An Unusual Case of Hypopituitarism in a 68 Year Old Man With a Normal Appearing Pituitary Gland and a Remote History of Severe Headache Attributed to Possible Apoplexy

Abstract A 66-year-old previously healthy man was admitted to the hospital with severe hypotension and gastroenteritis symptoms, which were attributed to food poisoning. No one else who ate with him got sick. Random morning cortisol was found to be 0.6, which was followed by the Cortrosyn stimulation test. Baseline cortisol was 0.9, which went up to 2.0 mcg/dL in 30 minutes after Cortrosyn stimulation and 2.9 mcg per dl after an hour. He was treated with high dose steroids during his inpatient stay and sent home on physiologic steroid doses. He followed up in the Endocrinology clinic after hospital discharge. A review of old records showed he was prescribed testosterone about ten years prior for symptoms of hypogonadism, but he never took it. Detailed workup revealed hypopituitarism. Serum prolactin, growth hormone, IGF-1, LH, FSH, Testosterone, TSH, and free T4 were all decreased. Brain/pituitary MRI, however, showed no pituitary abnormalities. All pituitary hormones were checked multiple times and were found to be consistently low. He was given hormone replacement therapy with levothyroxine and testosterone in addition to continuing steroids resulting in marked improvement. He gave a remote history of the worst headache of his life about twenty years ago. He stayed awake all night but never went to the hospital for an evaluation. A possible pituitary apoplexy several years ago was suspected in this case. We have not found any such case in the medical literature with hypopituitarism with a completely normal-appearing pituitary gland. This case illustrates the importance of detailed history, physical examination, hormonal testing, and appropriate hormone replacement in patients where an obvious acute cause may not be ascertained.

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Prolactin release, oestrogens and proliferation of prolactin-secreting cells in the anterior pituitary gland of adult male rats

Journal of Endocrinology ◽

10.1677/joe.0.1080399 ◽

1986 ◽

Vol 108 (3) ◽

pp. 399-403 ◽

Cited By ~ 29

Author(s):

R. L. Pérez ◽

G. A. Machiavelli ◽

M. I. Romano ◽

J. A. Burdman

Keyword(s):

Cell Proliferation ◽

Pituitary Gland ◽

Adult Male ◽

Anterior Pituitary ◽

Pituitary Hormones ◽

Anterior Pituitary Gland ◽

Male Rats ◽

Serum Prolactin ◽

Prolactin Release ◽

Experimental Conditions

ABSTRACT Relationships among the release of prolactin, the effect of oestrogens and the proliferation of prolactin-secreting cells were studied under several experimental conditions. Administration of sulpiride or oestradiol released prolactin and stimulated cell proliferation in the anterior pituitary gland of adult male rats. Clomiphene completely abolished the rise in cell proliferation, but did not interfere with the sulpiride-induced release of prolactin. Treatment with oestradiol plus sulpiride significantly increased serum prolactin concentrations and the mitotic index compared with the sum of the stimulation produced by both drugs separately. Bromocriptine abolished the stimulatory effect of oestradiol on the serum prolactin concentration and on cell proliferation. In oestradiol- and/or sulpiride-treated rats, 80% of the cells in mitoses were lactotrophs. The remaining 20% did not stain with antisera against any of the pituitary hormones. The number of prolactin-secreting cells in the anterior pituitary gland significantly increased after the administration of oestradiol or sulpiride. The results demonstrate that treatment with sulpiride and/or oestradiol increases the proliferation and the number of lactotrophs in the anterior pituitary gland of the rat. J. Endocr. (1986) 108, 399–403

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Idiopathic granulomatous hypophysitis presenting with galactorrhea, headache, and nausea in a woman: a case report and review of the literature

Journal of Medical Case Reports ◽

10.1186/s13256-019-2276-4 ◽

2019 ◽

Vol 13 (1) ◽

Author(s):

Guive Sharifi ◽

Mohammad Reza Mohajeri-Tehrani ◽

Behrouz Navabakhsh ◽

Bagher Larijani ◽

Touraj Valeh

Keyword(s):

