Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 54-year-old housewife became ill with transient diplopia followed by facial paralysis, tremor of the right hand and a progressively worsening disturbance in gait. Four years after the first appearance of the disease bilateral hypacusia, paralysis of the right hypoglossal nerve, dysarthria, severe spastic tetraparesis with ataxia, urinary retention and an organically induced character change were present. Lumbar puncture fluid contained 51/mm3 lymphocytes and 1164 mg/dl protein. Immunoglobulin A, G and M, synthesised locally, could be detected in cisternal fluid. The serum had a high antibody titre against Ixodes ricinus-Borrelia antigen and the same antibodies, formed locally, were present in the lumbar fluid. The neurological deficiencies improved markedly under parenteral penicillin treatment and the antibody titre decreased. The detection of Borrelian antibodies, especially those synthesised locally in the CSF, enabled an aetiological diagnosis to be made in seven other patients aged 18-47 years in whom the disease had been present for 1 to 8 years. These patients likewise presented symptoms characteristic of a disseminated disease of the CNS, with spastic pareses and evidence in the spinal fluid of chronic inflammation and disruption of CSF barriers in particular. This progressive encephalomyelitis differs from the common and spontaneously healing meningo-polyneuritis (Garin-Bujadoux-Bannworth), the usual manifestation of erythema chronicum migrans of the nervous system, in its progressive nature, its invasion of the CNS and the possible long lasting severe damage when not specifically treated.
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PMID:[Progressive Borrelia encephalomyelitis. Chronic manifestation of erythema chronicum migrans disease of the nervous system]. 400 60

The oral toxicity of capsaicin was investigated in mice and rats. Oral LD50 values were 118.8 mg/kg for male and 97.4 mg/kg for female mice, and 161.2 mg/kg for male and 148.1 mg/kg for female rats. Major toxic symptoms in mice were salivation, erythema of skin, staggering gait, bradypnea and cyanosis. Some animals showed tremor, clonic convulsion, dyspnea and lateral or prone position and then died 4 to 26 min after dosing. Survivors recovered within 6 hr in mice and 24 hr in rats. Toxic symptoms of rats were almost the same as mice, but rats showing higher incidence of cyanosis, clonic or tonic convulsion, dyspnea and lateral position, and the recovery was later than mice. The cause of death by capsaicin may be due to hypotension and respiratory paralysis in both animals, although the pathophysiology of death is not clearly understood. At pathological examination, erosion and ulcer of gastric fundus were seen in dead animals, while no pathological change was seen in surviving ones.
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PMID:Acute oral toxicity of capsaicin in mice and rats. 888 88

During a 4-month period, 34 dogs with tumors received a total of 60 doses of a single generic formulation of doxorubicin; 13 acute drug reactions were observed in these 34 dogs, and no acute reactions were observed after replacing the product with the proprietary brand. These reactions were characterized by one or more of the following signs: pruritus; head-shaking; urticaria; erythema of the pinnal, axillary, or inguinal regions; vocalization; vomiting; hyperemic or pale mucous membranes; high heart rate; and high respiratory rate. We propose that a component unique to generic doxorubicin was responsible for the unusually high number of acute drug reactions observed.
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PMID:Acute reactions in dogs treated with doxorubicin: increased frequency with the use of a generic formulation. 959 78

