In this paper, we reported a case of congenital aplasia of dorsal pancreas. This case in 35th case in Japan. The case is 72-year-old male. He feels general fatigability as chief complaint and was taken Diabetes Mellitus. In ERP examination, it was found a short main pancreatic duct of about 4.5 cm length and defect of pancreatic body and tail in Ultrasonogram and Computed Tomogram. In arteriography, it was not found feeding artery to pancreatic body and tail. Accordingly, we diagnosed this case as congenital defect of pancreatic body and tail. This one was normal range for P. F. D. andnormal exocrine pancreatic function. But, this one was operated because of taking cholecystolithiasis. On Retroperitoneal space that shoud be originally pancreatic body and tail, we confirmed only fat tissue without inflammation, fibrosis and carcinomatous tissue. We could not be confirmed Langerhans islet and pancreatic tissue in the biopsy sections of fat tissue.

A 60-year-old man who developed a nephrotic syndrome underwent a renal biopsy, and the case was diagnosed as membranoproliferative glomerulonephritis (MPGN). Despite chemotherapy using steroid, immunosuppresive and anticoagulant drugs, the patient exhibited persistently high urinary protein levels (above 8 g/day), and the renal function deteriorated gradually.
One and half years later, hemodialysis was started, but soon he had a high fever (above 38-40°C). Laboratory data revealed high levels of both antinuclear antibody titer and immune complex (IC) titer, and a low level of CH50.
Considering an active collagen disease like SLE, steroid pulse therapy and plasma exchange were instituted. The therapy was very effective this time.
It is well known that many patients with SLE and a long term history of hemodialysis develop a condition of so called “burn out” in which the activity of SLE declined to allow the withdrawal of steroid therapy. Also well known is the developement of hypocomplementemia in many patients with MPGN.
In our case, it was difficult to clarify what caused the high fever and other clinical symptoms. We must carefully observe the clinical symptoms of SLE.

In Oita prefecture, where ATL is relatively endemic, the authors carried out hematology analysis using an E-4000 hematology analyzer in a health examination. This analysis screened a group of 104 males and 181 females out of randomly collected 11, 568 persons in terms of a higher (exceeded 50%) W-SCR rate (i. e. lymphocyte rate in cell size distribution). The collected peripheral blood smears from this group were further subjected to the examination of lymphocyte morphology.
Abnormal lymphocytes exhibiting dyscaryosis, such as indentation or lobulation, were observed in 11 cases, and further examination of anti-ATLA antibody and earlobe blood smears revealed eight suspected cases of ATL-related condition.
Clinical symptoms characteristic of ATL were not observed in the above eight cases, though the anti-ATLA antibody titer measured by the ELISA method increased by more than 25. In one case, being diagnosed as chronic-type ATL, abnormal lymphocytes amounted to 70% and the leukocyte count was 28, 000/μl. In the other seven cases, abnormal lymphocytes amounted to only 1-11%, and the leukocyte counts ranged from 5, 300 to 11, 100/μl, which was almost within the normal limits.
The method in reported as an useful means for screening cases of nonsymptomatic chronic or smoldering type ATL through a health examination.