Pituitary Gland ◽

Inflammatory Disease ◽

Transsphenoidal Surgery ◽

Brain Magnetic Resonance Imaging ◽

Serum Prolactin ◽

Granulomatous Hypophysitis ◽

History Of ◽

Work Up ◽

Visual Complaints

Abstract Background Inflammation of the pituitary gland can occur in a variety of primary or secondary disorders. Idiopathic granulomatous hypophysitis is a rare inflammatory disease of the pituitary gland that can closely mimic a pituitary adenoma clinicoradiologically. Most authorities agree on minimally invasive transsphenoidal surgery as the mainstay in diagnosis and treatment of this disorder. There is still some controversy regarding pure medical management of idiopathic granulomatous hypophysitis in the literature. Case presentation A 47-year-old Iranian woman of Azeri ethnicity with a history of benign breast cysts with a chief complaint of galactorrhea presented to our endocrinology clinic. Her past medical history was negative for any menstrual irregularities, hirsutism, visual complaints, diplopia, polyuria and polydipsia or seizures. She was taking 100 mcg of levothyroxine daily. Her familial history and physical examination were unremarkable. Her initial laboratory work-up revealed hyperprolactinemia (82.4 ng/mL) with otherwise normal pituitary axes. Brain magnetic resonance imaging showed a pituitary macroadenoma for which she was treated with 0.5 mg of cabergoline weekly. Although her serum prolactin level dropped to 1.7 ng/mL and her galactorrhea was resolved, she continued to complain of headaches and nausea. Repeated imaging showed no decrease in size of the macroadenoma. Therefore, she underwent transsphenoidal surgery of the macroadenoma which was reported as chronic granulomatous hypophysitis by expert pathologists. Tuberculosis, sarcoidosis, Wegener’s granulomatosis, Langerhans cell histiocytosis, and syphilis were ruled out by appropriate tests and she was diagnosed as having idiopathic granulomatous hypophysitis. Fortunately, her condition was not complicated by hypopituitarism and she was symptom free 9 months after transsphenoidal surgery. Conclusions Idiopathic granulomatous hypophysitis, a rare inflammatory disease of the pituitary gland, is a diagnosis of exclusion for which both medical and surgical management are reported in the literature. We present a case of idiopathic granulomatous hypophysitis who was symptom free with no complications of hypopituitarism following its transsphenoidal resection after 9 months of follow-up.

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SERUM PROLACTIN IN PATIENTS WITH "FUNCTIONLESS" CHROMOPHOBE ADENOMAS BEFORE AND AFTER THERAPY

Acta Endocrinologica ◽

10.1530/acta.0.0840449 ◽

1977 ◽

Vol 84 (3) ◽

pp. 449-460 ◽

Cited By ~ 12

Author(s):

N. A. Samaan ◽

M. E. Leavens ◽

J. H. Jesse

Keyword(s):

Hormone Replacement ◽

Pituitary Surgery ◽

Pituitary Tumour ◽

Pituitary Hormones ◽

Thyroid Stimulating Hormone ◽

High Serum ◽

Primary Hypothyroidism ◽

Pituitary Function ◽

Serum Prolactin ◽

Before And After

ABSTRACT The immunoreactive serum human prolactin (PRL) level was measured before and after intravenous administration of 500 μg of thyrotrophinreleasing hormone (TRH) in 11 patients with "functionless" chromophobe adenomas before and after surgery and after radiotherapy in 6 of these patients. The results were compared to other pituitary function tests. Two of the patients studied had recurrent disease after previous pituitary surgery and radiotherapy. Five patients had pituitary surgery through the transfrontal route, while 6 had adenoma removal via the transnasal transsphenoidal route. Before surgery, the serum PRL concentration was abnormally high in 4 patients, before and after TRH administration. It was normal in 6 and subnormal in 1 patient who had had previous therapy. Two of the patients studied showed high serum thyroid-stimulating hormone (TSH) levels in the presence of low serum T3 and T4 suggesting primary hypothyroidism with a secondary TSH-producing pituitary tumour. After surgery all patients showed a significant decrease of the serum PRL level. This contrasts with more variable results in the measurements of other pituitary hormones. Post-operative radiotherapy produced no significant additional change in serum PRL levels in 5 of the 6 patients measured 6 months to 4 years after radiotherapy. Five of the 6 patients who had adenoma removed via the transsphenoidal route required no cortisol replacement and 4 remained euthyroid, whereas all 5 patients after transfrontal surgery required both cortisol and thyroid hormone replacement. These results indicate: (1) that measurement of serum PRL levels at basal and after TRH administration in patients with "functionless" chromophobe adenomas before and after treatment may be the best index for evaluating the effect of therapy; (2) that adenoma removal may be followed by preservation of normal pituitary function, but this is more likely to occur if the transsphenoidal approach is used; and (3) that primary thyroid insufficiency may be associated with a pituitary adenoma.

