Takao Kunori

Management of nodular goiters and their operative indications

It remains controversial whether or not nodular goiters should be treated surgically or conservatively. This report reviews our 9-year experience of treating nodular goiters in 334 patients, 44 of whom underwent surgery, and compares the methods of treatment employed from 1990 to 1999 with those employed from 1971 to 1989 when 171 operations were carried out. In accordance with diagnoses made using fineneedle aspiration biopsy (FNAB) and ultrasonography, patients were treated as follows. Those with cysts were given percutaneous ethanol injection therapy (PEIT), and those with solid tumors underwent surgery if cancer of >class 3 was suspected or if the tumors were >3cm. Consequently, 44 patients with solid tumors underwent surgery and 72 with cysts were treated by PEIT. The number of operations performed annually decreased to half of the pre-1990 figure. During the follow-up of those patients who did not undergo surgery, four with solid tumors and two with cysts later required surgery due to suspected carcinoma of > class 3 in 3 patients or as a result of personal choice in 3 patients. The growth of solid tumors was not able to be measured in most cases. These results indicate that the number of operations performed for nodular goiters can be reduced by PEIT. An accurate cytological diagnosis supports this therapeutic strategy.

Monitoring of B lymphocyte response with the protein-A plaque assay in kidney transplant patients.

The protein-A plaque assay was used for serial monitoring of spontaneous plaque-forming lymphocytes (PFC) in blood or thoracic duct lymph of 30 renal transplant patients. In patients experiencing early or delayed graft rejection, PFC manifested a 10-fold increase over the preoperative or control level within one month of the transplantation. Patients accepting the renal graft did not exhibit a remarkable PFC response. Among the factors examined (proportion of B cells, donor source, acute tabular necrosis, intraoperative blood transfusion, antilymphocyte serum, histocompatibility, and rejection), the PFC response was most closely related to graft rejection. Changes in serum immunoglobulin (Ig) did not appear to correlate with the PFC response. By using Ig-class-specific antisera, secreted Ig was identified as IgG, IgM, and IgA. This may indicate that renal grafts induce polyclonal activation of the recipients B cells.

SPONTANEOUS ANTIBODY-SECRETING CELLS IN THE STOMACH OF GASTRIC CANCER PATIENTS

The gastric mucosa has been regarded as an active site of humoral immunity since the discovery ofHelicobacter pylori. The present study was conducted to determine the in vivo activity of gastric B cells in 53 gastric cancer patients. B-cell activity was measured by protein-A plaque assay, in which IgA-, IgM-, and IgG-plaque-forming cells (PFC) were counted. The number of PFC was associated with the stage of cancer, but the response of lymphocytes in a non-tumorous area (NML) and tumor-infiltrating lymphocytes (TIL) differed. PFC in both sites were decreased compared to n0 cancer in n1 lymph node metastasis-positive cancer, while only NML showed raised PFC in n2+ (P<0.05, vs TIL). Cancer cells penetrating the submucosa caused the PFC of TIL (but not of NML) to decrease. Invasion of the intratumor capillary (V) or lymphatic (Ly) vessels also caused PFC to change, showing differences of Ig class; there was a decrease of PFC in V2 (IgG-and IgM-PFC) and in Ly2 (all Ig-PFC). IgA-PFC in Ly1 differed in TIL (decrease of PFC) and NML (increase). PFC also differed in TIL and NML in cancer cells, as follows: TILNML in papillary and signet ring cell adenocarcinoma. Changes in lymph node (LNL) and blood lymphocytes were similar to those in gastric PFC whose IgA value was 10 times as much as that of LNL. The 5-year survival rate was significantly better in patients with lower rather than higher PFC such as 89% vs 68%. Gastric B cells thus appear to be active and to reflect gastric mucosal immunity.