Influence of Hydrazine Sulfate on
Abnormal Carbohydrate Metabolism in Cancer Patients with Weight Loss *
[CANCER RESEARCH 44, 857-861, February 1984]
Rowan T. Chlebowski,** David Heber, Betsy Richardson, and
Jerome B. Block
Divisions of Medical Oncology [R.T.C., B.R., J.B.B.] and
Endocrinology and Metabolism [D.H.], Department of Medicine, University of California Los
Angeles School of Medicine, Harbor-UCLA Medical Center, Torrance, California 90509
Thirty-eight patients with advanced cancer and weight loss were tested in a prospectively
randomized, double-blind, placebo-controlled trial to evaluate the influence of hydrazine
sulfate on carbohydrate metabolism in cancer cachexia. All patients had an initial 3-day
inpatient metabolic evaluation including: standard 5-hr p.o. glucose tolerance test,
hormone studies, and total glucose production by infusion of [6-3H]glucose.
After 30 days of treatment with capsules containing either placebo or hydrazine sulfate in
a 60-mg, 3 times/day dosage, inpatient evaluation was repeated. A total of 62 metabolic
inpatient evaluations were performed. The pretreatment characteristics of age, sex, prior
therapy experience, nutritional parameters and tumor types were comparable in placebo and
hydrazine treatment groups. On initial evaluation, abnormal glucose tolerance and
increased glucose production were frequently seen. Serial assessment of glucose tolerance
showed no improvement after 30 days of placebo treatment. However, the glucose tolerance
was significantly improved in patients receiving 30 days of hydrazine sulfate [2-hr
glucose; initial 169 +/- 24 (S.E.) mg/d] versus final 128 +/- 12 mg/ dl; p<0.05]. In
addition, the rate of total glucose production was significantly decreased after 30 days
of hydrazine sulfate compared to placebo treatment (2.46 mg/kg/min versus 3.07 mg/kg/min,
respectively; p < 0.05). Toxic effects of hydrazine sulfate were minimal. Our results
suggest that hydrazine sulfate can influence the abnormal carbohydrate metabolism
associated with weight loss in patients with cancer.
Weight loss is a significant complication of cancer which adversely influences patient
outcome (7, 8). One of the earliest of the variety of hormonal (3, 26, 27) and metabolic
abnormalities described in cancer patients with weight loss was glucose intolerance, first
identified over 60 years ago (4, 18, 22, 25, 32). In addition, increased total glucose
production (4, 15-17, 21) as well as increased recycling of glucose through lactate (Cori
cycle) or alanine are seen in cancer patients with weight loss (16, 29 - 31). It has been
suggested that inappropriate activation of these gluconeogenic pathways could lead to
futile cycling and net host energy loss (13). If this hypothesis is correct, amelioration
of the abnormal carbohydrate metabolism in the cancer-bearing host could provide a
therapeutic approach to cancer cachexia.
Hydrazine sulfate inhibits the enzyme phosphoenolpyruvate carboxykinase which results in
interruption of gluconeogenesis in animals (11, 24). However, the ability of hydrazine
sulfate to influence glucose metabolism in humans has not been established previously. For
this reason, we conducted a randomized, placebo-controlled, double-blind trial to assess
the ability of hydrazine sulfate to correct the abnormal glucose metabolism associated
with weight loss in patients with cancer.
MATERIALS AND METHODS
Patients with metastatic cancer were eligible for study if they had lost 10% or more of
their usual body weight and had normal liver function and mental status. Patients with a
known history of diabetes mellitus were ineligible. Patients were entered either prior to
receiving systemic therapy or when a new systemic therapy program was initiated for
disease progression. After informed consent was obtained, patients were admitted to the
Clinical Research Center for a 3-day inpatient metabolic evaluation. No metabolic studies
were performed within 4 weeks of prior chemotherapy. Patients were subsequently randomized
in a double-blind fashion to receive either placebo or hydrazine sulfate. Patient
randomization was stratified on the basis of concurrent chemotherapy and conducted using
published random number tables. A hospital pharmacist held the code for the trial, thus
ensuring that the patient, treating physician, and evaluating physician remained blinded
to the treatment allocation. Capsules containing either hydrazine sulfate or placebo were
prepared by Anabolic, Inc. (Irvine, CA). Following 30 days of treatment with hydrazine or
placebo, the inpatient metabolic evaluation was repeated. In addition to the 38 cancer
patients randomized to receive hydrazine sulfate or placebo, an additional 10 age-matched,
cancer-free, control subjects had a similar 3day metabolic evaluation. These 10
cancer-free control patients were not treated with hydrazine.
