|LETTER TO THE EDITOR
|Year : 2012 | Volume
| Issue : 3 | Page : 476-477
Panhypopituitarism presenting as azoospermia
K. V. S. Hari Kumar1, Sai Priya2, RP Singh3, Richa Kalia1
1 Department of Endocrinology, Command Hospital, Lucknow, Uttar Pradesh, India
2 Department of Rheumatology , Command Hospital, Lucknow, Uttar Pradesh, India
3 Department of Gastroenterology, Command Hospital, Lucknow, Uttar Pradesh, India
|Date of Web Publication||5-May-2012|
K. V. S. Hari Kumar
Department of Endocrinology, Command Hospital, Lucknow - 226 002, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kumar KH, Priya S, Singh R P, Kalia R. Panhypopituitarism presenting as azoospermia. Indian J Endocr Metab 2012;16:476-7
|How to cite this URL:|
Kumar KH, Priya S, Singh R P, Kalia R. Panhypopituitarism presenting as azoospermia. Indian J Endocr Metab [serial online] 2012 [cited 2020 Nov 26];16:476-7. Available from: https://www.ijem.in/text.asp?2012/16/3/476/95732
Hypopituitarism is the term used to describe partial or complete loss of the hormones of the pituitary gland, leading to a state of systemic malfunction. The condition results from diseases of pituitary, hypothalamus or even the surrounding structures. The common underlying etiologies are neoplastic, infectious, inflammatory, vascular and traumatic lesions of the pituitary gland and its surroundings.  Panhypopituitarism refers to deficiency of all pituitary hormones and presents with growth failure in children and with local and systemic effects in adults.  The local features of a sellar mass lesion are common in adults and the secondary hormone deficiencies are silent because of gradual deficiency. Few conditions like apoplexy and lymphocytic hypophysitis have a dramatic presentation, but other etiologies have an obscure presentation. 
A 33-year-old man was referred to our department for evaluation of azoospermia. Detailed history revealed that the individual was symptomatic for about 8 months, when he developed a short febrile illness with headache and vomiting lasted for about 4-5 days. Fever subsided with antipyretics and he had residual asthenia and polyarthralgia. He was reviewed by rheumatologist and all relevant investigations were normal. He presented to a gastroenterologist the subsequent month, with pain abdomen and dyspepsia which was treated symptomatically with minimal improvement. He noticed gradual lack of libido coupled with erectile dysfunction and a urology review was sought. Semen analysis revealed azoospermia and the patient was referred to our department for further evaluation. The patient gave history of easy fatiguability, lack of sexual desire, weight gain of 3 kg over 8 months and no symptoms to suggest raised intracranial tension. He is a father of two children and denies features of decreased shaving frequency or gynecomastia. There was no similar history in the past or in any of the family members.
Examination revealed normal vital parameters with no evidence of goiter and midline/skeletal deformities. Visual fields by confrontation method and fundus examination were normal. General examination revealed supine blood pressure of 114/76 mm Hg and standing blood pressure of 106/74 mm Hg. There was no evidence of hyperpigmentation, xanthoma, myxedema, testicular atrophy (testicular volume 15 mL) and loss of secondary sexual characteristics. Other systemic examination was normal except for delayed relaxation of deep tendon jerks.
His investigations revealed normocytic normochromic anemia (Hb 11.2 g/dL) with normal hematological and biochemical parameters. Hormonal profile revealed the following: total triiodothyronine 68.9 ng/dL (normal 60-175 ng/dL), total thyroxine 3.7 μg/dL (normal 4-11.5 μg/dL), thyroid stimulating hormone 2.2 mIU/L (normal 0.3-4.5 mIU/L), thyroglobulin antibody 16.4 IU/mL (normal 0-20 IU/mL), thyroid peroxidase antibody 1.4 IU/mL (normal 0-15 IU/mL), insulin-like growth factor (IGF)-1 116 ng/mL (normal 90-340 ng/mL), serum prolactin 14 ng/mL (normal 0-15 ng/mL), luteinizing hormone (LH) 0.6 IU/L (normal 0-7 IU/L), follicle stimulating hormone (FSH) 3.5 IU/L (normal 2-10 IU/L), total testosterone 78 ng/dL (normal 300-1100 ng/dL), 8 a.m. cortisol 6.5 μg/dL (normal 5-25 μg/dL), adrenocorticotropic hormone (ACTH) 5.6 pmol/L (normal 4.5-22 pmol/L). In view of central hypothyroidism and hypogonadism, dynamic testing was done using insulin tolerance test. Peak cortisol after insulin-induced hypoglycemia was 5.4 μg/dL and peak growth hormone (GH) was 0.16 ng/mL. Dynamic and contrast-enhanced magnetic resonance imaging (MRI) study of sella and pituitary gland showed well-defined normal pituitary gland with bright spot. Rest of the brain parenchyma was normal. He was diagnosed to be a case of panhypopituitarism with no structural lesion.
He was treated with levothyroxine (uptitrated to 100 mcg/day), prednisolone (7.5 mg/day), testosterone depot (250 mg once a month), and subcutaneous growth hormone (1 U/day), along with calcium and vitamin D supplements. Evaluation after 3 months revealed significant improvement in the clinical features and the patient was explained about the need for lifelong replacement and stress dosing guidelines.
To the best of our knowledge, such a silent presentation of panhypopituitarism is not available in the published literature. Our patient had multiple visits to the various specialties before eventually he was diagnosed of panhypopituitarism. The onset of the disease in our patient was probably at the initial febrile illness resulting in hypophysitis and permanent damage to the anterior pituitary. Though he had no significant neurological deficit at that time, febrile illness coupled with headache and vomiting suggest raised intracranial tension. Subsequent symptomatology of easy fatiguability, listlessness, polyarthralgia suggest cortisol deficiency which is one of the first pituitary axis to get interrupted after lymphocytic hypophysitis. 
Our case had a unique feature of normal neuroimaging with adult panhypopituitarism. The common causes of adult panhypopituitarism are pituitary adenomas, sellar mass lesions, post radiation, Sheehans syndrome, pituitary apoplexy, granulomatous infiltrative disorders and empty sella syndrome. Most of these etiologies have characteristic imaging findings. Panhypopituitarism due to genetic mutations occasionally has a normal neuroimaging, but the defect appears in childhood and not in adult life.  Our patient probably had a lymphocytic hypophysitis initially, and the pituitary gland imaging after 8 months of illness is normal. This was described earlier in cases of lymphocytic hypophysitis that repeat neuroimaging revealed normal pituitary gland. The pattern of hormonal loss is unique to this condition with loss of ACTH initially followed by thyroid, gonadal and growth hormone axes. 
Panhypopituitarism may present as an acute illness with cortisol/thyroid deficiency or as a chronic disease with progressive hormonal deficiency. The symptoms are mostly nonspecific in the form of decreased exercise capacity, fatigue, pain abdomen, weight gain, loss of axillary/pubic hair, decreased libido, menstrual irregularity. Though our patient had most of these symptoms, the diagnosis was missed for 8 months. Other remarkable feature was that our patient led a practically normal life for 6 months despite the lack of all pituitary hormones.
To conclude, we report silent atypical presentation of panhypopituitarism in a young male as azoospermia. Our case highlights the need of detailed evaluation for hypopituitarism in a case of erectile dysfunction and azoospermia.
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