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Bacillary angiomatosis is known to be caused by a rickettsial organism; Rochalimaea henselae. This causative agent has been compared with different microorganisms and clinical conditions that appear in similar settings buy have been clearly differentiated from them; e.i. Cat-scratch disease (Afipia felis), Bartonella bacilliformis, other Rochalimaea sp., Kaposi's sarcoma, Lobular capillary hemangioma, Angiosarcoma, and Epithelioid hemangioma. Clinically the bacillary angiomatosis (BA) skin lesions vary from a single lesion to thousands. The cutaneous lesion appears as a bright-red round papule, subcutaneous nodule, or as a cellulitic plaque. When the lesion is biopsied it tends to blanch-out, bleed, and cause pain. The patient might present with signs and symptoms of chills, headaches, fever, malaise, and anorexia with or without weight loss. The extracutaneous lesions found in BA tend to be from multiple organs affecting from the oral lesions to anal mucosal lesions to widespread visceral lesions. The sites of preference for BA lesion manifestation tend to be the liver, spleen, lymph nodes, and bone. To diagnose bacillary angiomatosis the physician should prepare a differential diagnosis based primarily on its histopathological and clinical characteristics. To confirm the results from the stain, electron microscopy can identify the bacillus and pin-point the diagnosis of bacillary angiomatosis. The lesions presented by BA respond well to therapy with erythromycin 500 mg four times daily for a duration of 2 weeks to 2 months. In case of intolerance to erythromycin the second line of drug that successfully treats the BA bacillus is doxycyline. If relapses of the BA lesion recur, then a prolonged antibiotic therapy is necessary and in AIDS patients the duration may be extended as life-long suppressive therapy.
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PMID:Bacillary angiomatosis: microbiology, histopathology, clinical presentation, diagnosis and management. 870 69

A 35-year-old woman presented with a 6-month history of intermittent headaches, vomiting and dizziness. CT showed a plaque-like mass with tiny calcifications along the surface of the left frontal lobe. The mass exhibited heterogeneous enhancement with a few low-density foci. Underlying sulcal obliteration and enhancement and white matter oedema were also noted. Histopathological examination of excised material was consistent with tuberculoma. Recognition of this unusual presentation of intracranial tuberculoma may facilitate appropriate diagnosis and management.
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PMID:Tuberculoma en plaque: CT. 883 90

Bacillary angiomatosis is known to be caused by a rickettsial organism; Rochalimaea henselae. This causative agent has been compared with different microorganisms and clinical conditions that appear in similar settings but that have been clearly differentiated from them; e.i. Cat-scratch disease (Afipia felis), Bartonella bacilliformis, other Rochalimaea sp., Kaposi;s sarcoma, Lobular capillary hemangioma, Angiosarcoma, and Epithelioid hemangioma. Clinically the bacillary angiomatosis (BA) skin lesions vary from a single lesion to thousands. The cutaneous lesion appears as a bright-red round papule, subcutaneous nodule, or as a cellulitic plaque. When the lesion is biopsied it tends to blanch-out, bleed, and cause pain. The patient might present with signs and symptoms of chills, headaches, fever, malaise, and anorexia with or without weight loss. The extracutaneous lesions found in BA tend to be from multiple organs affecting from the oral lesions to anal mucosal lesions to widespread visceral lesions. The sites of preferences for BA lesion manifestation tend to be the liver, spleen, lymph nodes, and bone. To diagnose bacillary angiomatosis the physician should prepare a differential diagnosis based primarily on its histopathological and clinical characteristics. To confirm the results from the stain, electron microscopy can identify the bacillus and pin-point the diagnosis of bacillary angiomatosis. The lesions presented by BA respond well to therapy with erythromycin 500mg four times daily for a duration of 2 weeks to 2 months. In case of intolerance to erythromycin the second line of drug that successfully treats the BA bacillus is doxycycline. If relapses of the BA lesion recur, then a prolonged antibiotic therapy is necessary and in AIDS patients the duration may be extended as life-long suppressive therapy.
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PMID:Bacillary angiomatosis: microbiology, histopathology, clinical presentation, diagnosis and management. 891 40

