Multiple myeloma concealed by adrenal Cushing syndrome: a case report and review of the literature

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Term Occurence Count Dictionary
adrenal cortical adenoma 2 endocrinologydiseases
hypercalcemia 1 endocrinologydiseases
obesity 2 endocrinologydiseases
osteoporosis 2 endocrinologydiseases
mitotane 2 endocrinologydiseasesdrugs
adrenal adenoma 8 endocrinologydiseases
bortezomib 3 endocrinologydiseasesdrugs
cortisol 29 endocrinologydiseasesdrugs
cyclophosphamide 4 endocrinologydiseasesdrugs
dexamethasone 8 endocrinologydiseasesdrugs
hyperglycemia 1 endocrinologydiseases
melphalan 2 endocrinologydiseasesdrugs

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bortezomib 7661 set as the priority treatment to eliminate the clonal plasma cells. We decided to treat her with a bortezomib , cyclophosphamide, and dexamethasone (VCD) regimen consisting of: bortezomib 2 mg intravenously on
bortezomib 7738 decided to treat her with a bortezomib, cyclophosphamide, and dexamethasone (VCD) regimen consisting of: bortezomib 2 mg intravenously on days 1, 8, 15, and 22; cyclophosphamide 400 mg orally on days 1, 8, 15, and
bortezomib 11690 myeloma, MP melphalan/prednisolone, o,p’-DDD mitotane, VAD vincristine/doxorubicin/dexamethasone, VCD bortezomib /cyclophosphamide/dexamethasone, ASCT autologous stem cell transplantationKinugawa et al. reported a
cortisol 1269 association between adrenocorticotropic hormone-independent Cushing syndrome resulting from a left autonomous cortisol -secreting adrenal adenoma, and multiple myeloma.Electronic supplementary materialThe online version
cortisol 1584 authorized users.BackgroundCushing syndrome (CS) is a serious condition resulting from chronic exposure to cortisol excess, and it is associated with increased risks of cardiovascular, metabolic, and psychiatric complications,
cortisol 1752 cardiovascular, metabolic, and psychiatric complications, and osteoporosis. The causes of endogenous hyper cortisol ism are related to an overproduction of cortisol by the adrenal glands or of adrenocorticotropic hormone
cortisol 1800 complications, and osteoporosis. The causes of endogenous hypercortisolism are related to an overproduction of cortisol by the adrenal glands or of adrenocorticotropic hormone (ACTH) by the pituitary gland and ectopic sources
cortisol 2568 manifestations of the two diseases overlap, which lead to misdiagnoses by clinicians. Moreover, the hyper cortisol emic state could suppress the presentation of the MM.Case presentationA 33-year-old Thai woman presented
cortisol 3504 CS was therefore suspected.The provisional diagnosis of ECS was confirmed by a 24-hour urinary free cortisol (UFC) level of 529.4 μg/day, serum cortisol levels after 1 and 4 mg dexamethasone suppression of
cortisol 3550 diagnosis of ECS was confirmed by a 24-hour urinary free cortisol (UFC) level of 529.4 μg/day, serum cortisol levels after 1 and 4 mg dexamethasone suppression of 26 and 25.7 mcg/dL, respectively, and a loss of
cortisol 4101 adrenal CS, adrenal venous sampling (AVS) was performed to determine the potential side of the excess cortisol production. Using the reference method of William F. Young Jr et al., the AVS revealed a predominantly
cortisol 4269 Jr et al., the AVS revealed a predominantly left-sided ratio of adrenal venous to peripheral plasma cortisol (ratio, 3.21), which was compatible with a left cortisol-producing adrenal adenoma and a right, nonfunctioning
cortisol 4326 ratio of adrenal venous to peripheral plasma cortisol (ratio, 3.21), which was compatible with a left cortisol -producing adrenal adenoma and a right, nonfunctioning adrenal adenoma [[4]]. In addition to the investigations
cortisol 4875 1Tests for confirmation and subtypes of Cushing syndrome in our patientBasal levelResults 24-hour UFC cortisol level (mcg/day/g-Cr)529.36 Basal serum cortisol (mcg/dL)30.2 Basal plasma ACTH level (pg/mL)3.21,
cortisol 4925 syndrome in our patientBasal levelResults 24-hour UFC cortisol level (mcg/day/g-Cr)529.36 Basal serum cortisol (mcg/dL)30.2 Basal plasma ACTH level (pg/mL)3.21, 4.32, 3.43Diurnal variation8:00 a.m.4:00 p.m.12:00 a.m. Serum
cortisol 5059 plasma ACTH level (pg/mL)3.21, 4.32, 3.43Diurnal variation8:00 a.m.4:00 p.m.12:00 a.m. Serum total cortisol (mcg/dL)30.227.126.4Dexamethasone suppression tests 8:00 a.m. serum cortisol level after 1 mg DST
cortisol 5139 variation8:00 a.m.4:00 p.m.12:00 a.m. Serum total cortisol (mcg/dL)30.227.126.4Dexamethasone suppression tests 8:00 a.m. serum cortisol level after 1 mg DST (mcg/dL)26.0 8:00 a.m. serum cortisol level after 4 mg DST (mcg/dL)25.7 8:00 a.m.