A 15-year-old boy with T-cell acute lymphoblastic leukemia (ALL) (FAB L1), diagnosed in 1995, received combination chemotherapy consisting of 6 weeks of induction (vincristine, epirubicin, L-asparaginase, prednisolone) and 2 weeks of consolidation (cytosine arabinosides, etoposide). After achieving remission, for further maintenance of remission, he was treated with 14 cycles of intensive chemotherapy consisting of 6-MP, 10 mg/kg orally on the first 4 days, and cyclophosphamide, 1200 mg/m2, vincristine, 1.5 mg/m2, epirubicin, 15 mg/m2, and cytosine arabinoside, 40 mg/m2, intravenously on days 4, 11, 39, and 40, respectively. On day 18 of each cycle, he received intravenous methotrexate (MTX) infusion in a total dose of 150 mg/m2 plus oral leucovorin (30 mg/m2 ) rescue 36 h after starting MTX therapy. In addition, oral trimethoprim-sulfamethoxazole was given regularly to prevent Pneumocystis carinii infection. The patient achieved remission during the first course of treatment, but 8 months later the disease relapsed. He then received four doses of MTX (800 mg intravenously) plus leucovorin rescue in the following 4 months. During the last MTX therapy, small hemorrhagic bullae were found on the lateral side of the right ankle, but subsided after a few days. Due to partial remission of the disease, he was admitted again in January 1999 for high-dose MTX therapy. An initial hemogram on admission revealed hemoglobin 7.2 g/dL, white cell count 15,200/mm3, platelet count 153/mm3, blood creatinine 0.5 mg/dL, and alanine leucine aminotransferase (ALT) 20 U/L. He received 8500 mg of MTX (5000 mg/m2 ) as a continuous intravenous infusion for 24 h. Thirty-six hours after the start of MTX infusion, leucovorin (30 mg, intravenous) rescue was initiated every 6 h for 3 days. Another preventive measure to cover MTX toxicity included aggressive intravenous fluid replacement (4 L/m2 /day) and the addition of 25 meq/L sodium bicarbonate to the intravenous fluid to alkalinize the urine. Concurrent medication included 6-MP (50 mg) once daily and trimethoprim-sulfamethoxazole (120 mg, 600 mg) twice daily every other day. Plasma MTX levels were 52.36 micromol/L 24 h after MTX infusion, 1.87 micromol/L after 48 h, 0.57 micromol/L after 72 h, and 0.41 micromol/L after 96 h. These indicated delayed MTX plasma clearance. The blood creatinine level was mildly elevated from 0.5 mg/dL to 0.7 mg/dL. Thirty-six hours after the administration of MTX, the patient developed an erythematous painful swelling on the right middle finger. The erythema, with subsequent large bulla formation, progressed to all the fingers, toes, palms, and the soles of the feet. Some erythematous to hemorrhagic papules also appeared on the bilateral elbows. Subsequently, diffuse tender erythema with extensive erosions and focal tiny pustules developed on the back, abdomen, proximal extremities, and face (Fig. 1a,b). A positive Nikolsky's sign was also present. A biopsy specimen of the right dorsal hand lesion revealed parakeratosis, detached acanthotic epidermis with scattered necrotic keratinocytes, dyskeratotic cells and nuclear atypia, neutrophilic exocytosis, and many neutrophils in the papillary dermis (Fig. 2). The skin condition deteriorated rapidly. Toxic epidermal necrolysis-like lesions involved 90% of the total body surface on the fifth day after MTX infusion. Mucositis, diarrhea, involuntary tremor, fever, and chills were noted. The patient was then sent to the burn unit for intensive skin care. Ten days after MTX therapy, profound agranulocytosis and thrombocytopenia (white cell count 100/mm3, platelets 14,000/mm3, and hemoglobin 5.6 g/dL) were found. The patient was then started on granulocyte colony stimulation factor (G-CSF, 5 microg/kg/day), but his general condition deteriorated rapidly and he died 6 days later due to septic shock and multiple organ failure.
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PMID:Toxic epidermal necrolysis following combination of methotrexate and trimethoprim-sulfamethoxazole. 1097 34

In early safety assessment studies with the experimental anti-neoplastic drug XP315, a toxic reaction was observed in dogs immediately after intravenous (iv) infusion. The reaction was characterized by severe erythema around the ears, eyes, face and body; ocular hyperemia; head shaking; swelling around the eyes, face, paws, head, neck and legs; scratching; and reddened gums, which lasted several hours after dosing. By fractionating the drug substance using preparative HPLC and then infusing the residues into dogs by iv, this reaction was traced to an impurity in the drug substance. Following the preparative isolation of the toxic impurity, characterization was performed using a combination of NMR and mass spectral methods. The proposed impurity was found to be structurally related and nearly twice the molecular weight of XP315, resulting from a dimerization by ring fusion of two 3-aminonaphthalene fragments during the synthetic process. This paper details the steps taken to isolate the toxic impurity and characterize its structure using off-line methods.
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PMID:The isolation and identification of a toxic impurity in XP315 drug substance. 1168 40

A 71-year-old man with a history of allergic rhinitis for 6 years received spinal anesthesia using 2 ml of 0.3% dibucaine for transurethral prostatectomy. Two months previously he had undergone prostate biopsy and cystoscopy under spinal anesthesia with isobaric bupivacaine uneventfully. Forty five minutes after injection of dibucaine he complained of itching in the periorbital area, and developed tremor and muscle rigidity followed by loss of consciousness. Soon after, his blood pressure decreased to 40 mmHg, and erythema appeared over his body. Symptoms were relieved by epinephrine, hydrocortisone and antihistamine agents, but ten minutes after the treatment he again developed hypotension and erythema. Continuous infusion of epinephrine was needed for complete relief of symptoms. An intradermal test with 0.3% dibucaine carried out 6 days after surgery demonstrated a 12 x 8 mm wheal with flare. Although anaphylactic reaction to an amide local anesthetic has been reported to be quite rare, this is the 7th case report of anaphylactic reaction to dibucaine used for spinal anesthesia in Japan.
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PMID:[Anaphylactoid reaction to dibucaine during spinal anesthesia]. 1248 54

