of the parotid gland warrant consideration because of the potential for facial nerve injury occurring with surgical treatment and the risk of malignant conversion. Forty-eight cases of recurrent pleomorphic adenoma treated at the University of Michigan, Ann Arbor, between 1935 and 1975 were retrospectively analyzed. The results of surgical procedures for recurrence were determined with respect to tumor control and resultant facial nerve function. Malignant conversion developed in three (6%) of 48 cases. The results of this study underscore the importance of adequate surgical excision of initial recurrences as well as primary tumors to prevent tumor recidivism. Tumor control rates and facial nerve preservation are enhanced with formal parotidectomy for recurrent tumor when feasible. In cases in which facial nerve identification and dissection is not possible, en bloc total parotidectomy offers effective, though not absolute, control of extensive recurrence.Advances in surgical techniques -¿A-have markedly diminished the recurrence rate previously associated with surgical excision of pleomorphic adenoma of the parotid gland. Factors responsible for the recurrence of pleo¬ morphic adenoma have received extensive review over the past 50 years. While intraoperative tumor rupture and seeding, tumor multicentricity, metachronous tumor develop¬ ment, and histologie evidence of cap¬ sular penetration or hypercellularity are mentioned as factors possibly related to the development of recur¬ rence, clinical behavior of pleomor¬ phic adenomas is most closely corre¬ lated with the adequacy of surgical treatment. Rates of recurrence follow¬ ing primary surgery for pleomorphic adenoma of the parotid gland have been reported to be as high as 44%, this being attributed to inadequate surgical excision.1 Subsequent reports suggested that formal parotidectomy was associated with lower rates of recurrence than was simple excision,2 and comparisons of large groups treated within the same institution revealed a fourfold greater rate of recurrence from simple excision as compared with formal parotidectomy, whether superficial or total, with facial nerve preservation.3 Recent reports have documented that a surgi¬ cal treatment policy of formal paroti¬ dectomy for primary pleomorphic adenoma leads to recurrence rates that approach zero,46 and many sur¬ geons have adopted this policy. None¬
\s=b\Prior studies of impaired cellular immune reactivity in patients with head and neck squamous carcinoma (HNSC) suggest that immune deficiency associated with tumor growth may be related, in part, to alterations in immunoregulatory functions. To determine if production of soluble mediators of the immune response (lymphokines) is impaired in patients with HNSC, leukocyte migration inhibition in response to phytohemagglutinin was assessed in 32 patients with HNSC and 29 normal subjects and was correlated with levels of specific peripheral blood lymphocyte subpopulations to determine if quantitative levels of immunoregulatory lymphocyte subpopulations were related to in vitro lymphokine production. In the patients with cancer, leukocyte inhibitory factor production was consistently and significantly impaired and was directly related to levels of T4\ x=req-\ positive (helper/inducer) lymphocytes.Substantial differences in levels of individual subpopulations were not detected among normal subjects and patients with cancer; however, the mean T4/T8 ratio was substantially increased in the patients with cancer. The findings confirm and extend prior observations of impaired cellular immune mechanisms in patients with HNSC and suggest that impaired lymphokine production may be related to quantitative and qualitative alterations in lymphocyte subpopulations. (Arch Otolaryngol 1984;110:731-735) Impai red cellular immunoreactivity has been consistently demon¬ strated in patients with advanced immune deficiencies were character¬ ized by impaired delayed hypersensi¬ tivity1 and decreased T-lymphocyte levels2; however, more recent studies have documented the multifaceted nature of immune deficiencies in these patients. Such abnormalities have included impaired lymphocyte blastogenic response to mitogens,3·4 alterations in macrophage function,5·6 and increased levels of suppressor monocytes,7·8 immmunosuppressive proteins,9 and immune complexes in the blood of these patients.1011 These observations along with correlations of immune reactivity with tumor extent and prognosis have provided rationale for investigations of the mechanisms regulating immune re¬ sponses in anticipation that better characterization of the immune defi¬ ciency associated with head and neck cancer would permit rational design of immunotherapeutic approaches to tumor treatment.
Impaired cell-mediated immunity has been consistently associated with head and neck squamous carcinoma (HNSC). Previous work has implicated monocytes in this impairment. The present study shows that in a subgroup of untreated patients with advanced HNSC, monocytes are responsible for impaired in vitro lymphokine (leukocyte migration inhibitory factor) production. In view of recent studies suggesting interactions between lymphokines and monocytes in the immune response, the present findings may be relevant to future immunotherapeutic approaches.
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