gitelman 's syndrome ( gs ) is an autosomal recessive tubular disorder characterized by hypokalemic alkalosis , hypomagnesemia , and hypocalciuria . hypopituitarism can have varied etiologies including tumor in hypothalamo - pituitary region or its treatment , inflammatory , genetic , trauma , and hemorrhage , and can result in a host of hormonal and electrolyte abnormalities . both these disorders can cause significant morbidity and a combination of both can be potentially devastating . a few case reports are emerging which show a combination of inherited tubular disorders with pituitary abnormalities on imaging , but with normal hormonal profile . we report the first case of a post - menopausal lady who had a combination of gitelman 's syndrome with multiple pituitary hormone deficiencies ( mphd ) and was treated successfully by replacement of hormones and electrolytes . a 57-year - old lady , a known case of hypothyroidism for 7 years on levothyroxine replacement , presented with complaints of generalized weakness , postural giddiness , and intermittent episodes of spontaneous carpopedal spasms for past 9 months and was bedridden for past 1 month . she used to consume approximately 250 ml of milk products per day and had sunlight exposure for 10 minutes per week . there was no history of diuretic use , protracted vomiting or diarrhea , polydipsia , or polyuria . she was noted to have hypotension on several occasions over the past 9 months for which she was treated with intravenous fluids . she has three children ( last child birth 21 years back ) and there was no history of lactation failure . she attained menopause at the age of 47 years , prior to which her periods were regular . clinically , she was obese ( bmi 34.13 kg / m ) , and had supine hypotension ( bp 70/50 mmhg ) , pallor , bilateral non - pitting edema , acanthosis nigricans , and skin tags . trousseaus and chvosteks 's signs were positive . there was no goiter , deep tendon jerks were normal , and rest of the examination was normal . investigations revealed anemia ( hb 10.3 gm% ) , hyponatremia , hypokalemia , hypomagnesemia , hypocalcemia , hypophosphatemia , hypochloremia , and metabolic alkalosis [ table 1 ] . her serum 25-hydroxy vitamin d3level was 11.89 ng / ml and intact parathyroid hormone ( pth ) was 249 pg / ml ( 10.065.0 ) . urinary spot sodium ( 180 meq / l ) , potassium ( 13 meq / l ) , and chloride ( 161 24-hour urinary calcium [ 127 mg ( normal < 200 mg ) ] , phosphorus [ 412 mg ( normal < 1200 mg ) ] , and copper [ 8.3 g / d ( normal < 60 g / d ) ] excretion were normal . plasma renin activity 4.4 ng / ml / h ( 0.13.1 ) and plasma aldosterone 38.1 ng / dl ( 316 ) levels were high . plasma glucose levels ( ogtt ) , and renal and liver function tests were normal . qualitative test for urinary amino acids , hiv and antinuclear antibody ( ana ) serologies were negative . biochemical parameters pre- and postpresentation ( at 6-month follow - up ) thyroid profile at baseline was suggestive of hypothyroidism [ low t4 , thyroid stimulating hormone ( tsh ) 9.06 u / l ] , whereas it was normal at presentation . there was hypocortisolism ( random plasma cortisol : 164 nmol / l and peak cortisol during insulin - induced hypoglycemia : 453.2 nmol / l ) , relatively normal adrenocorticotropic hormone ( acth ) 11.6 pg / ml ( 7.263.3 ) , and low gonadotropins [ luteinizing hormone ( lh ) 1.36 miu / ml , follicle stimulating hormone ( fsh ) 4.00 miu / ml ] . serum prolactin [ 5.8 ng/ ml ( 525 ) ] and serum insulin - like growth factor 1 ( igf-1 ) [ 156 ng / ml ( 66310 ) ] were low normal . peak growth hormone level after iih was 5.6 ng / ml . anti - thyroid peroxide antibody levels were normal . mri sella showed loss of posterior pituitary bright spot [ figure 1 ] ; however , anterior pituitary was normal . in view of the above , a diagnosis of gitelman 's syndrome with mphd was made . she was treated with levothyroxine , hydrocortisone , and supplementation with vitamin d , sodium , potassium , magnesium , calcium , and chloride . she showed global improvement in symptoms , her carpopedal spasms resolved , blood pressure normalized , and biochemical parameters improved which are enumerated in table 1 . bartter 's and gitelman 's syndrome are two ends of a spectrum of inherited renal tubulopathies that are characterized by renal salt wasting , hypokalemic metabolic alkalosis , hyperreninemic - hyperaldosteronism with normal blood pressure , and hyperplasia of juxtaglomerular apparatus . gitelman 's syndrome ( gs ) , in addition , also exhibits hypomagnesemia and hypocalciuria . bartter 's syndrome is the more severe of two and presents in antenatal period or early childhood , whereas gitelman 's syndrome presents later in life and adult cases have