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Hypogonadotropic hypogonadism often develops in patients with hyperprolactinemia; it may be reversed with treatment of the hyperprolactinemia (See Hyperprolactinemia) Androgen replacement is discussed in the section on male hypogonadism Estrogen replacement is discussed in the section on female hypogonadism Women with hypopituitarism and androgen deficiency may be treated with compounded dehydroepiandrosterone (DHEA) in doses of about 50 mg/d orally DHEA therapy tends to increase pubic and axillary hair and may modestly improve libido, alertness, stamina, and overall psychologic well-being after 6 months of therapy To improve spermatogenesis, human chorionic gonadotropin (hCG) (equivalent to LH) may be given at a dosage of 2000 3000 units intramuscularly three times weekly and testosterone replacement is discontinued The dose of hCG is adjusted to normalize serum testosterone levels After 6 12 months of hCG treatment, if the sperm count remains low, hCG injections are continued along with injections of FSH: follitropin- (synthetic recombinant FSH) or urofollitropins (urine-derived FSH) An alternative for patients with an intact pituitary (eg, Kallmann s syndrome) is the use of leuprolide (GnRH analog) by intermittent subcutaneous infusion With either treatment, testicular volumes double within 5 12 months, and spermatogenesis occurs in most cases With

Selective transsphenoidal resection of pituitary adenomas can often restore normal pituitary function Cabergoline, bromocriptine, or quinagolide may reverse the hypogonadism seen in hyperprolactinomas (See Disorders of Prolactin Secretion) Disseminated Langerhans cell histiocytosis may be treated with bisphosphonates to improve bone pain; treatment with 2-chlorodeoxyadenosine has been reported to produce complete remission

polydipsia; hypernatremia occurs if fluid intake is inadequate Oxytocin deficiency causes lactation failure in postpartum women

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Diabetes insipidus is an uncommon disease characterized by an increase in thirst and the passage of large quantities of urine of low specific gravity (usually < 1006 with ad libitum fluid intake) The urine is otherwise normal It is caused by a deficiency of vasopressin or resistance to vasopressin Primary central diabetes insipidus (without an identifiable lesion noted on MRI of the pituitary and hypothalamus) accounts for about one-third of all cases of diabetes insipidus Many such cases appear to be due to autoimmunity against hypothalamic arginine vasopressin (AVP)-secreting cells; pituitary stalk thickening can often be detected on pituitary MRI scanning The cause may also be genetic Familial diabetes insipidus occurs as a dominant genetic trait with symptoms developing at about 2 years of age Diabetes insipidus also occurs in Wolfram syndrome, a rare autosomal recessive disorder that is also known by the acronym DIDMOAD (diabetes insipidus, type 1 diabetes mellitus, optic atrophy, and deafness) DIDMOAD manifestations usually present in childhood but may not occur until adulthood, along with depression and cognitive problems Secondary central diabetes insipidus is due to damage to the hypothalamus or pituitary stalk by tumor, hypophysitis, anoxic encephalopathy, surgical or accidental trauma, infection (eg, encephalitis, tuberculosis, syphilis), sarcoidosis, or multifocal Langerhans cell (eosinophilic) granulomatosis ( histiocytosis X ) Metastases to the pituitary are more likely to cause diabetes insipidus (33%) than are pituitary adenomas (1%) Vasopressinase-induced diabetes insipidus may be seen in the last trimester of pregnancy and in the puerperium; it is often associated with oligohydramnios, preeclampsia, or hepatic dysfunction A circulating enzyme destroys native vasopressin; however, synthetic desmopressin is unaffected The condition usually responds to desmopressin therapy (see below) and subsides spontaneously Nephrogenic diabetes insipidus is a disorder caused by a defect in the kidney tubules that interferes with water reabsorption The polyuria is unresponsive to vasopressin These patients have normal secretion of vasopressin Congenital nephrogenic diabetes insipidus is present from birth and is due to defective expression of renal vasopressin V2 receptors or vasopressin-sensitive water channels It occurs as a familial X-linked trait; adults often have hyperuricemia as well Acquired forms of vasopressin-resistant diabetes insipidus are usually less severe and are seen in pyelonephritis, renal amyloidosis, myeloma, potassium depletion, Sj gren s syndrome, sickle cell anemia, or chronic hypercalcemia The disorder may occur also as a corticosteroid effect or as an acute side effect of diuretics Certain drugs (eg, demeclocycline, lithium, foscarnet, or methicillin) may induce nephrogenic diabetes insipidus The recovery from acute tubular necrosis may also be associated with transient nephrogenic diabetes insipidus (See Kidney Disorders).

Mycosis fungoides may be confused with psoriasis, a drug eruption, an eczematous dermatitis, Hansen s disease (leprosy), or tinea corporis Histologic examination can distinguish these conditions

The disease is persistent but not life-endangering unless systemic lupus intervenes, which is uncommon Treatment with antimalarials is effective in perhaps 60% of cases Although the only morbidity may be cosmetic, this can be of overwhelming significance in more darkly pigmented patients with widespread disease Scarring alopecia can be prevented or lessened with close attention and aggressive therapy

Callen JP Cutaneous lupus erythematosus: a personal approach to management Australas J Dermatol 2006 Feb;47(1)13 27 [PMID: 16405478]

The treatment of mycosis fungoides is complex Early and aggressive treatment has not been proved to cure or prevent progression of the disease Topical mechlorethamine ointment or solution, topical corticosteroids, UVB and PUVA are all used for early patches and plaques Radiation therapy is effective for local lesions Photopheresis is used at some centers Systemic agents such as retinoids and immunomodulatory agents such as -interferon are used alone or in various combinations for more advanced disease or in patients who fail topical therapy Standard chemotherapeutic agents, except methotrexate, are used only when other approaches fail

CUTANEOUS T CELL LYMPHOMA (MYCOSIS FUNGOIDES)

Mycosis fungoides is usually slowly progressive (over decades) Prognosis is better in patients with patch or

FIGURE 8-1

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