Diagnosis and Treatment > Medication > Testosterone enanthate esters
You are looking at 1 - 4 of 4 items
Search for other papers by Yasufumi Seki in
Google Scholar
PubMed
Search for other papers by Satoshi Morimoto in
Google Scholar
PubMed
Search for other papers by Naohiro Yoshida in
Google Scholar
PubMed
Search for other papers by Kanako Bokuda in
Google Scholar
PubMed
Search for other papers by Nobukazu Sasaki in
Google Scholar
PubMed
Search for other papers by Midori Yatabe in
Google Scholar
PubMed
Search for other papers by Junichi Yatabe in
Google Scholar
PubMed
Search for other papers by Daisuke Watanabe in
Google Scholar
PubMed
Search for other papers by Satoru Morita in
Google Scholar
PubMed
Search for other papers by Keisuke Hata in
Google Scholar
PubMed
Search for other papers by Tomoko Yamamoto in
Google Scholar
PubMed
Search for other papers by Yoji Nagashima in
Google Scholar
PubMed
Search for other papers by Atsuhiro Ichihara in
Google Scholar
PubMed
Summary
Primary aldosteronism (PA) is more common than expected. Aberrant adrenal expression of luteinizing hormone (LH) receptor in patients with PA has been reported; however, its physiological role on the development of PA is still unknown. Herein, we report two unique cases of PA in patients with untreated Klinefelter’s syndrome, characterized as increased serum LH, suggesting a possible contribution of the syndrome to PA development. Case 1 was a 39-year-old man with obesity and hypertension since his 20s. His plasma aldosterone concentration (PAC) and renin activity (PRA) were 220 pg/mL and 0.4 ng/mL/h, respectively. He was diagnosed as having bilateral PA by confirmatory tests and adrenal venous sampling (AVS). Klinefelter’s syndrome was suspected as he showed gynecomastia and small testes, and it was confirmed on the basis of a low serum total testosterone level (57.3 ng/dL), high serum LH level (50.9 mIU/mL), and chromosome analysis. Case 2 was a 28-year-old man who had untreated Klinefelter’s syndrome diagnosed in his childhood and a 2-year history of hypertension and hypokalemia. PAC and PRA were 247 pg/mL and 0.3 ng/mL/h, respectively. He was diagnosed as having a 10 mm-sized aldosterone-producing adenoma (APA) by AVS. In the APA, immunohistochemical analysis showed co-expression of LH receptor and CYP11B2. Our cases of untreated Klinefelter’s syndrome complicated with PA suggest that increased serum LH levels and adipose tissues, caused by primary hypogonadism, could contribute to PA development. The possible complication of PA in hypertensive patients with Klinefelter’s syndrome should be carefully considered.
Learning points:
-
The pathogenesis of primary aldosteronism is still unclear.
-
Expression of luteinizing hormone receptor has been reported in aldosterone-producing adenoma.
-
Serum luteinizing hormone, which is increased in patients with Klinefelter’s syndrome, might contribute to the development of primary aldosteronism.
Search for other papers by Ken Takeshima in
Google Scholar
PubMed
Search for other papers by Hiroyuki Ariyasu in
Google Scholar
PubMed
Search for other papers by Tatsuya Ishibashi in
Google Scholar
PubMed
Search for other papers by Shintaro Kawai in
Google Scholar
PubMed
Search for other papers by Shinsuke Uraki in
Google Scholar
PubMed
Search for other papers by Jinsoo Koh in
Google Scholar
PubMed
Search for other papers by Hidefumi Ito in
Google Scholar
PubMed
Search for other papers by Takashi Akamizu in
Google Scholar
PubMed
Summary
Myotonic dystrophy type 1 (DM1) is an autosomal dominant multisystem disease affecting muscles, the eyes and the endocrine organs. Diabetes mellitus and primary hypogonadism are endocrine manifestations typically seen in patients with DM1. Abnormalities of hypothalamic–pituitary–adrenal (HPA) axis have also been reported in some DM1 patients. We present a case of DM1 with a rare combination of multiple endocrinopathies; diabetes mellitus, a combined form of primary and secondary hypogonadism, and dysfunction of the HPA axis. In the present case, diabetes mellitus was characterized by severe insulin resistance with hyperinsulinemia. Glycemic control improved after modification of insulin sensitizers, such as metformin and pioglitazone. Hypogonadism was treated with testosterone replacement therapy. Notably, body composition analysis revealed increase in muscle mass and decrease in fat mass in our patient. This implies that manifestations of hypogonadism could be hidden by symptoms of myotonic dystrophy. Our patient had no symptoms associated with adrenal deficiency, so adrenal dysfunction was carefully followed up without hydrocortisone replacement therapy. In this report, we highlight the necessity for evaluation and treatment of multiple endocrinopathies in patients with DM1.
