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PubMed1994

Full dose vincristine (without 2-mg dose limit) in the treatment of lymphomas.

BACKGROUND: Most current lymphoma protocols limit vincristine dose to 2 mg per single dose. Because a lower dose of vincristine may be associated with poorer outcome, there is some rationale to increase the dose of vincristine. METHODS: The feasibility of full dose vincristine (i.e., 1.4 mg/m2 without 2-mg dose limit) was prospectively evaluated in lymphoma patients treated with various combinations. After an initial dose of 1.4 mg/m2, patients were carefully monitored, and dose was modified according to toxicity. RESULTS: One hundred and four consecutive patients (31 with Hodgkin's disease and 73 with non-Hodgkin's lymphoma), aged 18-78 years were evaluated. The first dose was greater than 2 mg in 90% of the patients. The mean actual dose (percent of projected dose) was 100% in the first course and gradually decreased to 64% in the eighth course. The mean actual dose intensity of vincristine (percent of projected dose intensity) during the initial six cycles of prednisone, methotrexate, calcium leucovorin, doxorubicin, cyclophosphamide, etoposide, and mechlorethamine, vincristine, procarbazine, prednisone (ProMACE/MOPP), cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), and MOPP/doxorubicin, bleomycin, and vinblastine (MOPP/ABV) was 82% and MOPP/doxorubicin, bleomycin, and vinblastine was 82%, 83%, and 87%, respectively. Symptoms of neuropathy developed in 92% of the patients and were usually of mild or moderate severity. Toxicity included World Health Organization (WHO) Grades 3 and 4 constipation in 10 (10%), and WHO Grade 3 peripheral neurotoxicity in 16 (15%) patients. Rapid improvement was usually noticed within a few weeks after withdrawal of vincristine. The median duration of symptoms from discontinuation of vincristine was 3 months for paresthesiae and motor weakness and 5 months for muscle cramps. CONCLUSIONS: Full dose vincristine in lymphoma protocols is feasible but is associated with increased toxicity. The therapeutic advantage of full dose vincristine has yet to be proven.

Adolescent↗
PubMed2000

Frequency of minisatellite repeat number changes at the MS205 locus in human sperm before and after cancer chemotherapy.

To determine whether the measurement of repeat number mutations at a minisatellite locus could detect human germline mutations induced by chemotherapy, we performed a longitudinal study of the mutation frequencies in sperm from 10 patients treated for Hodgkin's disease. Polymerase chain reaction on small pools of DNA equivalent to 100 sperm and Southern blotting were used to screen at least 7900 sperm in each sample to quantify the mutation frequency at the minisatellite MS205 locus. Pretreatment and posttreatment semen samples were obtained at least 2 months after completion of therapy from 4 patients treated with a regimen (Novantrone, Oncovin, vinblastine and prednisone [NOVP]) that lacks alkylating agents and from three patients treated with regimens (Cytoxan, vinblastine, procarbazine and prednisone/Adriamycin, bleomycin, dacarbazine, lomustine, and prednisone [CVPP/ABDIC] or mechlorethamine, Oncovin, procarbazine and prednisone [MOPP]) containing alkylating agents. There were no effects of NOVP or CVPP/ABDIC on the mutation frequencies. In the 1 patient treated with MOPP, the treatment with the highest dose of gonadotoxic alkylating agents, there was a statistically significant increase in mutation frequency from 0.79% pretreatment to 1.14% posttreatment, indicating induction of mutations in stem spermatogonia. During-treatment semen samples obtained from 2 patients treated with ABVD, which does not contain gonadotoxic alkylating agents, and 1 with NOVP also did not show any increases above the baseline mutation frequencies, indicating no increase in the minisatellite mutation frequency in spermatocytes. Thus, measurement of repeat number changes at minisatellite MS205 appears to be able to detect induced germline mutations in human sperm. However, most chemotherapy regimens do not significantly increase this class of mutations.

Adult↗
PubMed2000

Protective effect of povidone iodine ointment against skin lesions induced by chemical and thermal stimuli.