During the 3 day inpatient evaluation, all patients received the following: (a)
anthropometrics including body weight, triceps skinfold thickness, midarm circumference,
and dietary history on Day 1; (b) p.o. glucose tolerance test on Day 2; and (c)
determination of total glucose production on Day 3. All patients received a
high-carbohydrate diet for 2 days prior to p.o. glucose tolerance testing. Total body
glucose production was determined by infusion of [6-3H]glucose in the fasting
state, using a primed constant infusion for 5 hr (31). Serial plasma supernatants were
sequentially passed through anion and cation exchange columns and evaporated to dryness to
remove labeled by-products of glucose metabolism and to eliminate any Vitiated water
formed by glucose metabolism. Production rate (PA) was calculated from the following:
glucose [cpm/dl X infusion rate (dl/min)]
|PA (mg/min) =
concentration at plateau (cpm/dl)
||Plasma glucose concentration
The data are expressed as glucose production rate in mg/kg/min. Standard
5-hr p.o. glucose tolerance was performed after 40 g/sq m glucose load with both glucose
and insulin response determined. Plasma glucose was measured using a Beckman glucose
analyzer. Insulin, growth hormone, glucagon, and cortisol were measured by established
The treatment program consisted of an escalating schedule of capsules containing either 60
mg of hydrazine sulfate or placebo until the full dosage of 60 mg. 3 times/day, given
before meals, was reached beginning on the eighth day. Patients were contacted weekly to
assess compliance and kept daily compliance diaries.
Statistically significant differences between hydrazine and placebo groups relative to any
pretreatment clinical factors were sought using chi squared contingency table analysis and
Students t test. The statistical differences between data generated at 2 time
periods were determined using the Students t test of the initial minus final values.
The statistical differences between hydrazine and placebo treatment were determined using
the 2 group t test; results are expressed as the mean +/- SEM.]
A total of 38 patients were randomized to receive either placebo or hydrazine sulfate
treatment. No statistically significant differences in the pretreatment patient
characteristics of the 2 treatment groups were seen (Table 1). Patients on the 2 arms were
comparable with respect to sex, performance score, and tumor types. Stratification
resulted in an equivalent number of patients receiving concurrent chemotherapy on both
arms. Non-small cell lung cancer accounted for 38% of placebo and hydrazine patients.
Other tumor types evaluated included adenocarcinomas of the gastrointestinal tract,
oropharyngeal carcinoma, and breast carcinoma. Sites of metastatic disease were also
closely comparable on the 2 arms with lung and liver prominent sites of involvement.
Measurable disease was not an entry criterion. In accordance with eligibility criteria,
all patients had experienced weight loss before entry on study. Weight loss prior to entry
was substantial; patients on the hydrazine arm lost 19% of their preillness weight, while
patients on the placebo arm lost 16% of their preillness weight. Consideration of other
pretreatment variables including prior chemotherapy and radiotherapy experience,
anthropometrics, and serum albumin revealed no significant differences between the
hydrazine- and placebo-treated groups (Table 1).