cortisol 5202 suppression tests 8:00 a.m. serum cortisol level after 1 mg DST (mcg/dL)26.0 8:00 a.m. serum cortisol level after 4 mg DST (mcg/dL)25.7 8:00 a.m. serum cortisol level after 8 mg DST (mcg/dL)25.6ACTH
cortisol 5265 DST (mcg/dL)26.0 8:00 a.m. serum cortisol level after 4 mg DST (mcg/dL)25.7 8:00 a.m. serum cortisol level after 8 mg DST (mcg/dL)25.6ACTH adrenocorticotropic hormone, DST dexamethasone suppression test,
cortisol 5395 (mcg/dL)25.6ACTH adrenocorticotropic hormone, DST dexamethasone suppression test, UFC urinary free cortisol Fig. 1Computed tomography showing a lipid-poor left adrenal adenoma of size 2.8 cm (arrow)Fig. 2Multiple
cortisol 7357 × 10). d Lambda-negative plasma cells (immunostained for lambda, × 10)Because our patient had hyper cortisol ism, the endogenous corticosteroid might have been suppressing plasma cell proliferation in the MM. She
cortisol 9166 report showed an adrenal cortical adenoma of size 2.0 × 2.4 × 0.6 cm (Fig. 4). Her serum cortisol level returned to 1 mcg/dL after the operation; she received a steroid replacement, which was gradually
cortisol 11106 [[5]]198955-year-old womanMM with Cushing diseaseIgG-lambda- Low dose of o,p’-DDD to control hyper cortisol emia- MP regimen for treatment of MM- After cortisol level was normalized, MM symptoms were exacerbatedKebapclar
cortisol 11158 diseaseIgG-lambda- Low dose of o,p’-DDD to control hypercortisolemia- MP regimen for treatment of MM- After cortisol level was normalized, MM symptoms were exacerbatedKebapclar et al. [[6]]200760-year-old manMM with subclinical
cortisol 11386 syndromeIgA- VAD regimen for MM treatment- Not applicableThis case201833-year-old womanMM with left cortisol -producing adrenal adenomaKappa light chain- VCD regimen with subsequent ASCT for treatment of MM- Left
cortisol 12432 ACTH-dependent and ACTH-independent CS. Pituitary microadenoma was confirmed as the source of the hyper cortisol ism by computed tomography and inferior petrosal sinus sampling. The clinical clues to the myeloma were
cortisol 13088 ultrasound) but without a Cushingoid appearance. Subclinical CS was confirmed by a high 24-hour UFC cortisol level (390 mcg/day), loss of diurnal variation of serum cortisol, and a low ACTH level (< 10 pg/mL).
cortisol 13153 was confirmed by a high 24-hour UFC cortisol level (390 mcg/day), loss of diurnal variation of serum cortisol , and a low ACTH level (< 10 pg/mL). A mild anemia (Hb 10.8 g/dL) and lytic lesions (evident in skull
cortisol 13395 MM.Treatment consideration varied by case. With the first, the patient was treated initially for hyper cortisol emia [[5]]. Although surgical resection of a pituitary adenoma is conventionally the first-line therapy
cortisol 13679 in accordance with her preferences. Successful treatment, demonstrated by a reduction in her plasma cortisol level, led to an exacerbation of the MM, which was then treated with melphalan and prednisolone. By
cortisol 13982 aggressive disease first. We decided to initiate therapy for the MM prior to surgical resection of the cortisol -producing adrenal tumor since our patient had well-controlled blood pressure and a stable CS condition.
