensitivity syndrome was first described in 1950, confusion still abounds regarding the syndrome. The triad of fever, rash and internal organ involvement occurring 1 to 8 weeks after exposure to an anticonvulsant heralds this rare (1 in 1,000 to 10,000 exposures) but serious reaction. Aromatic anticonvulsants [phenytoin, phenobarbital (phenobarbitone) and carbamazepine] are the most frequently involved drugs; however, there have also been several cases of anticonvulsant hypersensitivity syndrome associated with lamotrigine. Fever, in conjunction with malaise and pharyngitis, is often the first sign. This is followed by a rash which can range from a simple exanthem to toxic epidermal necrolysis. Internal organ involvement usually involves the liver, although other organs such as the kidney, CNS or lungs may be involved. Hypothyroidism may be a complication in these patients approximately 2 months after occurrence of symptoms. The aromatic anticonvulsants are metabolised to hydroxylated aromatic compounds, such as arene oxides. If detoxification of this toxic metabolite is insufficient, the toxic metabolite may bind to cellular macromolecules causing cell necrosis or a secondary immunological response. Cross-reactivity among the aromatic anticonvulsants may be as high as 75%. In addition, there is a familial tendency to hypersensitivity to anticonvulsants. Discontinuation of the anticonvulsant is essential in patients who develop symptoms compatible with anticonvulsant hypersensitivity syndrome. A minimum battery of laboratory tests, such as liver transaminases, complete blood count and urinalysis and serum creatinine, should be performed. Corticosteroids are usually administered if symptoms are severe. Patients with anticonvulsant hypersensitivity syndrome should avoid all aromatic anticonvulsants; benzodiazepines, valproic acid (sodium valproate) or one of the newer anticonvulsants can be used for seizure control. However, valproic acid should be used very cautiously in the presence of hepatitis. There is no evidence that lamotrigine cross-reacts with aromatic anticonvulsants. In addition, family counselling is a vital component of patient management.
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PMID:Anticonvulsant hypersensitivity syndrome: incidence, prevention and management. 1061 72

Diskitis, an inflammation of the intervertebral disk, is generally attributable to Staphylococcus aureus and rarely Staphylococcus epidermidis, Kingella kingae, Enterobacteriaciae, and Streptococcus pneumoniae. In many cases, no bacterial growth is obtained from infected intervertebral discs. Although anaerobic bacteria were recovered from adults with spondylodiscitis, these organisms were not reported before from children. The recovery of anaerobic bacteria in 2 children with diskitis is reported. Patient 1. A 10-year-old male presented with 6 weeks of low back pain and 2 weeks of low-grade fever and abdominal pain. Physical examination was normal except for tenderness to percussion over the spine between thoracic vertebra 11 and lumbar vertebra 2. The patient had a temperature of 104 degrees F. Laboratory tests were within normal limits, except for erythrocyte sedimentation rate (ESR), which was 58 mm/hour. Blood culture showed no growth. Magnetic resonance imaging with gadolinium contrast revealed minimal inflammatory changes in the 12th thoracic vertebra/first lumbar vertebra disk. There was no other abnormality. A computed tomography (CT)-guided aspiration of the disk space yielded bloody material, which was sent for aerobic and anaerobic cultures. Gram stain showed numerous white blood cells and Gram-positive cocci in chains. Cultures for anaerobic bacteria yielded heavy growth of Peptostreptococcus magnus, which was susceptible to penicillin, clindamycin, and vancomycin. The patient was treated with intravenous penicillin 600 000 units every 6 hours for 3 weeks, and then oral amoxicillin, 500 mg every 6 hours for 3 weeks. The back pain resolved within 2 weeks, and the ESR returned to normal at the end of therapy. Follow-up for 3 years showed complete resolution of the infection. Patient 2. An 8-year-old boy presented with low back pain and low-grade fever, irritability, and general malaise for 10 days. He had had an upper respiratory tract infection with sore throat 27 days earlier, for which he received no therapy. The patient had a temperature of 102 degrees F, and physical examination was normal except for tenderness to percussion over the spine between the second and fourth lumbar vertebrae. Laboratory tests were normal, except for the ESR (42 mm/hour). Radiographs of the spine showed narrowing of the third to fourth lumbar vertebra disk space and irregularity of the margins of the vertebral endplates. A CT scan revealed a lytic bone lesion at lumbar vertebra 4, and bone scan showed an increase uptake of (99m)technetium at the third to fourth lumbar vertebra disk space. CT-guided aspiration of the disk space yielded cloudy nonfoul-smelling material, which was sent for aerobic and anaerobic cultures. Gram stain showed numerous white blood cells and fusiform Gram-negative bacilli. Anaerobic culture grew light growth of Fusobacterium nucleatum. The organism produced beta-lactamase and was susceptible to ticarcillin-clavulanate, clindamycin, metronidazole, and imipenem. Therapy with clindamycin 450 mg every 8 hours was given parenterally for 3 weeks and orally for 3 weeks. Back pain resolved within 2 weeks. A 2-year follow-up showed complete resolution and no recurrence. This report describes, for the first time, the isolation of anaerobic bacteria from children with diskitis. The lack of their recovery in previous reports and the absence of bacterial growth in over two third of these studies may be caused by the use of improper methods for their collection, transportation, and cultivation. Proper choice of antimicrobial therapy for diskitis can be accomplished only by identification of the causative organisms and its antimicrobial susceptibility. This is of particular importance in infections caused by anaerobic bacteria that are often resistant to antimicrobials used to empirically treat diskitis. This was the case in our second patient, who was infected by F nucleatum, which was resistant to beta-lactam antibiotics. The origin of the anaerobic bacteria causing the infection in our patient is probably of endogenous nature. The presence of abdominal pain in the first child may have been attributable to a subclinical abdominal pathothology. The preceding pharyngitis in the second patient may have been associated with a potential hematogenous spread of F nucleatum. P magnus has been associated with bone and joint infections. This report highlights the importance of obtaining disk space culture for aerobic and anaerobic bacteria from all children with diskitis. Future prospective studies are warranted to elucidate the role of anaerobic bacteria in diskitis in children.
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PMID:Two cases of diskitis attributable to anaerobic bacteria in children. 1115