Characteristics of patients receiving placebo or hydrazine treatment
No differences between treatment arms were statistically significant.
|Tumor types evaluated
||61 +/- 2
||60 +/- 2
wt loss (%)
||16 +/- 2
||19 +/- 4
||16 +/- 3
||13 +/- 2
||24 +/- 2
||3.6 +/- 0.2
||3.5 +/- 0.2
The initial evaluation of p.o. glucose tolerance and glucose production in all 38 cancer
patients entered on study is compared to values observed in the 10 cancer-free,
age-matched controls in Table 2. Both significantly decreased glucose tolerance and
significantly increased glucose production were seen when the cancer patients were
compared to the cancer-free control population.
p.o. and glucose production on initial assessment of cancer patients compared to
||p.o. glucose tolerance
||95 +/- 8a
||142 +/- 13
||2.04 +/- 0.10
||98 +/- 6
||171 +/- 14b
||2.86 +/- 0.10b
significant difference comparing cancer to control patients; p<0.05.
Twenty-four of the 38 cancer patients randomized on study
completed 30 days of hydrazine or placebo treatment and had repeat inpatient metabolic
evaluations: 13 of 19 on hydrazine (68%) and 11 of 19 on placebo (57%). Almost all
remaining patients who were not restudied experienced disease progression during the
30-day treatment period, precluding metabolic reevaluation. Only one patient refused
repeat metabolic study.
|Chart 1. Influence of 30 days of treatment with placebo () or hydrazine sulfate () on p.o. glucose tolerance after 40 g/sq m glucose load in cancer
patients with weight loss. Initial ()
evaluation before treatment and final (----) evaluation after 30 days of treatment for
both glucose and insulin. The improvement in glucose tolerance after hydrazine
sulfate was statistically significant (p < 0.05). Bars, S.E.
The influence of 30 days of placebo treatment on the abnormal p.o. glucose tolerance seen
in cancer patients is illustrated in Chart 1. No change in either glucose or insulin
levels was seen when the initial assessment was compared to the final assessment performed
after 30 days of placebo therapy. In cancer patients randomized to receive hydrazine
sulfate for 30 days, however, a statistically significant improvement in glucose tolerance
was seen (Chart 1). Glucose levels decreased from 178 to 140 mg/dl at 1 hr and from 169 to
128 mg/dl at 2 hr (p < 0.05). No change in insulin levels accompanied the improved
glucose tolerance associated with hydrazine treatment. Growth hormone and cortisol
remained normal in all cases. Thirty days of hydrazine therapy also resulted in reduced
total glucose production. The influence of 30 days of placebo or hydrazine therapy on
total glucose production rates in all 24 cancer patients having repeat metabolic
evaluation is illustrated as a scattergraph in Chart 2. Consideration of the initial minus
final glucose production rate demonstrates a statistically significant (p < 0.05)
reduction in glucose production for patients receiving hydrazine sulfate (initial 2.78 +/-
0.17 versus final 2.46 +/- 0.19 on hydrazine) compared to those receiving placebo
treatment (initial 2.96 +/-0.24 versus final 3.07 +/- 0.34 on placebo).
|Chart 2. Influence of 30 days of treatment with placebo or hydrazine
sulfate on total glucose production rates in cancer patients with weight loss.
Initial evaluation before treatment and final evaluation after 30 days of treatment for
each patient completing repeat metabolic evaluation. The reduction in glucose
production after hydrazine sulfate was statistically significant (p < 0.05)
Twenty-five of the 38 patients entered were receiving concurrent chemotherapeutic regimens
in addition to hydrazine or placebo treatment for the 30-day study period. In all cases,
chemotherapy was given immediately following the initial metabolic evaluation, and repeat
metabolic evaluations were conducted at least 4 weeks after such chemotherapy
administration. The influence of chemotherapy on glucose metabolism is examined in Table
3. where initial and final glucose production rates are given for the 18 patients
receiving concurrent chemotherapy and compared to those seen in the 8 patients not
receiving concurrent chemotherapy. Although final values for 2-hr glucose and glucose
production rates were slightly lower in patients receiving concurrent chemotherapy, these
differences were not statistically significant. Chemotherapy treatment alone could not
account for the improvement in metabolic parameters seen when hydrazine-treated patients
are compared to those receiving one month of placebo treatment for 3 reasons. (a) A
comparable number of patients on both arms received concurrent chemotherapy (12 on the
placebo and 13 on the hydrazine arm). (b) As outlined in Table 3, glucose tolerance and
glucose production rates were not significantly influenced by concurrent chemotherapy
administration. (c) A comparable number of patients on both arms had an objective response
to chemotherapy. Objective response (a >50% decrease in tumor dimensions) in this
cancer patient population with advanced disease and extensive previous therapy was seen in
only one patient on the placebo arm (with breast cancer) and in 2 patients on the
hydrazine arm (one with lymphocytic lymphoma and one with gastric carcinoma). Since
measurable disease parameters and quantitative definition of all disease sites were not
entry criteria, no correlation between relative tumor burden and metabolic abnormalities
can be made. However, since only 3 of these 38 advanced-disease patients demonstrated
objective antitumor response, response to chemotherapy treatment was not a major
determinant of the metabolic changes seen.