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SUN-281 Pituitary Hyperplasia Secondary to Uncontrolled Primary Hypothyroidism

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.240 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

Author(s):

Jessica Lee Betancourt

Keyword(s):

Pituitary Gland ◽

Early Recognition ◽

Hormone Replacement ◽

Primary Hypothyroidism ◽

Laboratory Evaluation ◽

Complete Regression ◽

Pituitary Macroadenoma ◽

Free T4 ◽

Pituitary Hyperplasia ◽

Patient Reported

Abstract Background: There are several recognized causes of hyperplasia of the pituitary gland. These may present as sellar masses and be misdiagnosed as pituitary adenomas. Pituitary hyperplasia can occur in the presence of long standing primary hypothyroidism due to the loss of negative feedback caused by decreased secretion of thyroxine (T4) and triiodothyronine (T3) by the thyroid gland, leading to excessive thyrotropin releasing hormone (TRH) production by the hypothalamus causing Thyrotroph pituitary hyperplasia Clinical case: 51 y/o female with a past medical history that includes anxiety & depression, obesity, pre-diabetes and uncontrolled hypothyroidism due to Hashimoto’s, presented to the Endocrinology clinic for recent diagnosis of pituitary macroadenoma. Patient reported tiredness, decrease energy, myalgias, weight gain, abnormal menstrual periods and frontal headaches. On physical exam, she had a body mass index of 37.39kg/m2, blood pressure of 130/85mmHg, heart rate of 91 bpm. There was no thyromegaly noted on exam. No abdominal striae was noted. Overall, exam was unremarkable. Her neurological exam was normal and there were no obvious visual field deficits. Initial laboratory tests revealed a thyroid stimulating hormone (TSH) >150 uIU/mL (0.46–4.7 uIU/mL), free T4 0.3 ng/dL (0.7–1.3 ng/dL) and positive TPO antibodies. Other endocrine work up including ACTH, cortisol, prolactin, FSH, LH and IGF-1, were normal. An MRI of the pituitary revealed a heterogeneous enhancing mass replacing the pituitary gland in the sella that measured 16 x 17 x 11 mm. She was evaluated by Neurosurgery, for presumed diagnosis of pituitary macroadenoma. However, prompt recognition of uncontrolled primary hypothyroidism causing pituitary hyperplasia lead to medical management, first. She was started on weight based (1.6mcg/kg/day) levothyroxine at 175 mcg per day. Six weeks after thyroid replacement therapy laboratory evaluation showed improvement in thyroid function test with a TSH of 0.8mIU/mL, free T4 2.8ng/dL and total T3 307ng/dL. A repeat MRI of the pituitary showed decrease in size of the pituitary gland measuring 15 x 4 x 10 mm. Conclusion: This case illustrates the importance of early recognition of uncontrolled primary hypothyroidism during the evaluation of a pituitary mass. Complete regression of this pituitary gland abnormality can be achieved with thyroid hormone replacement avoiding the irreversible consequences of inappropriate pituitary surgery.

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SAT-244 Inflammatory Rathke Cleft Cyst Caused Hypothalamic Panhypopituitarism

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.187 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

Author(s):

Tangiku Mariko ◽

Tatsuo Ishizuka ◽

Kei Fujioka ◽

Saori Inui ◽

Hideki Tani ◽

...

Keyword(s):