Mustard gas (sulfur mustard, HD) is a powerful vesicant employed as a chemical weapon. The present study demonstrates the effect of povidone iodine (PI) ointment against skin toxicity caused by HD. Gross and histopathological examinations showed that application of PI 20 min or less following exposure to the vesicant resulted in marked skin protection. The shorter, interval between exposure and treatment, the better was the protection achieved. Povidone iodine was also effective against other mustards, such as carboxybutylchloroethyl sulfide (CBCS) and mechlorethamine. The fact that PI protected the skin against agents that cannot be oxidized, such as iodoacetic acid, divinylsulfone and cantharidine, indicated that the antidotal effect of PI was unrelated to oxidation of the nitrogen and sulfur atoms of the mustards. Furthermore, NMR spectroscopy of CBCS treated with iodine did not show oxidation of the sulfur atom. Clinical experience with patients after accidential heat burns (mostly of grade I) has shown that topical application of PI ointment immediately after the stimulus significantly reduced, and often prevented, skin lesions. Apart from being a safe and widely used disinfectant, PI ointment is recommended as an efficient protective agent against skin toxicity caused by hazardous chemicals and by heat stimuli.

Administration, Topical↗
PubMed1988

Subsequent development of acute non-lymphocytic leukemia in patients treated for Hodgkin's disease.

A nested case control study was carried out to investigate the association between treatment of patients with Hodgkin's disease (HD) and the risk of developing acute non-lymphocytic leukemia (ANLL). Seven Cancer Centers of the International Cancer Patient Data Exchange System of the UICC participated. A study cohort was selected consisting of 1,681 nonpretreated patients with HD, diagnosed from 1972 through 1978, and followed up through 1984. The median follow-up time was 66 months. Eighteen cases of leukemia were observed in the cohort. The risk of development of ANLL was significantly greater for male than for female patients. The treatment characteristics associated with an increased risk of developing ANLL were extensive radiotherapy, splenectomy and the chemotherapy combination of vincristine, procarbazine and mechlorethamine.

Acute Disease↗
PubMed1982

The hydrolysis of spirohydantoin mustard.

Spirohydantoin mustard (I) is a rationally designed anti-tumor agent with substantial in vivo activity against intracranially implanted tumors in mice. However, hydrolysis of I was much faster than that of mechlorethamine hydrochloride or melphalan, two parenterally administered mustards. The hydrolysis products of I were identified by GC-MS of their silylated derivatives. The decomposition of I (at 25 degrees in 10% dimethylacetamide at pH 4-6), as monitored by GLC was pseudo first-order. The half-life of I ranged from 20 min at pH 4.0 to 14 min at pH 6.0. Nonionic surfactants enhanced the stability of I, but this effect was diminished at lower pH, presumably due to decreased solubility of I in the micelle as more drug was protonated. Several dilute parenterally suitable solvents exhibited no marked effect on the hydrolysis of I. The drug was most stable in a 10% fat emulsion system where the time for 10% decomposition of I was 49 +/- 5 min. Plots of the concentration of I versus time were linear indicating the disappearance was zero order in the 10% fat emulsion system.

Animals↗
PubMed2006

APE chemotherapy for children with relapsed Hodgkin disease: a Pediatric Oncology Group trial.

BACKGROUND: MOPP (mechlorethamine, vincristine, procarbazine, prednisone) and ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) are effective therapies for Hodgkin disease (HD) that may cause long-term toxicities in children. APE (cytosine arabinoside, cisplatin, etoposide) is a non-cross-resistant regimen with limited toxicities. We evaluated this regimen for patients with recurrent or refractory disease. METHODS: Patients with recurrent Hodgkin disease who were <or=21 years of age and had previously received standard alkylating agent and doxorubicin-based therapy, were treated with APE chemotherapy (cytosine arabinoside 750 mg/m(2), cisplatin 15 mg/m(2), etoposide 20 mg/m(2)) every 12 hr, administered three or four times per cycle. Response, Event-free survival (EFS), and overall survival (OS) were assessed. RESULTS: Thirty-one patients in first (n = 25) or second (n = 6) relapse of Hodgkin disease were eligible and evaluable. APE chemotherapy was well-tolerated, with the major toxicity consisting of short duration, grade 3/4 hematopoietic toxicity. The CR/PR response rate was 68% (42% CR, 26% PR). Allowing subsequent stem cell transplantation in some patients, 4-year EFS and OS were 27% +/- 8% and 49% +/- 9%, with 8-year EFS and OS of 23% +/- 9% and 34% +/- 10%. DISCUSSION: APE is an efficacious regimen with minimal toxicity. Novel regimens are necessary to: (1) re-induce remission, (2) treat newly diagnosed patients, and (3) augment therapy in patients with slow response to standard regimens. This regimen had minimal toxicity and an excellent response rate that facilitated long term survival, often in conjunction with transplantation. The Children's Oncology Group is using a similar regimen to augment therapy for slow responders on a current Hodgkin disease trial.