of concurrent chemotherapy on glucose tolerance production in cancer patients with weight
no case was chemotherapy administered less than 4 weeks before the final metabolic
evaluation. No differences between the 2 groups were statistically significant.
(mg/dl) (2-hr glucose level)
|No concurrent chemotherapy
||173 +/- 18a
||159 +/- 14
||2.93 +/- 0.25
||2.89 +/- 0.27
||175 +/- 11
||153 +/- 9
||2.84 +/- 0.19
||2.71 +/- 0.21
|a Mean +/- S.E.
Patient tolerance to the p.o. 60-mg, 3 times/day dosage of hydrazine sulfate was
excellent. Hypoglycemia was not seen. Transient dizziness was experienced by 2 patients.
Therapy was discontinued by one patient on the hydrazine and one patient on the placebo
arm, both for the reason of intolerable nausea.
The study protocol, including the 30day period of treatment and the patient entry
criteria, was specifically designed to determine whether hydrazine sulfate could influence
the abnormal glucose metabolism associated with cancer cachexia. The study protocol was
not designed to assess whether any changes in metabolic parameters would be associated
with clinical benefit. However, in the advanced-disease cancer patients receiving
hydrazine treatment in this study, 7 of 9 patients with improved p.o. glucose tolerance
(manifested by decreased 2-hr glucose levels after 30 days of therapy) either improved or
stabilized their weight, while all 4 patients without improvement in p.o. glucose
tolerance lost weight. As expected from a population of patients with solid tumors of
these primary sites, almost all patients (with the exception of the 3 showing objective
responses) demonstrated no measurable change in tumor dimensions during the 1-month period
of observation (Table 4).
Change in disease
parameter over 30-day period of hydrazine treatment grouped by change in glucose tolerance
||Major disease parameter
||Change in parameter over 30 days
|Glucose tolerance not improved, lost weight
| Patient A
| Patient B
||No change in size, alkaline phosphate
| Patient C
| Patient D
||Slight increase in size, (not measurable)
|Glucose tolerance improved, lost weight
| Patient E
||No measurable parameter
| Patient F
||Liver size slightly greater on physical examination
|Glucose tolerance improved, weight stable
| Patient G
| Patient H
| Patient I
||Approximate 25% increase in size
| Patient J
||25% decrease in size on physical examination a
| Patient K
| Patient L
||No change in liver, slight decrease in adenopathy
| Patient M
|a Went on to achieve partial
In the present study, both a decrease in glucose tolerance and an increase in the rate of
total glucose production were seen in cancer patients with weight loss compared to
age-matched, healthy controls. Such abnormalities of glucose metabolism have been reported
previously in patients with cancer cachexia (4, 16, 17, 22, 25). The abnormal carbohydrate
metabolism in our patients was not associated with major changes in the levels of hormones
such as insulin, glucagon, and cortisol usually involved in regulating glucose tolerance
and production. The increase in glucose production seen in cancer patients with weight
loss differs from the situation in normal subjects experiencing weight loss due to
starvation, where a decrease in total glucose production has been reported (17).
