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Clinical study of Japanese spotted fever and its aggravating factors

 Twenty-eight patients with Japanese spotted fever were clinically investigated. The diagnosis was determined by confirming an increase of specific antibody. All patients were treated with minocycline, and all recovered, excluding one patient with a fulminant course. Fever and exanthema were observe...

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Detalles Bibliográficos
Autores principales: Kodama, Kazuya, Senba, Takanori, Yamauchi, Hayato, Nomura, Tetsuhiko, Chikahira, Yoshimi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer-Verlag 2003
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102015/
https://www.ncbi.nlm.nih.gov/pubmed/12673413
http://dx.doi.org/10.1007/s10156-002-0223-5
Descripción
Sumario: Twenty-eight patients with Japanese spotted fever were clinically investigated. The diagnosis was determined by confirming an increase of specific antibody. All patients were treated with minocycline, and all recovered, excluding one patient with a fulminant course. Fever and exanthema were observed in all patients, and an eschar was pointed out in 20 (71%) patients. The platelet count was 10 × 10(4)/μl or lower in 8 (28%) patients. The fibrin degradation product (FDP)-level was abnormally high, 10 μg/ml or more, in 16 (57%) patients. The creatine kinase (CK) value was high in 14 of 22 patients, suggesting the presence of myositis. The leukocyte count, FDP, C-reactive protein, and soluble interleukin 2 receptor (sIL2-R) levels were significantly higher in severe cases. In the group without concomitant steroid therapy, mean times of 54.7 h and 101.4 h were required to reduce the temperature to 38°C and 37°C or lower, respectively, after the initiation of tetracycline treatment. There were 6 severe cases: 1 with disseminated intravascular coagulation, 2 with multiorgan failure, 1 with acute respiratory distress syndrome, and 2 with meningoencephalitis. These severe cases formed a group that required 6 or more days to initiate therapy after the onset (P < 0.005 vs non-severe group), showing that delay in diagnosis and therapy is the major cause of aggravation. In the 2 patients complicated by multiorgan failure, the sIL2-R level, produced by activated lymphocytes, was 10 000 U/ml or higher, suggesting that an sIL2-R level of more than 10 000 U/ml can be used as a marker of poor prognosis. It may be better that moderate to severe cases are treated with minocycline plus short-term steroid therapy.