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VASOPRESSIN IN DEPRESSION
164 with early screening of sexually active females and/or those with a history of in-utero exposure to diethylstilboestrol. 1129 East Second,
Casper, Wyoming 82601, U.S.A.
SAM T. SCALING
VASOPRESSIN IN DEPRESSION al.’ have suggested that arginine vasopressin (A.v.P.) plays a role in human affective disorder: the specific proposal was that plasma-A.v.p. levels are decreased in depression. We present here preliminary results from our investigations of plasma-A.v.p. in depressed patients and the response of plasma-A.v.p. to electroconvulsive therapy (E.C.T.).
SiR,--Gold
et
Seven female patients (mean age S4-4±$-6) were studied while in hospital for treatment of depressive illness. They all had a major depressive disorder.2 Seven female controls (mean age 52±6-3) were selected from hospital personnel. The patients and controls were nonsmokers and in good general health. Subjects in the following categories were excluded: those with orthostatic hypotension or other clinical evidence of hypovolaemia; those with a history of ingestion, in the 4 weeks before the study, of any psychotropic medications or drugs suspected to affect A.v.p. release; those who had drunk alcohol within 24 h of study or who had had heavy alcohol consumption within a week; and known alcoholics.
A.V.P.
([JtU/ml) RESPONSE TO E.C.T.
hypothesis that A.V.P. function is decreased in depression remains purely speculative. The secretion of A.V.P. stimulated by E.c.T. is of interest. The mechanism is unclear. This observation may be relevant in light of the speculation that A.V.P. has antidepressant activity.1 A.V.P. may be a brain active hormone with effects on behaviour.4 Release of this hormone by E.C.T. might play some role in the mechanism of action of this poorly understood but ever, the
highly effective5 antidepressant treatment. Geriatric Research, Education, and Clinical Center,
V.A.Hospital, Seattle, Washington 98108, U.S.A. and Department of Psychiatry and Behavioral Sciences,
MURRAY RASKIND
University of Washington
Department of Psychiatry and Behavioral Sciences,
University of Washington
HERBERT ORENSTEIN
Department of Medicine and Pediatrics, University of California at Los Angeles
RICHARD E. WEITZMAN
HASSALL’S CORPUSCLES
SiR,—Dr Forresterzis
correct
in
stating that
some
thymo-
cytes die in Hassall’s corpuscles. However, recent evidence indicates that these corpuscles function as part of the reticuloendothelial system, taking up vital dyes and colloidal particles from the circulation as well as homologous and foreign serumproteins. Furthermore they enlarge during involution and
during reconstitution, bearing an inverse relationship in the thymus gland. Like Hassall himself, these corpuscles are busy bodies.
regress
to D.N.A. turnover
Department of Pathology, Guy’s Hospital Medical School, London, SE1 9RT
*Significantly higher than baseline, p < 0 - 01. tNot included in statistical analysis because of insufficient numbers.
J. N.
BLAU
ANAEROBIC BREAST ABSCESSES
SiR,—The report by Mr Leach and colleagues (Jan. 6, p. Subjects deprived of fluids after midnight, blood being collected between 7 A.M. and 10 A.M. while subjects were in a comfortable supine position. Two blood-samples were taken 10 min apart through an indwelling needle inserted 15 min beforehand. Individual A.V.P. values are the means of these two samples. A.V.P. was measured by radioimmunoassay.3 The normal range was 0.5-2.0 p.U/ml. Serumsodium was determined by flame photometry. In four patients, plasma-A.v.p. was measured again after successful E.C.T. and full recovery. The acute response of plasma A.V.P. to E.C.T. (five treatments in the four patients) was also determined, blood being sampled before premedication and 2 min afterwards and 5 min and 15 min after cessation of seizure activity. Results are expressed as means ± s.E. and analysed by t test, paired t test, or analysis of variance. Plasma-A.v.p. in the depressed patients (1-66±0-20 tU/ml) did not differ significantly from that in the control subjects (1·36±0·23). Nor did serum-sodium (means 141 and 140 were
mmot/1 respectively). There was no significant difference between plasma-A.v.p. during illness (1· 16±0·29 U/ml, range
and after recovery (1.02+0-$jU/mt, 0.23-2.60). Plasma-A.v.p. rose significantly after E.c.T. (see table). Values were highest 5 min after E.c.T. These results do not support the hypothesis that plasma-A.v.p. is decreased in depression. More subtle abnormalities of A.V.P. function might occur in depression, perhaps involving altered secretion into cerebrospinal fluid or altered responsivity to osmolar and/or volume regulatory stimuli. At present, how-
0.67-1.85)
1. Gold, P. W., Goodwin, F. K., Reus, V. I. Lancet, 1978, i, 1233. 2. Spitzer, R. L., Endicott, J., Robins, E. Am. J. Psychiat. 1975, 132, 1187. 3. Skowsky, W. R., Rosenbloom, A. A., Fisher, D. A. J. clin. Endocr. Metab.