Hydrazine sulfate has a demonstrated capacity to inhibit gluconeogenesis in animal systems
(11, 24). The use of hydrazine sulfate to influence the abnormal glucose metabolism in
cancer cachexia has been proposed as a therapeutic approach to weight loss in the cancer
patient (12). Previous experience with the use of hydrazine sulfate in patients with
cancer has come from 2 types of clinical studies. In uncontrolled trials of hydrazine
sulfate where subjective parameters were assessed, benefit was reported by investigators
both in North America (13) and Russia (12). In uncontrolled trials of hydrazine sulfate,
where reduction in tumor size was used as the major therapeutic endpoint in patients with
far advanced disease, no benefit was seen (19, 23, 28). A major difficulty complicating
interpretation of the previous clinical hydrazine experience has been study designs which
were not controlled and did not evaluate changes in metabolic parameters. As a result,
both the positive (12, 14) and negative (19, 23. 28) clinical trials have not given
incontrovertible results. No prior clinical study has evaluated the influence of hydrazine
sulfate on the abnormal carbohydrate metabolism seen in patients with cancer cachexia.
Therefore, we addressed this specific question using a randomized, placebo-controlled,
In the present trial, hydrazine sulfate treatment resulted in significant improvement in
the abnormal glucose metabolism seen in patients with weight loss and cancer. One month of
placebo treatment had no influence on the decreased glucose tolerance seen in cancer
patients in this trial. Total glucose production rates also remained elevated after 1
month of placebo treatment. Patients receiving 1 month of hydrazine treatment had a
significant improvement in glucose tolerance and a significant decrease in total glucose
production rates compared to those receiving 1 month of placebo. The improvement in
glucose tolerance following hydrazine therapy occurred without major change in insulin
levels, suggesting that hydrazine results in an increase in insulin sensitivity in cancer
patients. Improved glucose tolerance may occur either as a result of an increase in the
rate of exogenous glucose disposition or as a result of an impairment of new glucose
formation. Further study, assessing incorporation of gluconeogenic substrates such as
alanine or lactate into glucose, will be required to directly assess the mechanism
mediating the hydrazine effect. However, the observation of a significant decrease in
total glucose production following hydrazine therapy in the current trial indicates at
least some influence on new glucose production.
The important question of whether the improvement in metabolic indices associated with
hydrazine use in the present trial will result in improved clinical outcome for cancer
patients with weight loss remains to be determined. Although the contribution of abnormal
glucose metabolism to the net energy loss reported to occur in cancer cachexia (10) has
not been quantified, the capacity of hydrazine sulfate to influence abnormal glucose
metabolism in patients with weight loss and cancer suggests further study of this agent is
indicated, especially in prospective clinical trials correlating metabolic, nutritional,
and clinical out-come parameters.
For many types of cancer, an extremely poor prognosis is associated with weight toss (7,
8). Anorexia, leading to a decrease in caloric intake, frequently occurs in cancer
patients with weight loss (6,9). As a result, nutritional supportive therapy has been
studied as a means of improving the prognosis of such patients. However, in several
randomized trials, provision of nutritional support using tong-term parenteral nutrition
has had only limited impact on clinical outcome in this population (1, 20). The present
study illustrates the use of a nonchemotherapeutic agent to ameliorate abnormal host
metabolism in patients with weight loss and cancer. Correction of the abnormal metabolism
associated with cancer cachexia using hydrazine sulfate or other agents (2, 27) may
provide an alternative approach to the treatment of the cancer patient with weight loss.
In summary, we conclude: (a) abnormal glucose metabolism is commonly present in patients
with weight loss and cancer; (b) hydrazine sulfate can influence the abnormal glucose
metabolism associated with cancer cachexia; and (c) further studies of hydrazine sulfate
correlating metabolic, nutritional, and clinical parameters are indicated in the cancer
* Supported by Grant RD-163 from the American Cancer Society,
and by the General Clinical Research Center Grant RR-00425, NIH. This study was
published and presented in part in abstract form (5).
** To whom requests for reprints should be addressed, at
Division of Medical Oncology, Harbor-UCLA Medical Center, 1000 W. Carson St., Torrance, CA
90509. Received November 5, 1982; accepted November 8, 1983.
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