cortisol 14720 complications.ConclusionWe have reported the first case of ACTH-independent CS from a left autonomous cortisol -secreting adrenal adenoma in a patient with myeloma.Additional fileAdditional file 1:Timeline. (DOCX
cyclophosphamide 7673 priority treatment to eliminate the clonal plasma cells. We decided to treat her with a bortezomib, cyclophosphamide , and dexamethasone (VCD) regimen consisting of: bortezomib 2 mg intravenously on days 1, 8, 15, and
cyclophosphamide 7795 dexamethasone (VCD) regimen consisting of: bortezomib 2 mg intravenously on days 1, 8, 15, and 22; cyclophosphamide 400 mg orally on days 1, 8, 15, and 22; and dexamethasone 40 mg orally on days 1, 8, 15, and 22. The
cyclophosphamide 8353 collection was made after this cycle. The protocol for stem cell mobilization consisted of 4000 mg of cyclophosphamide in normal saline (250 mL) administered intravenously for 4 hours on day 1, and filgrastim 600 mcg
cyclophosphamide 11701 melphalan/prednisolone, o,p’-DDD mitotane, VAD vincristine/doxorubicin/dexamethasone, VCD bortezomib/ cyclophosphamide /dexamethasone, ASCT autologous stem cell transplantationKinugawa et al. reported a case of Cushing disease
dexamethasone 3584 24-hour urinary free cortisol (UFC) level of 529.4 μg/day, serum cortisol levels after 1 and 4 mg dexamethasone suppression of 26 and 25.7 mcg/dL, respectively, and a loss of physiologic diurnal variation. ACTH-independent
dexamethasone 5346 (mcg/dL)25.7 8:00 a.m. serum cortisol level after 8 mg DST (mcg/dL)25.6ACTH adrenocorticotropic hormone, DST dexamethasone suppression test, UFC urinary free cortisolFig. 1Computed tomography showing a lipid-poor left adrenal
dexamethasone 7695 eliminate the clonal plasma cells. We decided to treat her with a bortezomib, cyclophosphamide, and dexamethasone (VCD) regimen consisting of: bortezomib 2 mg intravenously on days 1, 8, 15, and 22; cyclophosphamide
dexamethasone 7857 intravenously on days 1, 8, 15, and 22; cyclophosphamide 400 mg orally on days 1, 8, 15, and 22; and dexamethasone 40 mg orally on days 1, 8, 15, and 22. The treatment was recycled every 28 days, with a total of six cycles.
dexamethasone 11671 syndrome, MM multiple myeloma, MP melphalan/prednisolone, o,p’-DDD mitotane, VAD vincristine/doxorubicin/ dexamethasone , VCD bortezomib/cyclophosphamide/dexamethasone, ASCT autologous stem cell transplantationKinugawa et
dexamethasone 11718 melphalan/prednisolone, o,p’-DDD mitotane, VAD vincristine/doxorubicin/dexamethasone, VCD bortezomib/cyclophosphamide/ dexamethasone , ASCT autologous stem cell transplantationKinugawa et al. reported a case of Cushing disease (CD) and
dexamethasone 12061 older than the one in our case. The confirmatory laboratory test for CS was positive with a low-dose dexamethasone suppression test, an increase in urinary excretion of 17-hydroxycorticosteroids (17-OHSC), and a loss
dexamethasone 12244 17-hydroxycorticosteroids (17-OHSC), and a loss of diurnal variation of serum cortical steroid. The 8-mg overnight dexamethasone suppression test and ACTH level were evaluated to discriminate between ACTH-dependent and ACTH-independent
melphalan 11598 adrenalectomy- MM in complete response- CS in remissionCS Cushing syndrome, MM multiple myeloma, MP melphalan /prednisolone, o,p’-DDD mitotane, VAD vincristine/doxorubicin/dexamethasone, VCD bortezomib/cyclophosphamide/dexamethasone,
melphalan 13757 reduction in her plasma cortisol level, led to an exacerbation of the MM, which was then treated with melphalan and prednisolone. By comparison, the sequence of our treatment was different as we preferred to manage
mitotane 11633 response- CS in remissionCS Cushing syndrome, MM multiple myeloma, MP melphalan/prednisolone, o,p’-DDD mitotane , VAD vincristine/doxorubicin/dexamethasone, VCD bortezomib/cyclophosphamide/dexamethasone, ASCT autologous
mitotane 13543 of a pituitary adenoma is conventionally the first-line therapy of CD, the patient was treated with mitotane (also known as o,p’-DDD) in accordance with her preferences. Successful treatment, demonstrated by