Adolescent↗
PubMed1988

Glucocorticoids attenuate taste aversions produced by toxins in rats.

Conditioned taste aversions (CTAs) develop if toxicosis is induced after an animal eats or drinks. Usually, if a second drug is administered after consumption and prior to the toxin, it either adds to the CTA produced by the toxin or else has no noticeable effect. However, glucocorticoids (dexamethasone, cortisol, methylprednisolone, and prednisolone) attenuate CTAs produced by cyclophosphamide. Dexamethasone was tested most extensively and is also effective against CTAs produced by carmustine, cisplatin, copper sulfate, cytarabine, dactinomycin, doxorubicin, lithium chloride, and mechlorethamine. Delta-9 THC, domperidone, haloperidol, metoclopramide, and scopolamine were ineffective against CTAs produced by cyclophosphamide, although they are used medically for palliative purposes. Prochlorperazine attenuated CTAs but to a much smaller extent than the glucocorticoids. These results are interpreted as cross-validation of recent reports that glucocorticoids alleviate clinically observed distress produced by cancer chemotherapies.

Animals↗
PubMed1985

Clonogenic response of cells of murine intestinal crypts to 12 cytotoxic drugs.

The in situ response of clonogenic cells in murine intestinal crypts to graded doses of 12 clinically used cytotoxic drugs has been measured by the crypt microcolony assay. For the alkylating agents mechlorethamine hydrochloride and BCNU, survival curves down to three logs of crypt depletion could be obtained. However, with isopropyl methane sulphonate only one log of depletion was measurable, and for a fourth alkylating agent, cyclophosphamide, no crypt killing occurred before other toxicities resulted in death of the animal in less than 3-4 days. This is the major constraint on the use of the microcolony assay with cytotoxic drugs. Of four antibiotics, survival curves were obtainable for adriamycin, bleomycin and mitomycin C, but not for actinomycin D. 5-Fluorouracil gave only a limited degree of crypt kill. Of three S-phase-specific drugs, hydroxyurea and vincristine resulted in little or no crypt depletion, but there was dose-dependent crypt depletion after methotrexate. The complexities of applying cellular-kinetic classifications of cytotoxic drugs to in situ endpoints are discussed.

Alkylating Agents↗
PubMed1975

Problems of nomenclature III: ambiguous abbreviations and catchwords.

To avoid ambiguity, the following emendations are advocated: (1) 2H, in place of H2, to designate the second histamine receptor; (2) HN-2, in place of HN2, to designate mechlorethamine (MBA);(3) 'pre-drug', in place of 'pro-drug', to describe molecular species which must undergo biotransormation before yielding an effective drug.

Abbreviations as Topic↗
PubMed2000

DNA guanine-guanine crosslinking sequence specificity of isophosphoramide mustard, the alkylating metabolite of the clinical antitumor agent ifosfamide.

PURPOSE: The purpose of this investigation was to determine the base sequence specificity of isophosphoramide mustard (IPM), the alkylating metabolite of ifosfamide, by crosslinking of designed DNA oligomers in comparison with the clinical alkylating agents mechlorethamine (ME) (nitrogen mustard) and phosphoramide mustard (PM), the alkylating metabolite of cyclophosphamide. METHODS: IPM, as well as PM and ME were each reacted with three dodecameric duplexes, which were designed to detect interstrand crosslinking between guanines in 5'-GC-3' (I), 5'-GNC-3' (II) or 5'-GNNC-3' (III) sequences (N = A or T). RESULTS: All three agents preferentially react with 5'-GNC-3' target sequences. The 5'-GNNC-3' target sequence is less reactive by a factor of approximately 2.5- to 10-fold, while 5'-GC-3' is of even lower reactivity. CONCLUSION: These results indicate that all three agents show approximately equal preference for reaction with a 5'-GNC-3' target sequence in spite of the fact that IPM yields a 7-atom crosslink, while the other two agents yield 5-atom crosslinks.

Antineoplastic Agents, Alkylating↗
PubMed1994

Effect of sulfhydryl compounds and glutathione depletion on rat heart myocyte toxicity induced by 4-hydroperoxycyclophosphamide and acrolein in vitro.

