-A 57 years-old male, known to be hypertensive

-On presentation he was bound to a wheelchair

-5 months ago, he complained of: epigastric pain, vomiting, GERD symptoms

-After repeated admissions to different hospitals, he was subjected to: laboratory investigations and several upper G.I. endoscopies, he received treatments including N.S.A.I.Ds in one occasion, then repeated P.P.Is and anti H.pylori drugs.

-During the previous course his s.creatinine level reached 2.5 mg/dl

-In the last occasion of admission, he was revealed to have:

-elevated s.calcium level: 16 mg/dl

-Parathyroid hormone level:1057 pg/ml (normal: 15 to 65 pg/mL)

-He was then undergone parathyroid isotopic scan which revealed: mild diffuse symmetrical enlargement, diffuse homogenous tracer uptake, no focal lesions and negative adenoma behavior.

-Then he developed bilateral lower limbs weakness forcing him to be wheelchair bound.

-On presentation and with retrograde history he was revealed to have:

-recurrent renal stones formation for 17 years with multiple interventions

-his abdominal pain and vomiting were associated with severe psychological disturbance pushing him to neglect feeding and hydration, he was severely dehydrated on presentation

-his daughter revealed to be also renal stones passer

-In view of his general condition (bed ridden, dehydration, psychic disturbance), I considered him to be in a well-established medical emergency, especially in acute hypercalcemia which may be fatal, mandating rapid resuscitation, just keeping him alive then regaining his fair general condition.

 -It is to be noted that the patient was about to have further contrast-imaging plans, despite his critical condition, but we postponed this step until stabilizing the patient's condition as his s.creatinine level reached 4 mg/dl by the time we saw him.

-Also, I considered that this case scenario is not that a typical behaviour of, pure primary hyperparathyroidism, and other primary factors should be considered as mentioned above especially after revising history and additional clinical notes.    

Compare this case of primary hypercalcemia with compensation exposed to hazardous investigations with the previous case of secondary hypercalcemia which is strongly due to granulomatous process.