Pituitary Gland ◽

High Intensity ◽

Rare Case ◽

Hormone Replacement ◽

Ct Scanning ◽

Serum Cortisol ◽

Pituitary Hormones ◽

Posterior Lobe ◽

Lh Rh ◽

T2 Weighted Images

Abstract Background: Hypothalamic panhypopituitarism was a rare disease which was caused by brain tumors such as Rathke cyst, germinoma, malignant lymphoma and craniopharyngioma, and vascular accidents such as thrombosis and hemorrhage. We have found a rare case of hypothalamic panhypopituitarism occurred by the inflammation of Rathke cyst. Case presentation: A 77-year-old woman was admitted to our hospital because of severe headache, nausea, vomiting and fever. Hyponatremia (Na 131 meq/L) and increased CRP level (0.20 mg/dl) and no finding of gastroenterological examination and abdominal CT scanning were observed. Endocrinological examination revealed low levels of anterior pituitary hormones such as GH, LH, FSH and ACTH and increased PRL levels and low level of serum cortisol. Simultaneous CRH, TRH and LH-RH stimulations tests indicated low responses of TSH, LH, FSH and PRL and hyperesponse of ACTH (from 2.4 to 251 pg/ml). Radiological examination by enhanced MRI revealed high intensity of T2-weighted images and low and partial high intensities of T1-weighted images in swelling of pituitary gland and vanishment of high intensity of posterior lobe in T2-weighted images suggesting that the inflammatory wall of Rathke cyst. We searched previous data of ACTH and cortisol levels which showed normal level of ACTH (55.2 pg/ml) and cortisol 18.8 μ;g/dl) when headache and nausea arouse on 50 days before. Based on above results patient was diagnosed as hypothalamic hypopituitarism due to inflammatory Rathke cyst. Therefore, patient was treated with hormone replacement therapy by 20 mg of hydrocortisone. After these treatment, polyuria, urinary low osmotic pressure and hypernatremia appeared due to partial diabetes insipidus caused by the impairment of posterior lobe in pituitary gland, and diagnosed by the examination of vasopressin test. This patient was also treated by the oral desmopressin acetate hydrate (60 μ;g/day), and has been well-tolerated in the outpatient clinic. Conclusion: These results suggested that inflammatory Rathke cyst with inflammatory changes in hypothlamo-pituitary system raised a rare case of hypothalamic panhypopituitarism.Reference: Nishioka H. et al.: Clin Endocrinology (Oxf) 2006:64:184–188

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Hypophysitis, the Growing Spectrum of a Rare Pituitary Disease

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/clinem/dgab672 ◽

2021 ◽

Author(s):

Fabienne Langlois ◽

Elena V Varlamov ◽

Maria Fleseriu

Keyword(s):

Differential Diagnosis ◽

Pituitary Gland ◽

Hormone Replacement ◽

Mass Effect ◽

High Dose ◽

Drug Induced ◽

Presumptive Diagnosis ◽

Primary Tumors ◽

Pituitary Dysfunction ◽

Pituitary Disease

Abstract Hypophysitis is defined as inflammation of the pituitary gland that is primary or secondary to a local or systemic process. Differential diagnosis is broad (including primary tumors, metastases, and lympho-proliferative diseases) and multifaceted. Patients with hypophysitis typically present with headaches, some degree of anterior and/or posterior pituitary dysfunction, and enlargement of pituitary gland and/or stalk, as determined by imaging. Most hypophysitis causes are autoimmune, but other etiologies include inflammation secondary to cellar tumors or cysts, systemic diseases, and infection or drug-induced causes. Novel pathologies such as IgG4-related hypophysitis, immunotherapy-induced hypophysitis and paraneoplastic pituitary-directed autoimmunity are also included in a growing spectrum of this rare pituitary disease. Typical magnetic resonance imaging reveals stalk thickening and homogenous enlargement of the pituitary gland, however, imaging is not always specific. Diagnosis can be challenging and ultimately, only a pituitary biopsy can confirm hypophysitis type and rule out other etiologies. A presumptive diagnosis can be made often without biopsy. Detailed history and clinical examination are essential, notably for signs of underlying etiology with systemic manifestations. Hormone replacement and in selected cases careful observation is advised with imaging follow-up. High-dose glucocorticoids are initiated mainly to help reduce mass effect. A response may be observed in all auto-immune etiologies, but also in lymphoproliferative diseases, and as such should not be used for differential diagnosis. Surgery may be necessary in some cases to relieve mass effect and allow a definite diagnosis. Immunosuppressive therapy and radiation are sometimes also necessary in resistant cases.