1974, 38, 278.
35)
prompts
us to
report
a
similar
case.
A
30-year-old
multi-
presented with a 12-year history of recurrent breast abscesses which persisted despite repeated incisions and various courses of chemotherapy. Biopsy showed non-specific, chronic inflammatory change only. When the patient was first seen by us a year ago the abscess yielded Bacteroides melaninogenicus resistant to penicillin, B. oralis, anaerobic streptococci, parous
woman
and Escherichia coli. Treatment with metronidazole, 400 mg 8-hourly and latterly with 200 mg 8-hourly, resulted in almost complete healing of the abscesses, which, however, have always recurred at varying intervals after cessation of chemotherapy. Tests of phagocytic function3 indicated an impaired response; the patient’s white blood-cells and homologous serum produced only a 14-fold reduction in the count of a culture of Proteus mirabilis, whilst the cells and serum of a normal control patient produced a 1000-fold decrease under identical conditions. Further evidence that polymorph function was abnormal was obtained when only 5% of the patient’s neutrophils proved capable of reducing nitroblue tetrazolium when stimulated with crude endotoxin, whereas 25% of the neutrophils of a control patient reduced the dye under the same conditions. The patient’s serum showed no obvious abnormality when screened for defects of humoral immunity (immunoglobulin and so on) and her serum did not affect the phagocytic ability of normal control cells. We suspect, therefore, that the defect 4. de Wied, D. Life Sci. 1977, 20, 195. 5. Br. J. Psychiat. 1977, 131, 251. 2. Forrester, J. Lancet, 1978, ii, 1360. 3. Ingham, H. R., Sisson, P. R., Thargonnet, D., Lancet, 1977, ii, 1252.
Selkon, J. B., Codd, A.
A.
Casper, Wyoming 82601, U.S.A.
SAM T. SCALING
VASOPRESSIN IN DEPRESSION al.’ have suggested that arginine vasopressin (A.v.P.) plays a role in human affective disorder: the specific proposal was that plasma-A.v.p. levels are decreased in depression. We present here preliminary results from our investigations of plasma-A.v.p. in depressed patients and the response of plasma-A.v.p. to electroconvulsive therapy (E.C.T.).
SiR,--Gold
et
Seven female patients (mean age S4-4±$-6) were studied while in hospital for treatment of depressive illness. They all had a major depressive disorder.2 Seven female controls (mean age 52±6-3) were selected from hospital personnel. The patients and controls were nonsmokers and in good general health. Subjects in the following categories were excluded: those with orthostatic hypotension or other clinical evidence of hypovolaemia; those with a history of ingestion, in the 4 weeks before the study, of any psychotropic medications or drugs suspected to affect A.v.p. release; those who had drunk alcohol within 24 h of study or who had had heavy alcohol consumption within a week; and known alcoholics.
A.V.P.
([JtU/ml) RESPONSE TO E.C.T.
hypothesis that A.V.P. function is decreased in depression remains purely speculative. The secretion of A.V.P. stimulated by E.c.T. is of interest. The mechanism is unclear. This observation may be relevant in light of the speculation that A.V.P. has antidepressant activity.1 A.V.P. may be a brain active hormone with effects on behaviour.4 Release of this hormone by E.C.T. might play some role in the mechanism of action of this poorly understood but ever, the
highly effective5 antidepressant treatment. Geriatric Research, Education, and Clinical Center,
V.A.Hospital, Seattle, Washington 98108, U.S.A. and Department of Psychiatry and Behavioral Sciences,
MURRAY RASKIND
University of Washington
Department of Psychiatry and Behavioral Sciences,
University of Washington
HERBERT ORENSTEIN
Department of Medicine and Pediatrics, University of California at Los Angeles
RICHARD E. WEITZMAN
HASSALL’S CORPUSCLES
SiR,—Dr Forresterzis
correct
in
stating that
some
thymo-
cytes die in Hassall’s corpuscles. However, recent evidence indicates that these corpuscles function as part of the reticuloendothelial system, taking up vital dyes and colloidal particles from the circulation as well as homologous and foreign serumproteins. Furthermore they enlarge during involution and
during reconstitution, bearing an inverse relationship in the thymus gland. Like Hassall himself, these corpuscles are busy bodies.
regress
to D.N.A. turnover
Department of Pathology, Guy’s Hospital Medical School, London, SE1 9RT
*Significantly higher than baseline, p < 0 - 01. tNot included in statistical analysis because of insufficient numbers.