The goals of stable angina pectoris treatment are: (i) symptom relief and increase in angina-free walking time; and (ii) reduction of mortality and adverse outcome. Strategies used for plaque stabilisation resulting in a reduction in cardiovascular mortality and morbidity are: smoking cessation; aspirin (acetylsalicylic acid); blood pressure control; lipid lowering agents when low density lipoprotein cholesterol is elevated despite dietary therapy; coronary bypass surgery in patients with left main stem disease or triple vessel coronary disease and diminished left ventricular function; and use of estrogen in postmenopausal women. For symptom relief and to increase angina-free walking time, long acting nitrates, beta-blockers, calcium antagonists and potassium channel openers can be used. Drugs from these 3 classes are all effective when used optimally and choice of initial therapy should consider the presence of concomitant disease and underlying left ventricular function. However, none of the long acting nitrates provide continuous prophylaxis because nitrate tolerance develops during long term therapy. In patients with uncomplicated stable angina, nitrates, beta-blockers and calcium antagonists are all effective. Intermittent nitrate therapy is not associated with tolerance, but headache is a common adverse effect and the patient is unprotected at night and in the early hours of the morning. Concomitant treatment with a beta-blocker may be beneficial if the patient experiences withdrawal or early morning angina. For patients with stable angina and hypertension, therapy with a beta-blocker or a calcium antagonist rather than nitrate is indicated. beta-Blockers are preferred in patients who have had a myocardial infarction, or in those with a history of supraventricular tachyarrhythmias. beta-Blockers may produce excessive slowing of the heart rate, fatigue and bronchospasm in susceptible patients. Calcium antagonists are indicated as initial therapy when beta-blockers are either not tolerated or contraindicated. beta-Blockers and nondihydropyridine calcium antagonists should not be used in patients with sinus bradycardia and those with greater than first degree atrioventricular (AV) block because of the possibility of further slowing of heart rate and/or the development of high grade AV block. When monotherapy with one class is ineffective or associated with adverse effects, the patient should be switched to another class rather than given an additional drug. Optimal monotherapy is often as effective as combination therapy. If maximum monotherapy is only partially effective, a combination therapy which is not additive in terms of adverse effects should be chosen. Triple therapy may be deleterious and no more effective than dual therapy.
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PMID:Choosing the most appropriate treatment for stable angina. Safety considerations. 967 56

Progression of cutaneous T-cell lymphoma (CTCL) is associated with profound defects in cell-mediated immunity and depressed production of cytokines, which support cell-mediated immunity. Because we have observed marked defects in interleukin-12 (IL-12) production in CTCL and because IL-12 is critical for antitumor cytotoxic T-cell responses, we initiated a phase I dose escalation trial with recombinant human IL-12 (rhIL-12) where patients received either 50, 100, or 300 ng/kg rhIL-12 twice weekly subcutaneously or intralesionally for up to 24 weeks. Ten patients were entered: 5 with extensive plaque, 3 with Sezary syndrome, and 2 with extensive tumors with large cell transformation. One patient with Sezary syndrome dropped out after 1 week for personal reasons. Subcutaneous dosing resulted in complete responses (CR) in 2 of 5 plaque and partial responses (PR) in 2 of 5 plaque, and 1 of 2 Sezary syndrome (overall response rate CR+PR 5 of 9, 56%). A minor response also occurred in 1 of 5 plaque patients. Intralesional dosing resulted in individual tumor regression in 2 of 2 patients. Biopsy of regressing lesions showed a significant decrease in the density of the infiltrate in all cases and complete resolution of the infiltrate among those with clinical lesion resolution. An increase in numbers of CD8-positive and/or TIA-1-positive T cells were observed on immunohistochemical analysis of skin biopsy specimens obtained from regressing skin lesions. Adverse effects of rhIL-12 on this regimen were minor and limited and included low-grade fever and headache. One patient discontinued rhIL-12 at week 6 because of depression. These results suggest that rhIL-12 may augment antitumor cytotoxic T-cell responses and may represent a potent and well-tolerated therapeutic agent for CTCL.
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PMID:Interleukin-12 therapy of cutaneous T-cell lymphoma induces lesion regression and cytotoxic T-cell responses. 1041 80

