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PURPOSE: To investigate the effect of direct current treatment (DCT) on the growth of mammary carcinomas in rats by MR-volumetry. METHODS: Chemically induced mammary adenocarcinomas in a control group (n = 17) were compared with treated tumours (18 C/cm3 in group A: n = 7 or 36 C/cm3 in group B: n = 12). 31 untreated tumours were situated near a treated tumour (group C). Experiments were carried out using one positive electrode in the tumour centre and three negative electrodes in the periphery. The tumour volume was measured by MRI before, and 1, 3, 6, 9 and 12 weeks after treatment. RESULTS: 12 weeks after DCT, the mean tumour volume in group A (164% +/- 158%, p < 0.05) and group B (13% +/- 24%, p < 0.001) was significantly reduced compared to the control group (434% +/- 230, Mann-Whitney U-Test). Complete tumour regression occurred in 42% of tumours in group B and was not achieved in group A, C and control group. Tumour growth in group C was decreased compared to the control group. CONCLUSIONS: The effectiveness of DCT was found to depend on the applied dosage -36 C/cm3 was more effective than 18 C/cm3. The effect of DCT is not limited to the area between the electrodes.

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Nine patients with unrecognized incomplete cervical spinal cord injury are discussed. Four were sent home as normal, three were called hysterical, and two went undiagnosed during stupor or coma. A literature search revealed 28 additional cases. Eighty percent of these were males, two thirds were over 50 years old, and most had central or posterior cord syndromes. Falls with hyperextension, spondylosis, or disc disease, and motor vehicle accidents were the most common causes. Only one of the 37 had a cervical fracture. In some the neurologic problem was missed altogether; in others it was attributed to hysteria, intoxication, or to other neurologic or systemic diseases. Minor injuries without cervical fracture or dislocation, advanced age, unusual or changeable neurologic deficits, intoxication, and psychiatric problems all contributed to the confusion.

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Recent studies have described an association between high-risk lipoprotein profiles and anabolic steroid abuse by athletes. However, none have included a comprehensive evaluation of diet as a confounding variable. The risk of cardiovascular disease (CVD) and its associations with drug abuse, dietary patterns, and training regimens were evaluated in 18 steroid-using (SU) and 17 non-steroid-using (NSU; no history of drug use or greater than or equal to 1 year drug-free) male bodybuilders. CVD risk was also evaluated in 10 control males. Fasting serum total cholesterol (TC), high-density lipoprotein cholesterol (HDL) and HDL subfractions 2 and 3, low-density (LDL) and very-low-density (VLDL) lipoprotein cholesterol, apoproteins (APO) A-1 and B, and triglycerides (TG) were analyzed at baseline (greater than or equal to 6 months drug-free) and the peak of steroid self-administration in SU. NSU were tested at similar times. Baseline CVD risk factor ratios (TC/HDL) were elevated (greater than 4.97) in 44% of SU and 24% of NSU. When baseline LDL and HDL values were compared to National Cholesterol Education Program CVD risk guidelines, these percentages stayed the same. At the peak of steroid administration significant changes were observed in LDL (22% increase), HDL (63% decrease), HDL-2 (86% decrease), HDL-3 (54% decrease), and TC/HDL (85% increase). No similar measures were observed among NSU or controls. Diets of all bodybuilders were similar, and included a daily intake of 5739 (+/- 2500) kcal, 324 (+/- 163) g protein, 637 (+/- 259) g carbohydrate, 214 (+/- 109) g fat, 5 (+/- 8) g alcohol, 1413 (+/- 1151) mg cholesterol, and a P/S ratio of 0.6 (+/- 0.3). Significant relationships between dietary fats and serum lipids were observed in the NSU. Polyunsaturated fatty acids were correlated with TG and VLDL (r = 0.69; p = 0.01), and TC/HDL (r = 0.06; p = 0.04). Total fats were correlated with TG (r = 0.57; p = 0.05), HDL-3 (r = -0.62; p = 0.04), and VLDL (r = 0.57; p = 0.05), and saturated fats with HDL-3 (r = -0.59; p = 0.055). Diet was moderately associated with lipoproteins in SU, but steroids had a much greater influence on CVD risk. Despite disease promoting diets NSU had relatively average CVD risk that may be attributed to protective effects of rigorous training.

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This report describes a patient who presented with extensive inguinal lymphadenopathy while taking quinidine for the treatment of arrhythmias. An excisional lymph node biopsy specimen demonstrated atypical, reactive, follicular hyperplasia. Immunologic assessment utilizing 20 monoclonal antibodies indicated a reactive process with follicles shown to be polyclonal B cell. The patient's adenopathy resolved within one month of discontinuation of quinidine and he remains well 15 months later. The histologic and immunologic findings as well as the clinical response are typical for a drug-induced reactive lymphadenopathy.