This paper aims to remind paediatric clinicians to suspect and confirm 'PFAPA' syndrome (Periodic Fever, Aphthous stomatitis, Pharyngitis and cervical Adenitis syndrome). We report two cases of PFAPA syndrome: a 3-year-old healthy boy with atopic rhinitis and a boy aged 8 years 5 months who simultaneously had lymphocytic vasculitis syndrome treated with immunosuppressive drugs. Both met Marshall's criteria. The literature regarding PFAPA syndrome was complied using a Medline search for articles published between 1963 and 1998 and we then reviewed the reference lists of the articles. The Medline search revealed 28 cases with available clinical manifestations, management and prognosis. Our study describes two additional cases. We divided the cases into typical (28 cases) and atypical (two cases) PFAPA syndrome. In typical PFAPA, the age of onset was less than 5 years in most cases and the patients presented 4.9 +/- 1.4 days of fever (100%), pharyngitis (89.3%), cervical adenitis (72.1%), stomatitis (71.4%), malaise (64.3%), headache (60.7%), abdominal pain (53.6%) and nausea/vomiting (17.9%). Afebrile intervals were 3.2 +/- 2.4 months and increased with age. The time from initial onset to final episode was 3 years 7 months +/- 3 years 6 months. The total number of episodes was 8.3 +/- 2.5 (range 6-14). Effective treatment included steroids, tonsillectomy/adenoidectomy and cimetidine. The general outcome was good. In atypical PFAPF, the clinical manifestations were similar to those of typical PFAPA except that the age of onset was more than 5 years, and life-threatening intestinal perforation happened once in a patient with underlying Fanconi's anaemia. It was concluded that typical PFAPA syndrome is benign and can be diagnosed by detailed history-taking and from physical findings during repeated febrile episodes with tests to rule out other periodic fever syndromes. A review of the literatures since the first report in 1987 has shown that typical PFAPA syndrome is not associated with significant long-term sequelae and has a good response to steroids. One patient with atypical PFAPA, who received low-dose steroids for over 1 year, developed intestinal perforation after an increment of the 7-day steroid dose. If an underlying problem requires long-term immunosuppressive medication, it is wiser to choose cimetidine rather than increasing the steroid dosage to resolve atypical PFAPA.
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PMID:PFAPA syndrome (Periodic Fever, Aphthous stomatitis, Pharyngitis, Adenitis). 1120 45

Primary HIV can be asymptomatic or result in a severe symptomatic illness. Common symptoms are pyrexia, pharyngitis, malaise, lethargy, maculopapular rash, mucous membrane ulceration, lymphadenopathy and headache. It can be reliably diagnosed by a positive virologic test in the absence of HIV-specific antibodies. Progression to late-stage disease is influenced by the severity of the symptoms in primary HIV infection, the duration of the illness, the presence of neurological symptoms and the presence of oral candidiasis. This stage is characterized by a very high viral load and infectiousness. Currently the experimental data are insufficient to recommend whether or not those diagnosed with primary HIV infection should routinely receive antiretroviral therapy.
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PMID:Primary HIV infection. 1183 60

Infectious mononucleosis is usually produced as primoinfection by Epstein-Barr virus, but the second most common cause is cytomegalovirus. Clinical presentation of infectious mononucleosis is a pharyngitis and tonsillitis, associated to neck nodes, fever and general malaise, as well as haematological features such as an absolute lymphomonocytosis. Occasionally it is the neck node that is more severe, even without initial lymphomonocytosis. We report a deep neck abscess within a neck node as subacute presentation of infectious mononucleosis by cytomegalovirus. We review the clinical presentation of infectious mononucleosis, specially due to cytomegalovirus, as well as the importance that this disease could have while dealing with diagnosis and management of neck masses.
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PMID:[The neck cysts and infectious mononucleosis due to cytomegalovirus]. 1205 10


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