also been described . our patient presented with nonspecific features of generalized weakness that can be explained on the basis of severe dyselectrolytemia and hypopituitarism . postural giddiness can be a manifestation of gitelman 's syndrome per se or that of hypotension that our patient had . loss of fluid and electrolytes leads to activation of renin  angiotensin  aldosterone system ( ras ) resulting in hyperaldosteronism on one hand and renal release of vasodilator prostaglandins ( pge2 and prostacyclins ) on the other . hence , blood pressure remains normal despite hyperaldosteronism as prostaglandin - induced vasodilatation counters the hypertensive effects of overactive ras . association of conn 's syndrome that results in hyporeninemic - hyperaldosteronism has also been recently reported with gs . our patient , however , had hyperreninemic - hyperaldosteronism and normal adrenals on mri , hence such an association is ruled out . hypokalemic metabolic alkalosis occurs due to hyperreninemic - hyperaldosteronism leading to increased potassium and hydrogen ion secretion in the collecting tubules . magnesium wasting in distal convoluted tubules as a result of inhibition of its uptake in the presence of hypokalemia and metabolic alkalosis leads to hypomagnesemia in gitelman 's syndrome , as was seen in our case . hypochloridemia with increased urinary chlorine excretion is also a feature of bartter 's syndrome and an overlap of both the conditions can not be denied in our case . hypocalcemia in our patient is thought to have occurred due to poor oral intake of milk products ; vitamin d deficiency , and possibly reduction in 1-hydroxylase activity . an overlap with bartter 's syndrome is seen in many patients and this could also possibly have worsened hypocalcemia . hypophosphatemia in our patient can be explained by poor oral intake , hypovitaminosis d , and secondary hyperparathyroidism . panhypopituitarism , on the other hand , refers to total or partial loss of pituitary hormone secretion as a result of pituitary or hypothalamic dysfunction resulting in loss of anterior pituitary hormones with or without loss of antidiuretic hormone . our patient had low lh , fsh levels despite having attained menopause ; acth was relatively normal in spite of low cortisol and stimulated cortisol level was suggestive of compensated adrenal insufficiency . her tsh value was mildly elevated despite low total t4 that is seen in subclinical hypothyroidism , but can also occur in secondary hypothyroidism . due to the presence of above combination of hormonal profile and abnormality in pituitary on imaging , a diagnosis of pituitary failure was made . diuretic use and protracted vomiting or diarrhea as a possible cause of hyokalemia was were excluded by history taking . secondary causes for tubulopathy were excluded including fanconi 's syndrome , renal tubular acidosis , systemic lupus erythematosus , wilson 's disease , and hiv . in the light of above , we diagnosed our patient to be suffering from gitelman 's syndrome though she had some overlapping features of bartter 's syndrome as well . both these syndromes are autosomal recessive disorders caused by an inactivating mutation of the thiazide - sensitive sodium - chloride cotransporter in the loop of henle and distal renal tubule , namely slc12a3 and clcnkb genes , encoding the chloride channel . mphd can be due to tumor or its treatment in the hypothalamo - pituitary region , which was ruled out by history and imaging . autoimmune etiology is another important factor ; however , surrogate antibodies ( anti - tpo and ana ) were negative in our patient to rule out autoimmune disrorder . also , there was no history of lactation failure to suggest sheehan 's syndrome as a possible cause . barring these , inherited causes can give rise to mphd which could be a causative factor in our patient . the tubular defect in bartter 's or gitelman 's syndrome can not be corrected and lifelong magnesium and potassium supplementation is required , whereas treatment of mphd is replacement of deficient hormones , as was done in our patient . the combination of nonsteroidal anti - inflammatory drugs ( nsaids ) to reduce renal pg synthesis and a potassium - sparing diuretic to raise the plasma potassium concentration toward normal partially reverses the metabolic alkalosis and corrects the hypomagnesemia . to conclude , gitelman 's syndrome is an often overlooked cause of hypokalemia and hypomagnesemia in adults . hence , a clinician should be alert to such a possibility as the outcome can be rewarding . it remains to be seen , however , whether association of gitelman 's syndrome with pituitary abnormalities with or without mphd is just a chance association or there is a common genetic link .