Learning points:
-
DM1 patients could be affected by a variety of multiple endocrinopathies.
-
Our patients with DM1 presented rare combinations of multiple endocrinopathies; diabetes mellitus, combined form of primary and secondary hypogonadism and dysfunction of HPA axis.
-
Testosterone treatment of hypogonadism in patients with DM1 could improve body composition.
-
The patients with DM1 should be assessed endocrine functions and treated depending on the degree of each endocrine dysfunction.
Search for other papers by Ana G Ferreira in
Google Scholar
PubMed
Search for other papers by Tiago N Silva in
Google Scholar
PubMed
Search for other papers by Henrique V Luiz in
Google Scholar
PubMed
Search for other papers by Filipa D Campos in
Google Scholar
PubMed
Search for other papers by Maria C Cordeiro in
Google Scholar
PubMed
Search for other papers by Jorge R Portugal in
Google Scholar
PubMed
Sellar plasmacytomas are rare and the differential diagnosis with non-functioning pituitary adenomas might be difficult because of clinical and radiological resemblance. They usually present with neurological signs and intact anterior pituitary function. Some may already have or eventually progress to multiple myeloma. We describe a case associated with extensive anterior pituitary involvement, which is a rare form of presentation. A 68-year-old man was referred to our Endocrinology outpatient clinic due to gynecomastia, reduced libido and sexual impotence. Physical examination, breast ultrasound and mammography confirmed bilateral gynecomastia. Blood tests revealed slight hyperprolactinemia, low testosterone levels, low cortisol levels and central hypothyroidism. Sellar MRI showed a heterogeneous sellar mass (56 × 60 × 61 mm), initially suspected as an invasive macroadenoma. After correcting the pituitary deficits with hydrocortisone and levothyroxine, the patient underwent transsphenoidal surgery. Histological examination revealed a plasmacytoma and multiple myeloma was ruled out. The patient was unsuccessfully treated with radiation therapy (no tumor shrinkage). Myeloma ultimately developed, with several other similar lesions in different locations. The patient was started on chemotherapy, had a bone marrow transplant and is now stable (progression free) on lenalidomide and dexamethasone. The presenting symptoms and panhypopituitarism persisted, requiring chronic replacement treatment with levothyroxine, hydrocortisone and testosterone.
Learning points:
-
Plasmacytomas, although rare, are a possible type of sellar masses, which have a completely different treatment approach, so it is important to make the correct diagnosis.
-
Usually, they present with neurological signs and symptoms and a well-preserved pituitary function, but our case shows that anterior pituitary function can be severely compromised.
-
Making a more extensive evaluation (clinical and biochemical) might provide some clues to this diagnosis.
Search for other papers by Lourdes Balcázar-Hernández in
Google Scholar
PubMed
Search for other papers by Guadalupe Vargas-Ortega in
Google Scholar
PubMed
Search for other papers by Yelitza Valverde-García in
Google Scholar
PubMed
Search for other papers by Victoria Mendoza-Zubieta in
Google Scholar
PubMed
Search for other papers by Baldomero González-Virla in
Google Scholar
PubMed
Summary
The craniopharyngiomas are solid cystic suprasellar tumors that can present extension to adjacent structures, conditioning pituitary and hypothalamic dysfunction. Within hypothalamic neuroendocrine dysfunction, we can find obesity, behavioral changes, disturbed circadian rhythm and sleep irregularities, imbalances in the regulation of body temperature, thirst, heart rate and/or blood pressure and alterations in dietary intake (like anorexia). We present a rare case of anorexia–cachexia syndrome like a manifestation of neuroendocrine dysfunction in a patient with a papillary craniopharyngioma. Anorexia–cachexia syndrome is a complex metabolic process associated with underlying illness and characterized by loss of muscle with or without loss of fat mass and can occur in a number of diseases like cancer neoplasm, non-cancer neoplasm, chronic disease or immunodeficiency states like HIV/AIDS. The role of cytokines and anorexigenic and orexigenic peptides are important in the etiology. The anorexia–cachexia syndrome is a clinical entity rarely described in the literature and it leads to important function limitation, comorbidities and worsening prognosis.
Learning points:
-
Suprasellar lesions can result in pituitary and hypothalamic dysfunction.
-
The hypothalamic neuroendocrine dysfunction is commonly related with obesity, behavioral changes, disturbed circadian rhythm and sleep irregularities, but rarely with anorexia–cachexia.
-
Anorexia–cachexia syndrome is a metabolic process associated with loss of muscle, with or without loss of fat mass, in a patient with neoplasm, chronic disease or immunodeficiency states.
-
Anorexia–cachexia syndrome results in important function limitation, comorbidities that influence negatively on treatment, progressive clinical deterioration and bad prognosis that can lead the patient to death.
-
Anorexia–cachexia syndrome should be suspected in patients with emaciation and hypothalamic lesions.