Neonatal rat heart myocytes were used to study the acute cardiotoxic effects of cyclophosphamide (CTX) metabolites. The myocytes were equi-sensitive to 4-hydroperoxycyclophosphamide (4HPC) and acrolein in vitro with 50% inhibitory concentrations (IC50) of 123 microM and 152 microM, respectively. The parent compound, CTX, was inactive and the myocytes were much less sensitive to the bis-chloroethylamine alkylator, mechlorethamine (IC50 = 1161 microM). Cellular glutathione (GSH) levels were initially reduced and then transiently elevated following exposure to 4HPC. With acrolein, GSH levels were reduced to unmeasurable levels at all time points. With the addition of 0.5 mM L-buthionine sulfoximine (BSO), myocyte GSH levels were reduced from control values of 120 nmol/mg protein to < 10 nmol/mg protein without causing direct cytotoxicity. However, pretreatment with BSO significantly enhanced the cardiotoxic effects of 4HPC. Finally, two exogenous sulfhydryl-containing compounds were shown to block the myotoxic effects of both 4HPC and acrolein. Mesna and N-acetylcysteine increased at concentrations of 0.01 microgram/ml and 0.1 microgram/ml roughly increased the IC50 of 4HPC by 2-3-fold. These results suggest that acrolein and 4HPC are equipotent cytotoxins and that a transient depletion in GSH accompanies this toxic effect in cardiac myocytes.

Acrolein↗
PubMed1992

Pancopride, a potent and long-acting 5-HT3 receptor antagonist, is orally effective against anticancer drug-evoked emesis.

Pancopride ((+-)N-(1-azabicyclo-[2,2,2]-oct-3-yl)-2-cyclopropylmethoxy-4-ami no-5-chlorobenzamide) is a new potent and selective 5-HT3 receptor antagonist, orally and parenterally effective against cytotoxic drug-induced emesis. In vitro, pancopride displayed high affinity (Ki = 0.40 nM) for [3H]GR65630-labelled 5-HT3 recognition sites in membranes from the cortex of rat brains. In vivo, pancopride antagonized 5-HT-induced bradycardia in anaesthetized rats when administered i.v. 5 min (ID50 = 0.56 microgram/kg) or p.o. 60 min (ID50 = 8.7 micrograms/kg) before 5-HT challenge. A single oral dose (10 micrograms/kg) of pancopride produced a significant inhibition of the bradycardic reflex over an 8-h period. Pancopride dose dependently inhibited the number of vomiting episodes and delayed the onset of vomiting induced by cisplatin in dogs (ID50 = 3.6 micrograms/kg i.v. and 7.1 micrograms/kg p.o.). Pancopride was also effective in blocking mechlorethamine- and dacarbazine-induced emesis. Unlike metoclopramide, pancopride was shown to lack any measurable antidopaminergic activity both in vitro and in vivo. These results support clinical data, indicating that pancopride will be a useful drug for treating cytostatic-induced emesis in humans.

Animals↗
PubMed1984

Interaction of alpha adrenergic antagonists with calmodulin.

Several alpha-adrenergic antagonists inhibited the activation of calmodulin-stimulated phosphodiesterase at concentrations that had little or no effect on basal phosphodiesterase activity. The most potent of these compounds were phenoxybenzamine and dibenamine (IC50 values of about 1 microM); the amino acid ergot alkaloids ergocryptine, ergocristine, ergotamine and their dihydrogenated derivatives were less potent calmodulin-inhibitors (IC50 values of 35-80 microM). The amino ergot alkaloids ergonovine and methysergide were essentially devoid of inhibitory activity. A variety of other alpha 1-antagonists (phentolamine, tolazoline and prazosin), an alpha 2-antagonist (yohimbine), alpha-agonists (norepinephrine, phenylephrine and clonidine), beta-adrenergic antagonists (propranolol and practolol) and the beta-adrenergic agonist methoxyphenamine displayed little or no anti-calmodulin activity (IC50 values greater than 300 microM). Similarly, the alkylating agents chlorambucil and mechlorethamine also failed to inhibit calmodulin activity. Phenoxybenzamine and dibenamine inhibited calmodulin activity irreversibly, whereas the inhibition caused by other alpha adrenergic blocking agents was reversible. Phenoxybenzamine inhibited calmodulin activity by binding directly to it. This binding was calcium-dependent and irreversible. The irreversible binding and inhibition of calmodulin activity by phenoxybenzamine (or dibenamine) may serve as a useful tool for studying the sites at which drugs bind to calmodulin and may also be useful for studying the distribution and turnover of calmodulin.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1996

Mutagenic damage to mammalian cells by therapeutic alkylating agents.