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The histologic, immunophenotypic, and clinical findings in 24 cases of "well-differentiated" lymphoproliferative disorders are presented, with an emphasis on small lymphocytic lymphoma (SLL; well-differentiated lymphocytic lymphoma, WDLL). SLL was diagnosed in 18 patients, Waldenström's macroglobulinemia in one, mantle zone lymphoma (MZL) in four, and intermediate differentiated lymphocytic lymphoma (IDL) in one. Immunophenotypic analysis revealed one SLL to be of T-cell derivation, while a monoclonal B-cell phenotype was found in the remaining 23 patients; 20 of these neoplasms co-expressed the pan-T-cell antigen Leu-1. This included three of the four patients with MZL and the patient with IDL. All SLLs with pseudofollicular growth centers stained for transferrin receptor. Additionally, a survey of 248 non-Hodgkin's lymphomas of all types revealed four of 70 patients with B-cell large cell lymphoma (LCL; diffuse histiocytic lymphoma, DHL) that also co-expressed the same Leu-1 antigen. Immunoperoxidase study of both frozen tissue sections and cytocentrifuge preparations eliminated the limitations of faint antigen expression and/or interstitial immunoglobulin staining. In addition to detailing the immunophenotype of SLL, the immunologic kinship of MZL/IDL to SLL and the uncommon co-expression of Leu-1 in B-cell LCLs are demonstrated.

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Of 34 patients with primary amyloidosis seen at the University of Arizona between 1973 and 1984, 25 had amyloidosis in association with overt multiple myeloma. Response to treatment was evaluable in 16 of the 25 patients. Median survival in the seven patients (44 percent) with response to treatment was 28 months versus a median of seven and a half months for the nine patients without response (p less than 0.001). Although there were no absolute predictors of response, patients with response were much less likely to have cardiac amyloid (14 percent versus 78 percent, p = 0.02), but more likely to have unusually high serum beta 2-microglobulin (above 15 micrograms/dl in three of four with response versus in neither of two without response) and kappa subtype monoclonal protein (57 percent versus 33 percent). Renal amyloid and/or serum creatinine levels above 2 mg/dl in three of seven (43 percent) patients with response did not preclude a good outcome. It is concluded that a chemotherapy induction trial is worthwhile in primary amyloidosis associated with myeloma since a subset of patients can have prolonged survival (more than two years).

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The usefulness of the mouse rosette (MR) assay in differentiating among various "well to intermediate differentiated" lymphoproliferative disorders (LPD) is presented. Thirty patients with a suspected LPD were studied. By standard histologic, cytologic, immunologic (surface immunoglobulin and monoclonal antibody markers), and clinical criteria, the following diagnoses (independent of MR data) were made: chronic lymphocytic leukemia (CLL) (n = 12), CLL in transformation (n = 2), well-differentiated lymphocytic lymphoma (WDLL) (n = 5), intermediate-differentiated lymphoma (IDL) (n = 2), hairy cell leukemia (HCL) (n = 3), prolymphocytic leukemic (PLL) (n = 1), poorly differentiated lymphocytic lymphoma (PDL) (n = 1), and no disease or reactive lymphocytosis (n = 4). There were 11 B-CLL cases and one T-CLL case. The percent of MR in all cases of B-CLL ranged from 26 to 76% (m = 62%); 10/11 cases had greater than or equal to 50% MR. The case with 26% MR was atypical in that it occurred in a 26-year-old patient. The percent of MR ranged from 0 to 42% (m = 16%) in the cases of well to intermediate differentiated lymphomas. Similar to previous reports intermediate proportions of MR were seen in HCL (12-41%); and low values were seen in PDL (4%) and PLL (4%). In summary, the MR assay may be a useful tool for differentiating CLL from other well to intermediate differentiated LPD involving the peripheral blood. Also, since the MR receptor is normally found only on functionally immature cells, this differential mouse rosetting capability suggests that CLL arises from a less mature cell than WDLL or IDL.

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Eleven patients with mature or peripheral T-cell lymphoma (PTL), other than mycosis fungoides, were identified using an extensive battery of T- and B-cell markers. Eight cases had a histologic diagnosis of either diffuse large cell or mixed lymphoma, three of small cell type. All cases had one or more "mature" T-antigens and an absence of B- and immature T-antigens. Assessment of T-antigens included E-rosettes (Er), anti-Leu 1-7 and Tdt. The authors delineated striking heterogeneity of T-antigen expression: 9 different immunotypes in 11 cases. Subset T-antigen assessment indicated T-helper neoplastic cells in five cases and T-suppressor in two. The remaining four had universal T-antigens alone. Seven cases appeared to have "novel" T-phenotypes not corresponding to normal T-ontogeny phenotypes. Novel or idiosyncratic phenotypes may be a key characteristic of PTL. Since no single T-antigen, including Er and Er receptor (Leu-5), was expressed in all cases, a battery of monoclonal antibodies is necessary to detect PTL. Clinically, the authors found PTL unexpectedly aggressive, despite mature immunotype. Most patients were elderly (median age 69); all had extranodal disease with cutaneous involvement (six cases) most frequent. Responses to chemotherapy frequently proved transient, with median survival of nine months. A fulminant course was noted even with localized presentation. Clinical outcome suggests PTL requires new therapeutic strategies.

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