Hemorrhagic fever with renal syndrome (HFRS) was first found in Japan in about 120 residents of Osaka City during the decade of 1960. As 22 cases of them were admitted to Osaka University Hospital between 1961 and 1970, we studied and summarized the clinical manifestations of these cases as group A. The HFRS developed again in the staffs of animal laboratories in Osaka University Medical School between 1980 and 1982, and we also studied the clinical features of 5 of these cases as group B. The HFRS in group A was mediated by wild urban rats, but one in group B was considered to be mediated by experimental animals.
High fever of 39-41°C for 3-7 days and proteinuria were always observed in patients of both groups. Anorexia, lassitude, emesis, myalgia, abdominal pain and headache were main complaints in the majority of patients. Injection of the oral and conjunctival mucosa, coating of the tongue, tenderness in the abdomen, petechiae on the palate and hepatomegaly were common manifestations observed in most cases. Development of microscopic hematuria, various casts and polynuclear giant cells in the urinary sediment, leukopenia with a marked neutrophilia and shift to the left and extremely low sedimentation rate during the initial stage, leukocytosis with an increase of lymphocytes, development of atypical lymphocytes, thrombocytopenia, polycythemia and increases in serum enzymes such as GOT, GPT, LDH and CPK were common abnormalities in the laboratory data. Moreover, transient glycosuria, glucose intolerance or low serum cholesterol levels, which have not been reported previously, were also frequently observed. However, azotemia (BUN>23 mg/dl) was seen only in 30% of all cases.
In group A, some severe cases manifested petechiae on the body (7/22), epistaxis (5/22) and/or hypotension (6/22), and two cases were fatal, but none in group B showed such serious symptoms. Marked proteinuria over 3 g/day was observed in 10 cases (45%) of group A, but urinary protein was slight and very transient in most cases of group B. On the contrary, serum GOT and GPT levels were generally higher in group B than in group A. It is, therefore, suggested that the HFRS which develops in the animal laboratories in Japan may cause more severe damages in the liver than in the kidney.
When the clinical manifestations of our cases (including both group A and B) are compared with those reported from other Eastern Asian countries, they are generally mild and their course cannot be distingwished so clearly as reported by Sheedy, et al. (1954). The clinical feature, which shows relatively serious hepatic complications with high serum enzyme levels and rather mild renal syndrome with a slight azotemia, seems to be something different from those in other countries and be characteristic ofthe HFRS in Japan.
The course of illness and the clinical features of HFRS in Japan, which generally consists of mild cases, are almost clarified in this study by summarization and analysis of the patients experienced in Osaka University Hospital in the 1960's and the 1980's.
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