Cytotoxic alkylating agents used as therapeutics include nitrogen mustards, ethyleneimines, alkyl sulfonates, nitrosoureas and triazenes. Their reactivity with DNA, RNA and proteins can cause cell death. Side-effects of treatment include tissue toxicity and secondary malignancies, likely due to the genetic damage induced. The full mutagenic potential of alkylating agents may only be realised after they undergo metabolic activation, principally by cytochromes P450. Mutagenicity is related to the ability of alkylating agents to form crosslinks and/or transfer an alkyl group to form monoadducts in DNA. The most frequent location of adducts in the DNA is at guanines. Expressed mutations involve different base substitutions, including all types of transitions and transversions. The mutational spectra of alkylating agents on mammalian cells is distinct from that induced in bacterial cells, reflecting the different codon usage by bacteria and differences in DNA repair and replication enzymes. Mutations are induced by busulfan, chlorambucil (CAB), cyclophosphamide (CP, or its metabolite), dacarbazine, mechlorethamine, melphalan, mitomycin-C (MMC), nitrosoureas and thiotepa. Although dose-dependent, the relationship is not always linear. The molarities at which alkylating agents induce cell killing and mutations vary over three orders of magnitude. The mutagenic efficiency, of alkylating agents also varies, with some agents inducing three times more mutations for equivalent cell killing. The induction of micronuclei, sister chromatid exchanges, or chromosome aberrations is variable, but has been observed for CP, CAB, MMC, melphalan and triethylenemelamine. There is insufficient information to determine whether any synergistic effects of alkylating agents used in combination will influence the cytotoxic and mutagenic damage equally. Understanding the potential synergy of alkylating agents at the cellular and molecular level should allow improvement of the therapeutic efficacy of alkylating agents without increasing the unwanted mutation induction.

Alkylating Agents↗
PubMed1986

The effects of nitrogen mustards on the proliferative and Ig synthetic response of human peripheral blood lymphocytes.

Maximal inhibition of pokeweed mitogen-stimulated Ig production and [3H]thymidine incorporation was shown to occur when unfractionated human peripheral blood mononuclear cells were cultured with concentrations of the nitrogen mustards melphalan, mechlorethamine or chlorambucil in the 20-100-microM range, whereas concentrations of microsome-activated cyclophosphamide (A-Cy) in the 2-mM range were required for equivalent inhibition. Around 400 microM A-Cy, IgM secretion was not inhibited, but secretion of IgA and IgG was. The [3H]thymidine incorporation of enriched populations of both large and small B and T cells all showed about 20-50-fold greater sensitivity to melphalan than to A-Cy, despite a difference of only 6-fold in alkylating activity between these drugs. Large (250 micron 3) B and T cells were only marginally more sensitive to melphalan and A-Cy than small (210 micron 3) T and B cells. Kinetic studies showed that IgG and IgA secreted by day 7 could be maximally inhibited by melphalan added as late as day 3, and IgM synthesis as late as day 2. In contrast, inhibition of Ig production by A-Cy steadily declined after the first day, especially IgM, which was no longer inhibitable by A-Cy on day 3. Inhibition of cumulative Ig production did not occur when A-Cy or melphalan was added on day 5 or later. Cell recombination experiments performed with drug pulsed and untreated monocytes plus B cells and irradiated T cells showed that inhibition of [3H]thymidine or Ig production was most striking when monocytes + B cells (rather than T cells) were exposed to melphalan in the first 16 h. When A-Cy was used in the first 16 h, inhibition of Ig production was partial and inconsistent, and inhibition of monocytes + B cell or T cell [3H]thymidine incorporation was not evident. We conclude that the nitrogen mustards melphalan and A-Cy can inhibit pokeweed mitogen-stimulated DNA synthesis by human T or B cells and Ig production in vitro, but that their mechanisms of action differ.

Adult↗
PubMed1990

The effect of chemotherapy on the in vivo frequency of glycophorin A 'null' variant erythrocytes.