We describe a case with simultaneous occurrence of cluster headache-like pain and multiple sclerosis. Both neuroimaging and neurophysiology (trigeminal evoked potentials) revealed a demyelination plaque in the pons, at the trigeminal root entry zone, on the side of pain. Although that type of lesion is usually associated with trigeminal neuralgia pain, we hypothesize that in this case it may be linked with the concomitant cluster headache, possibly by activation of trigemino-vascular mechanisms.
Cephalalgia 1999 Oct
PMID:Cluster headache-like pain in multiple sclerosis. 1057 Jul 29

A previously healthy 7-year-old white boy presented to St. Louis Children's Hospital with a 1-day history of headache, malaise, temperature of 38.7 degrees C, and a progressively erythematous, tender calf with central dusky purpura. On the morning of admission, his mother noticed a 2-mm crust on the patient's right calf with a 3-cm x 3-cm area of surrounding erythema. No history of recent trauma or bite was obtained. He had suffered two episodes of nonbloody, nonbilious emesis during the last day. In addition, over the previous 12 h, he presented brown urine without dysuria. His mother and brother had suffered from gastroenteritis over the previous week without bloody diarrhea. On initial physical examination, there was a 6-cm x 11-cm macular tender purpuric plaque with a central punctum on the right inner calf, which was warm and tender to the touch, with erythematous streaking towards the popliteal fossa (Fig. 1). The inguinal area was also erythematous with tender lymphadenopathy and induration, but without fluctuance. Laboratory studies included an elevated white blood cell count of 20, 800/microL with 6% bands, 86% segs, and 7% lymphocytes, hemoglobin of 12.5 g/dL, hematocrit of 35.1%, and platelets of 282,000/microL. The prothrombin time/activated partial tissue thromboplastin was 10. 4/28.0 s (normal PT, 9.3-12.3 s; normal PTT, 21.3-33.7 s) and fibrinogen was 558 mg/dL (normal, 192-379 mg/dL). Urinalysis showed 1+ protein, 8-10 white blood cells, too numerous to count red blood cells, and no hemoglobinuria. His electrolytes, blood urea nitrogen (BUN), and creatine were normal. The urine culture was negative. Blood culture after 24 h showed one out of two bottles of coagulase negative Staphylococcus epidermidis. The patient's physical examination was highly suggestive of a brown recluse spider bite with surrounding purpura. Over the next 2 days, the surrounding rim of erythema expanded. The skin within the plaque cleared and peeled at the periphery. The coagulase negative staphylococci in the blood culture were considered to be a contaminant. Cefotaxime and oxacillin were given intravenously. His leg was elevated and cooled with ice packs. The patient's fever resolved within 24 h. The lesion became less erythematous and nontender with decreased warmth and lymphadenopathy. The child was discharged on Duricef for 10 days. Because the patient experienced hematuria rather than hemoglobinuria, nephritis was suggested. In this case, poststreptococcal glomerulonephritis was the most likely cause. His anti-streptolysin-O titer was elevated at 400 U (normal, <200 U) and C3 was 21.4 mg/dL (normal, 83-177 mg/dL). His urine lightened to yellow-brown in color. His blood pressure was normal. Renal ultrasound showed severe left hydronephrosis with cortical atrophy, probably secondary to chronic/congenital ureteropelvic junction obstruction. His right kidney was normal.
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PMID:A child with spider bite and glomerulonephritis: a diagnostic challenge. 1080 79

