Browsing by Subject "Hypogonadism"
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Item CONGENITAL IDIOPATHIC HYPOGONADOTROPIC HYPOGONADISM: A CASE REPORT(2014-03) Sumko, Dan; Soutt, William; Wong, Long; Weis, StephenAbstract: Congenital idiopathic hypogonadotropic hypogonadism (IHH) is caused by the lack of production or physiological response to gonadotropin releasing hormone (GnRH). A wide variety of genetic mutations have been implicated in the disorder demonstrating autosomal dominant, recessive, and X-linked inheritance patterns. Diagnosis of IHH is complicated by its similarity in presentation to a constitutional delay of puberty and often goes undiagnosed in patients under the age of 18. Once IHH is identified, the effects of the disturbed HPA axis must be addressed. In this report, we offer a brief overview of the diagnosis and management of IHH and present the case of a 27-year old male with undiagnosed IHH. We present the following case: A 27-year old male presented to a family medicine clinic with complaint of a changing skin lesion that was a melanoma in situ. As a result he had a full-skin exam and was found to have a microphallus, undescended testes, and minimal pubic hair distribution. He had a normal sense of smell. Laboratory evaluation showed total testosterone to be 26 ng/dL (250-1100 normal), LH 0.4 mIU/mL (1.5-9.3 normal), and FSH 1.6 mIU/mL (1.6-8.0 normal). Prolactin, PTH, and calcium were within normal limits, as well as his CBC and BMP. MRI of the brain showed no lesions of the hypothalamus or pituitary gland. An abdominal CT confirmed undescended testes. DEXA scan revealed osteopenia. He was diagnosed as IHH. The patient was provided with supplementary vitamin D, calcium, and referrals to endocrinology and urology for orchiopexy. Purpose: (a): Congenital idiopathic hypogonadotropic hypogonadism (IHH) is caused by the lack of production or physiological response to gonadotropin releasing hormone (GnRH). A wide variety of genetic mutations have been implicated in the disorder demonstrating autosomal dominant, recessive, and X-linked inheritance patterns. Diagnosis of IHH is complicated by its similarity in presentation to a constitutional delay of puberty and often goes undiagnosed in patients under the age of 18. Once IHH is identified, the effects of the disturbed HPA axis must be addressed. In this report, we offer a brief overview of the diagnosis and management of IHH and present the case of a 27-year old male with undiagnosed IHH. Methods (b): A 27-year old male presented to a family medicine clinic with complaint of a changing skin lesion that was a melanoma in situ. As a result the patient had a full-skin exam and was found to have a microphallus, undescended testes, and minimal pubic hair distribution. He had a normal sense of smell. Laboratory evaluation showed total testosterone to be 26 ng/dL (250-1100 normal), LH 0.4 mIU/mL (1.5-9.3 normal), and FSH 1.6 mIU/mL (1.6-8.0 normal). Prolactin, PTH, and calcium were within normal limits, as well as his CBC and BMP. MRI of the brain showed no lesions of the hypothalamus or pituitary gland. An abdominal CT confirmed undescended testes. DEXA scan revealed osteopenia. Results (c): The patients was diagnosed as IHH. The patient was provided with supplementary vitamin D, calcium, and referrals to endocrinology and urology for orchiopexy. Conclusions (d): The diagnosis of IHH in this patient was critical for his future health. Osteoporosis, increased risk of testicular cancer secondary to cryptorchidism, and infertility are just a few of the more serious sequelae associated with IHH. When diagnosed early, these comorbidities can be reduced or even eliminated. This case highlights the value of obtaining a detailed history and performing a thorough physical examination as this patient’s risk of cancer, fractures, and infertility could have been dramatically reduced with an earlier diagnosis.Item The role of aging and length of hypogonadism on the neuroprotective effects of dietary genistein following focal cerebral ischemia(2021-05) Oppong-Gyebi, Anthony; Schreihofer, Derek A.; Singh, Meharvan; Sumien, Nathalie; Yang, Shaohua; Shi, XiangrongThe risk of ischemic stroke increases with increasing age. Women beyond menopause have an exponential increase in stroke risk with worse post-stroke prognosis and mortalities compared to men of similar ages. One of the key reasons for this discrepancy is the sudden and drastic drop in the levels of the circulating principal female sex hormones estrogen and progesterone after menopause. Both sex hormones have been shown in several studies to provide neuroprotection against ischemic insults in stroke models and other disease models including Alzheimer's Disease and Parkinson's Disease. However, from clinical studies, neither estrogen nor progesterone alone or in combination has met clinical needs for the prevention of chronic cardiovascular diseases. These clinical failures were mainly evidenced by the absence of benefits in the human population or an increased predisposition to adverse side effects. Reports from studies including the Women's Health Initiative and Nurse's Health Study showed that the timing of initiation and age of recipients significantly influence the outcome of estrogen therapy. In this dissertation project, we investigated the plant-based estrogenic compound genistein as a possible alternative to estrogen therapy. It was hypothesized that the neuroprotective benefits of genistein will be less sensitive to the length of hypogonadism and age under experimental ischemic conditions. We used a rodent model of transient middle cerebral artery occlusion under varied lengths of estrogen deprivation and age to test the neuroprotection of dietary genistein. Findings from this dissertation show that early initiation of dietary genistein after hypogonadism improves aspects of cognition, an effect that is diminished following the long absence of circulating estrogen. Furthermore, pre-treatment with dietary genistein improves age-associated locomotor deficits after long-term hypogonadism after stroke. This dissertation, therefore, provides new considerations on the time-dependent sensitivity of the brain to genistein's effect as a potential therapeutic option to improve aspects of cognition and reduce the severity of stroke in the target population with low circulating estrogens.