A human in vivo somatic cell assay based on the enumeration of variant erythrocytes lacking expression of an allelic form of the cell-surface sialoglycoprotein, glycophorin A, was applied to the study of blood samples from patients obtained prior to, during, and following chemotherapy for malignant disease in order to determine the effect of mutagenic chemical agents on the frequency of variant cells. In 22 patients assayed prior to therapy, the mean variant cell frequency was 11.9 per million, which was not significantly different from that observed in healthy controls. In an initial cross-sectional survey, blood samples were obtained at various times during and after therapy from 30 patients diagnosed with a variety of malignancies who were treated with one or more known mutagenic agents including adriamycin, bleomycin, cis-platinum, cyclophosphamide, dacarbazine, etoposide, lomustine, mechlorethamine, melphalan, mitomycin C, and procarbazine. Significant elevations in the mean frequency of variant cells over pre-therapy and normal levels were observed in samples obtained during and after therapy. In a time-series study, 14 breast cancer patients treated with CAF (cyclophosphamide, adriamycin, 5-fluorouracil), CMF (cyclophosphamide, methotrexate, 5-fluorouracil), or VMF (vinblastine, methotrexate, 5-fluorouracil) adjuvant chemotherapy were sampled repeatedly during and after therapy. For the CAF and CMF patients an increase in the frequency of variant cells was observed with a lag in the appearance of induced variants after initiation of therapy; variant frequencies gradually increased during therapy reaching a maximum at or shortly after the end of therapy, then declined to near pre-therapy levels within 6 months. The maximum level of induced variants ranged from 2- to 7-fold over pre-therapy or normal levels depending on the combination of agents used. The breast cancer patients treated with both adriamycin and cyclophosphamide showed consistent elevations in the frequency of variant cells; patients treated only with cyclophosphamide showed lower and more variable elevations. The data demonstrate that mutagenic chemotherapy agents induce elevated levels of glycophorin A variant erythrocytes consistent with the hypothesis that variant cells result from somatic mutation. The elevations in variant cells were transient, suggesting that these agents primarily affect the rapidly cycling committed erythroid cell population.

Adolescent↗
PubMed1990

Combination of ABVD and radiotherapy in early stages of Hodgkin's disease: analysis of a series of 94 patients. Pierre and Marie Curie Group (GPMC).

In order to reduce, if not completely suppress, late complications of combined chemotherapy and radiotherapy in Hodgkin's disease (HD), MOPP regimen (mechlorethamine, vincristine, procarbazine and prednisone) was replaced by ABVD (doxorubicin, bleomycin, vinblastine and dacarbazine). Ninety-four patients with HD clinical stages I to IIIA with no staging laparotomy were treated by three courses of ABVD followed by radiotherapy. Irradiation was performed on extended fields in 41 cases and on involved fields in 53 others. Consolidation chemotherapy was planned in 67 cases with at least one unfavorable prognostic factor, but achieved only in 33 cases. Seventeen patients relapsed within 1 to 46 months after the beginning of treatment. Ten patients died, 7 of HD and 3 of intercurrent diseases or accident. Disease-free survival rate with a median follow-up of 60 months is 80%. This study showed, on the one hand, many digestive and general side-effects after ABVD and, on the other, a satisfactory hematological tolerance. Furthermore, mediastinitis or cardiovascular complications were not more frequent than with MOPP. These results point out the development and use of better tolerated regimens for initial chemotherapy in HD, without jeopardizing the good results of the treatment.

Adult↗
PubMed1991

Testicular dysfunction in Hodgkin's disease before and after treatment.

Over a 7-year period, semen analysis was performed in 92 male patients with Hodgkin's disease prior to therapy. In 67% of patients semen revealed a decreased chance for fertility (i.e. oligozoospermia, asthenozoospermia and/or teratozoospermia). The mean basal levels of follicle-stimulating hormone (FSH), luteinising hormone, testosterone and prolactin were in the normal range. In 77 patients in complete remission after alternating MOPP/ABVD (mechlorethamine, vincristine, procarbazine, prednisone; doxorubicin, bleomycin, vinblastine, dacarbazine), testicular function was assessed. 87% of patients were azoospermic, 9% had semen abnormalities and only 4% were normospermic. Recovery of spermatogenesis was documented in only 17 of 42 (40%) reassessed patients after a median time of 27 months and was generally not affected by pretreatment sperm quality. After chemotherapy, the mean value of FSH [20.45 (S.E. 1.7) mUI/ml] was significantly superior compared with that of the mean pretreatment values. No difference was documented in the mean testosterone and prolactin values tested before and after treatment. Our findings indicate that, of patients with Hodgkin's disease, about half are affected by hypogonadism before starting chemotherapy. By utilising alternating MOPP/ABVD, persistent testicular dysfunction was documented in half of the patients.

Adolescent↗