PRESENTING FEATURES: A 70-year-old African American man was admitted with a history of fever, chills, and malaise of several days' duration. His past medical history was notable for end-stage renal disease requiring hemodialysis, coronary artery disease, and aortic stenosis requiring a bioprosthetic aortic valve replacement. On the day of admission, the patient was noted to have a shaking chill while undergoing dialysis through his catheter and was admitted to the hospital. He complained of pain at the catheter insertion site, shortness of breath, and dyspnea on exertion, but denied chest pain. On physical examination, the patient had a temperature of 100.4 degrees F, with a heart rate of 64 beats per minute, blood pressure of 127/72 mm Hg, and an oxygen saturation of 97% on room air. He was a mildly obese man in no apparent distress. He had shotty cervical lymphadenopathy and a right subclavian dialysis catheter in place, with erythema and pus at the entry site. His jugular venous pressure was 10 cm H(2)O. Lung examination showed bibasilar rales. Heart sounds were normal, with no rub or gallop. He had a 2/6 systolic ejection murmur best heart at the left sternal border as well as a 3/6 holosystolic murmur at the apex that radiated to his left axilla. Examination of the abdomen and extremities was unremarkable. The patient's neurological examination was unremarkable, and he was alert and oriented to person, place, and time. Laboratory studies showed an elevated white blood cell count of 16,700 cells/microL. His blood urea nitrogen level was 43 mg/dL and his serum creatinine level was 4.9 mg/dL. Multiple blood cultures grew methicillin-resistant Staphylococcus aureus. An admission, chest radiograph showed no infiltrate. An admission electrocardiogram showed normal sinus rhythm with first degree atrioventricular block, left anterior fascicular block, and left ventricular hypertrophy. shows rhythm strips from lead II electrocardiograms 5 months before admission (top), on admission (middle) and 5 days after admission (bottom). What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. 1514 15

A new antimicrobial ear cleanser was evaluated for the treatment of bacterial and yeast ear infection in dogs. Forty-five dogs with erythemato-ceruminous or purulent otitis externa were randomly allocated to two treatment groups: reference ear cleanser (Epiotic, Virbac) or test ear cleanser (Epiotic Advanced, Virbac). Ear cleansing was performed twice daily for 2 weeks, and no other treatment was allowed. By week 2, clinical (exudate quantity, erythema, stenosis, excoriation, and odor) and discomfort (pain, ear scratching, and head shaking) scores were significantly decreased (P < .0001 for all) and no microbial overgrowth could be detected in 25 (64.1%) and 32 (68.1%) ears treated with Epiotic and Epiotic Advanced, respectively. The new pH-balanced, propylene glycol-free test ear cleanser, which incorporates microbial adhesin-blocking carbohydrates, proved as effective as the reference acidic formula.
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PMID:The efficacy of an antiseptic and microbial anti-adhesive ear cleanser in dogs with otitis externa. 1659 80

This paper proposed a support vector machine (SVM) based classification method to identify diversified pathological voices. Sound signals were sampled from the pronunciation of a vowel "a" vocalized by 214 subjects, including 181 patients suffered from various dysphonias (such as polypoid degeneration, adductor spasmodic dysphonia, vocal fatigue, vocal tremor, vocal fold edema, hyperfunction, and erythema), and 33 healthy subjects. 25 acoustic parameters were calculated from the sampled data for each subject. The original acoustic dataset was first transformed via principal component analysis (PCA) method into a new feature space. To learn the identification boundary for healthy and pathological voices, a soft-margin SVM and three kinds of kernels were examined. The results under different combination of parameters and kernels were investigated. The effectiveness of SVM-based approach seems to be promising in the application of pathological voice identification.
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PMID:SVM-based identification of pathological voices. 1800 22

The disease of Lyme is a tick-borne infection. It involves skin, the nervous system, joints and the heart. Spirochaeta Borrelia burgdorferi is the etiologic agent of the disease. In the majority of cases, clinical symptoms, like migrating erythema, occur from 3 to 30 days, sometimes to 3 months after a bite from a tick. The early disseminated infection involves multiple migrating erythema, neuroborreliosis, arthritis, myocarditis and other organ-related symptoms. The late stage of chronic infection involves chronic atrophic leg dermatitis, neurological and rheumatological symptoms, and other organ-related symptoms which persist for above 12 months. The diagnosis of the disease of Lyme is based upon specific clinical symptoms confirmed by serologic tests. The two-step diagnostic protocol including the ELISA method, confirmed by the Western-blot test, is optimal. The present article describes a case of a 59-year-old man, a computer specialist, who often spends his free time walking in woods for recreation, and who was bitten by a tick 3 years before hospitalization. The bite resulted in migrating erythema that subsided without antimicrobial treatment. In spite of this, the man had not changed his hobby exposing himself to bites from ticks. One year later, multiple migrating erythema and extrapyramidalis symptoms appeared without any other organ malfunctions. In the current year, the patient was admitted to the Infectious Diseases Hospital, and received antibiotics (ceftriaxon) with following neurological improvement. Several months later, extrapyramidal symptoms increased. On the day of admission to the hospital, the neurologic examination showed abnormalities of upper and lower limbs movements (propulsive walking and the right lower leg traction), the right hand tremor, pouts of the face, and sleepiness.
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PMID:Neuroborreliosis with extrapyramidal symptoms: a case report. 1861 83


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