To determine whether some constitutional symptoms of influenza, such as headache, myalgia and nausea, could represent a viral infection of brain, muscle, and liver, we inoculated juvenile Balb/c mice intranasally with 103 plaque forming units of influenza B/Lee virus. Blood, brain, liver, skeletal muscle, and lung tissues were removed aseptically and assayed for infectivity by a plaque assay, viral RNA by reverse transcriptase-polymerase chain reaction (RT - PCR), viral antigen by immunoperoxidase staining, and histologic changes by light microscopy. Mice became ill 2 - 3 days post inoculation (PI). A productive viral infection of the lungs developed from days 1 - 8 with maxima of virus titers, pneumonia, and the number of immunoperoxidase staining lung cells occurring on days 2 - 6 PI. Virus isolation from blood was rare and viral RNA was detected intermittently in blood by RT - PCR. In many animals, a non-permissive or abortive infection of brain occurred from days 1 - 8 and peaked on days 3 - 4 PI. Viral RNA was detected in brain tissue and viral antigen was seen in cerebral endothelial cells but infectious virus was rarely isolated from brain. In liver, viral RNA was detected and viral antigen was seen occasionally in hepatocytes. In skeletal muscle, viral RNA was detected but neither infectious virus nor viral antigen was seen. A correlation existed between the severity of the illness, pneumonia, lung virus titer, viral antigen in lung cells, and extent of a non-permissive viral infection of brain and liver but not muscle. These studies demonstrate that following intranasal infection of influenza virus in mice, a viral pneumonia develops with subsequent intermittent viremia and non-permissive or abortive infection of brain, liver and muscle.
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PMID:Experimental influenza causes a non-permissive viral infection of brain, liver and muscle. 1117 25

A randomized, controlled, double-blinded study was conducted to determine safety and immunogenicity of five live attenuated dengue vaccines produced by Aventis Pasteur (AvP). The study was completed with 40 flavivirus non-immune volunteers: five recipients of each monovalent (dengue-1, dengue-2, dengue-3, or dengue-4) vaccine, ten recipients of tetravalent (dengue-1, dengue-2, dengue-3, and dengue-4) vaccine, and ten recipients of vaccine vehicle alone. All vaccines were administered in a single subcutaneous dose (range, 3.6-4.4 log(10) plaque forming units). No serious adverse reactions occurred in volunteers followed for 6 months after vaccination. Five vaccine recipients developed fever (T > or = 38.0 degrees C), including four tetravalent vaccinees between days 8 and 10 after vaccination. Dengue-1, dengue-2, dengue-3, or dengue-4 vaccine recipients reported similar frequency of mild symptoms of headache, malaise, and eye pain. Tetravalent vaccinees noted more moderate symptoms with onset from study days 8-11 and developed maculopapular rashes distributed over trunk and extremities. Transient neutropenia (white blood cells < 4000/mm3) was noted after vaccination but not thrombocytopenia (platelets < 100,000/mm3). All dengue-3, dengue-4, and tetravalent vaccine recipients were viremic between days 7 and 12 but viremia was rarely detected in dengue-1 or dengue-2 vaccinees. All dengue-2, dengue-3, and dengue-4, and 60% of dengue-1 vaccine recipients developed neutralizing and/or immunoglobulin M antibodies. All tetravalent vaccine recipients were viremic with dengue-3 virus and developed neutralizing antibodies to dengue-3 virus. Seven volunteers also had multivalent antibody responses, yet the highest antibody titers were against dengue-3 virus. The AvP live attenuated dengue virus vaccines are safe and tolerable in humans. The live attenuated tetravalent dengue vaccine was most reactogenic, and preferential replication of dengue-3 virus may have affected its infectivity and immunogenicity.
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PMID:Safety and immunogenicity of attenuated dengue virus vaccines (Aventis Pasteur) in human volunteers. 1131 14

A rare case of a diffuse calvarial meningioma in a sixty-three year-old female is reported. The patient presented with headache, painful proptosis and chemosis of the left eye. Imaging showed that the frontoparietal calvarium on both sides and the left orbital roof were thickened. The thickened bone showed patchy rarefaction. In relationship to the thickened bone, there was an enhancing en-plaque meningioma. The tumour extended on to the superolateral aspect of the left orbit and resulted in proptosis. Excision of the left frontoparietal calvarium and the orbital tumour was performed. The management of diffuse calvarial meningioma is discussed and the relevant literature is briefly reviewed.
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PMID:Diffuse calvarial meningioma: a case report. 1183 3


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