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The emergence of psychosis in a patient with severe hypothyroidism: A case report and literature review

European Psychiatry ◽

10.1016/j.eurpsy.2017.01.1662 ◽

2017 ◽

Vol 41 (S1) ◽

pp. s842-s842

Author(s):

M.L. Turk ◽

J. Rosen

Keyword(s):

Psychiatric Symptoms ◽

Hormone Replacement ◽

Psychotic Symptoms ◽

Free T4 ◽

Thyroid Hormone Replacement ◽

History Of ◽

Speed Up ◽

Competing Interest ◽

Shed Light ◽

Basic Medical

Hypothyroidism is associated with changes in mental state that can range from mild cognitive impairment to depression to florid myxedema coma. A few cases have linked the occurence of psychotic symptoms in the context of severe hypothyroidism, an event referred in the literature as “myxedema madness”. We describe the case of a 48-year-old male with no past psychiatric history and a past medical history of hypertension and hypothyroidism who presented to the psychiatric unit for management of new-onset psychosis, particularly paranoid delusions. On basic medical screening, the patient was found to have severe hypothyroidism manifested by a TSH level of 51.85 and a free T4 level less than 0.4. The patient was treated with both an antipsychotic and thyroid hormone replacement, after which his hypothyroid symptoms and his psychosis improved. Liothyronine was also prescribed to speed up the recovery course, as his delusions were thought to be due to his hypothyroidism. The aim of this poster is to shed light on the possibility of development of psychosis concomitantly with severe hypothyroidism, given the rarity of such events, as well as to illustrate the importance of treating the underlying medical cause rather than only focusing on the treatment of the psychiatric symptoms. The use of Liothyronine proved to be beneficial in this case, as the patient's symptoms drastically improved after its administration. This could potentially illustrate the importance of using Liothyronine particularly in the treatment of delusional disorder in severe hypothyroidism.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Effects of 8-prenylnaringenin on the hypothalamo-pituitary-uterine axis in rats after 3-month treatment

Journal of Endocrinology ◽

10.1677/joe.1.06384 ◽

2006 ◽

Vol 188 (3) ◽

pp. 397-405 ◽

Cited By ~ 29

Author(s):

J Christoffel ◽

G Rimoldi ◽

W Wuttke

Keyword(s):

Pulse Generator ◽

Receptor Gene ◽

Concomitant Administration ◽

Pituitary Hormones ◽

Gnrh Receptor ◽

Serum Prolactin ◽

High Dose ◽

Uterine Weight ◽

Complement Protein ◽

17Β Estradiol

Phytoestrogens are increasingly consumed in artificially high doses as herbal preparations and nutritional supplements. The flavanone 8-prenylnaringenin (8PN) is a potent phytoestrogen, but its benefits and risks after long-term application are poorly identified. Therefore, we tested two doses of 8PN and 17β-estradiol-3-benzoate (E2B) (effective doses: 6.8 and 68.4 mg/kg body weight (BW) of 8PN, and 0.17 and 0.7 mg/kg BW of 17β-estradiol (E2)) and compared their effects on uterine weight, pituitary hormones (LH, FSH and prolactin) and the expression of estrogen-regulated genes and of estrogen receptor (ER)α and ERβ in the hypothalamus, pituitary and uterus. Both doses of E2 and the high dose of 8PN suppressed serum LH and FSH, and stimulated serum prolactin levels, uterine weight, and progesterone receptor, insulin-like growth factor I and complement protein C3 mRNA transcripts. In the preoptic and the mediobasal areas of the hypothalamus, all treatments had negligible effects on ERα and ERβ and gonadotropin-releasing hormone (GnRH) receptor gene expression, while ERβ and GnRH receptor transcripts in the anterior pituitary were reduced under both E2 doses and the high 8PN dose. The mRNA concentrations of the LHα and -β subunits in the pituitary were suppressed by E2 and 8PN. In summary, 8PN had very similar though milder effects than E2 on all tested parameters. Inhibition of climacteric complaints by E2 takes place in the hypothalamus, where it inhibits the overactive GnRH pulse generator. Hence, 8PN may be used to inhibit climacteric symptoms effectively. Human pharmacologic studies will show whether the stimulatory effect on the uterus that was found in the present animal model would require the concomitant administration of progestins to prevent endometrial overstimulation.