Select Disease Character Offset Disease Term Instance
adrenal adenoma 1288 adrenocorticotropic hormone-independent Cushing syndrome resulting from a left autonomous cortisol-secreting adrenal adenoma , and multiple myeloma.Electronic supplementary materialThe online version of this article (10.1186/s13256-018-1731-y)
adrenal adenoma 3841 level of 3.21 pg/mL (Table 1), and computed tomography of her upper abdomen showed a lipid-poor left adrenal adenoma (size, 2.8 cm) and a lipid-poor right adrenal adenoma (size, 1.1 cm; Fig. 1). Due to the bilateral
adrenal adenoma 3896 of her upper abdomen showed a lipid-poor left adrenal adenoma (size, 2.8 cm) and a lipid-poor right adrenal adenoma (size, 1.1 cm; Fig. 1). Due to the bilateral adrenal nodules, an atypical finding in adrenal CS, adrenal
adrenal adenoma 4345 venous to peripheral plasma cortisol (ratio, 3.21), which was compatible with a left cortisol-producing adrenal adenoma and a right, nonfunctioning adrenal adenoma [[4]]. In addition to the investigations for CS, plain films
adrenal adenoma 4389 3.21), which was compatible with a left cortisol-producing adrenal adenoma and a right, nonfunctioning adrenal adenoma [[4]]. In addition to the investigations for CS, plain films of the lumbosacral spine were obtained
adrenal adenoma 5455 dexamethasone suppression test, UFC urinary free cortisolFig. 1Computed tomography showing a lipid-poor left adrenal adenoma of size 2.8 cm (arrow)Fig. 2Multiple lytic bone lesions on X-rays. a Skull lateral X-ray (arrow). b
adrenal adenoma 11405 regimen for MM treatment- Not applicableThis case201833-year-old womanMM with left cortisol-producing adrenal adenoma Kappa light chain- VCD regimen with subsequent ASCT for treatment of MM- Left adrenalectomy- MM in complete
adrenal adenoma 14739 complications.ConclusionWe have reported the first case of ACTH-independent CS from a left autonomous cortisol-secreting adrenal adenoma in a patient with myeloma.Additional fileAdditional file 1:Timeline. (DOCX 15 kb
adrenal cortical adenoma 9082 transplant, a left laparoscopic adrenalectomy was successfully undertaken. The pathological report showed an adrenal cortical adenoma of size 2.0 × 2.4 × 0.6 cm (Fig. 4). Her serum cortisol level returned to 1 mcg/dL after
adrenal cortical adenoma 9686 treatments, and outcome was provided in Additional file 1.Fig. 4Histopathological findings from left adrenal cortical adenoma consisting of lipid-rich (clear vacuolated) cells and lipid-depleted (compact eosinophilic) cellsDiscussionGlucocorticoid
hypercalcemia 2146 abnormal plasma cells, which produce monoclonal immunoglobulin. The clinical signs and symptoms include hypercalcemia , renal failure, anemia, bone pain, and pathological fractures. The standard treatment for MM consists
hyperglycemia 8054 with a total of six cycles. While she was receiving this chemotherapy regimen, she did not develop hyperglycemia or dyslipidemia. After six cycles, she finally achieved a very good partial response, according to
obesity 3280 history of occasional use of Chinese herbs and weight loss pills. On examination, a rounded face, truncal obesity , and wide purplish striae on her abdominal wall and right thigh were observed. Her blood pressure was
obesity 11895 reported a case of Cushing disease (CD) and MM [[5]]. The clinical features were a rounded face, central obesity , and hypertension, so CS was suspected. That patient was older than the one in our case. The confirmatory
osteoporosis 1708 is associated with increased risks of cardiovascular, metabolic, and psychiatric complications, and osteoporosis . The causes of endogenous hypercortisolism are related to an overproduction of cortisol by the adrenal
osteoporosis 9861 and lipid-depleted (compact eosinophilic) cellsDiscussionGlucocorticoid excess, the common cause of osteoporosis , can affect the bone function and leads to a high morbidity among patients. Osteoporotic fractures and

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