J. N.
BLAU
ANAEROBIC BREAST ABSCESSES
SiR,—The report by Mr Leach and colleagues (Jan. 6, p. Subjects deprived of fluids after midnight, blood being collected between 7 A.M. and 10 A.M. while subjects were in a comfortable supine position. Two blood-samples were taken 10 min apart through an indwelling needle inserted 15 min beforehand. Individual A.V.P. values are the means of these two samples. A.V.P. was measured by radioimmunoassay.3 The normal range was 0.5-2.0 p.U/ml. Serumsodium was determined by flame photometry. In four patients, plasma-A.v.p. was measured again after successful E.C.T. and full recovery. The acute response of plasma A.V.P. to E.C.T. (five treatments in the four patients) was also determined, blood being sampled before premedication and 2 min afterwards and 5 min and 15 min after cessation of seizure activity. Results are expressed as means ± s.E. and analysed by t test, paired t test, or analysis of variance. Plasma-A.v.p. in the depressed patients (1-66±0-20 tU/ml) did not differ significantly from that in the control subjects (1·36±0·23). Nor did serum-sodium (means 141 and 140 were
mmot/1 respectively). There was no significant difference between plasma-A.v.p. during illness (1· 16±0·29 U/ml, range
and after recovery (1.02+0-$jU/mt, 0.23-2.60). Plasma-A.v.p. rose significantly after E.c.T. (see table). Values were highest 5 min after E.c.T. These results do not support the hypothesis that plasma-A.v.p. is decreased in depression. More subtle abnormalities of A.V.P. function might occur in depression, perhaps involving altered secretion into cerebrospinal fluid or altered responsivity to osmolar and/or volume regulatory stimuli. At present, how-
0.67-1.85)
1. Gold, P. W., Goodwin, F. K., Reus, V. I. Lancet, 1978, i, 1233. 2. Spitzer, R. L., Endicott, J., Robins, E. Am. J. Psychiat. 1975, 132, 1187. 3. Skowsky, W. R., Rosenbloom, A. A., Fisher, D. A. J. clin. Endocr. Metab.
1974, 38, 278.
35)
prompts
us to
report
a
similar
case.
A
30-year-old
multi-
presented with a 12-year history of recurrent breast abscesses which persisted despite repeated incisions and various courses of chemotherapy. Biopsy showed non-specific, chronic inflammatory change only. When the patient was first seen by us a year ago the abscess yielded Bacteroides melaninogenicus resistant to penicillin, B. oralis, anaerobic streptococci, parous
woman
and Escherichia coli. Treatment with metronidazole, 400 mg 8-hourly and latterly with 200 mg 8-hourly, resulted in almost complete healing of the abscesses, which, however, have always recurred at varying intervals after cessation of chemotherapy. Tests of phagocytic function3 indicated an impaired response; the patient’s white blood-cells and homologous serum produced only a 14-fold reduction in the count of a culture of Proteus mirabilis, whilst the cells and serum of a normal control patient produced a 1000-fold decrease under identical conditions. Further evidence that polymorph function was abnormal was obtained when only 5% of the patient’s neutrophils proved capable of reducing nitroblue tetrazolium when stimulated with crude endotoxin, whereas 25% of the neutrophils of a control patient reduced the dye under the same conditions. The patient’s serum showed no obvious abnormality when screened for defects of humoral immunity (immunoglobulin and so on) and her serum did not affect the phagocytic ability of normal control cells. We suspect, therefore, that the defect 4. de Wied, D. Life Sci. 1977, 20, 195. 5. Br. J. Psychiat. 1977, 131, 251. 2. Forrester, J. Lancet, 1978, ii, 1360. 3. Ingham, H. R., Sisson, P. R., Thargonnet, D., Lancet, 1977, ii, 1252.
Selkon, J. B., Codd, A.
A.