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Opioid-induced hypoadrenalism resulting in fasting hypoglycaemia

BMJ Case Reports ◽

10.1136/bcr-2019-230551 ◽

2019 ◽

Vol 12 (12) ◽

pp. e230551 ◽

Cited By ~ 2

Author(s):

Eddy J Tabet ◽

Antonia Jean Clarke ◽

Stephen M Twigg

Keyword(s):

Patient Outcomes ◽

Adrenocorticotropic Hormone ◽

High Dose ◽

Acth Level ◽

Secondary Adrenal Insufficiency ◽

Morning Cortisol ◽

History Of ◽

Synacthen Test ◽

Secondary Hypoadrenalism ◽

Short Synacthen Test

An 18-year-old woman with a history of hollow visceral myopathy presented with a small-bowel obstruction. High-dose opioid analgesia was required subsequently during hospital admission. She suffered two episodes of documented fasting hypoglycaemia, despite adjustment of parenteral carbohydrate administration. Investigations for non-insulin-mediated hypoglycaemia revealed a low morning cortisol of 109 nmol/L and an inappropriately low Adrenocorticotropic hormone (ACTH) level of 2.2 pmol/L. A diagnosis of secondary adrenal insufficiency was confirmed on repeat cortisol and ACTH testing. The 250 µg short Synacthen test cortisol response was normal, suggestive of acute rather than chronic ACTH deficiency. This pattern was consistent after further opioid exposure. Adrenal recovery occurred shortly after opioid cessation. Opioid-induced hypoadrenalism is likely an under-recognised clinical entity with potentially serious adverse patient outcomes. There are reported cases involving commonly prescribed opioids including fentanyl and tramadol. However, we believe this is the first reported clinical case of acute transient opioid-induced secondary hypoadrenalism associated with fasting hypoglycaemia.

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Pancytopenia in a Patient With Severe Hypothyroidism: A Case Report

Journal of the Endocrine Society ◽

10.1210/jendso/bvab048.1934 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. A946-A947

Author(s):

Aysegul Bulut ◽

Khaled AlSibai ◽

Catalina Norman

Keyword(s):

Thyroid Hormone ◽

Reference Range ◽

Hormone Replacement ◽

Macrocytic Anemia ◽

Normocytic Anemia ◽

Free T4 ◽

Left Femur ◽

Thyroid Hormone Replacement ◽

Myxedema Coma ◽

History Of

Abstract Introduction: Hypothyroidism usually affects red blood cell line most commonly seen as normochromic normocytic anemia. We present a unique case of a patient with pancytopenia in the setting of severe hypothyroidism, which improved following IV thyroid hormone replacement. Case: An 85-year-old female with history of type II diabetes mellitus and hypothyroidism who was admitted for open reduction and internal fixation (ORIF) of a displaced left femur fracture following a mechanical fall. Patient has a long-standing history of hypothyroidism on replacement with levothyroxine 75 mcg, which was inadvertently discontinued at the nursing home 2 weeks prior to presentation. CBC on admission was notable for pancytopenia with macrocytic anemia with hemoglobin of 6.2 g/dl (baseline of 11), leukopenia with WBC of 4.2 x103/ul and thrombocytopenia with platelet of 77 X 103 /ul. TSH was 83 uIU/mL (reference range: 0.34 - 5.6) and Free T4 was < 0.11 ng/dl (reference range: 0.93 - 1.7). Patient was on the verge of developing myxedema coma as she presented with hypotension with blood pressure of 103/55 mmHg, hyponatremia 133 mmol/L and mild change in mental status. There was no evidence for hypothermia or bradycardia. Presence of a small thigh hematoma on examination partially explained the acute drop in hemoglobin. Iron panel, folic acid and vitamin B12 levels were found to be within normal range. Patient had no active of infection to suggest sepsis and she did not receive any myelosuppressive medication. Rapid replacement with IV levothyroxine was started before proceeding with surgery to prevent development of myxedema coma. Free T4 normalized at 1.05 ng/dl after receiving a total of 700 mcg of IV levothyroxine on day 5 of hospitalization. ORIF was done with no complications. Pancytopenia resolved upon thyroid replacement therapy and she was discharged on her regular dose of levothyroxine 75 mcg daily. Discussion: Most common hematologic abnormality associated with hypothyroidism is normochromic normocytic anemia. Currently, there are less than 10 reported cases of pancytopenia associated with hypothyroidism. The exact mechanism is unclear but proposed hypothesis is transient bone marrow hypoplasia. The most common clinical presentation, as seen in our patient, is profound hypothyroidism with ultimate outcome of myxedema coma. Most of these patients had resolution of pancytopenia following adequate thyroid hormone replacement. Interestingly, all cases have been reported in female patient population. Further research is needed to understand pathophysiology, risk factors, prognosis and the risk of pancytopenia recurrence in patients with severe hypothyroidism. More importantly, hypothyroidism must certainly be entertained as a differential diagnosis of pancytopenia.

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