Table 2.

The prevalence of individual routine clinicopathological features of both hypoadrenocorticism and ‘atypical’ hypoadrenocorticism compiling data from the most relevant case series [14, 18, 25, 26, 28, 29, 37, 38, 42, 46, 66]. In most cases of primary hypoadrenocorticism, mineralocorticoid deficiency was presumed because of associated electrolyte abnormalities. In most cases of ‘atypical’ hypoadrenocorticism, electrolyte abnormalities were not present and while glucocorticoid deficiency was confirmed, mineralocorticoid production was not usually evaluated. Secondary hypoadrenocorticism was confirmed in only a small number of these cases but included two cases with hyponatraemia

Abnormality	Hypoadrenocorticism		“Atypical” hypoadrenocorticism
	No. affected (No. evaluated)	%	No. affected (No. evaluated)	%
Haematology
Anaemia	130 (507)	27.0	23 (68)	33.8
Neutrophilia	82 (334)	24.5	16 (68)	23.5
Eosinophilia	81 (441)	18.4	13 (66)	19.7
Relative erythrocytosis	64 (369)	17.3	0 (68)	0
Lymphocytosis	38 (367)	10.4	14 (68)	20.6
Biochemistry
Hyperkalaemia	467 (535)	87.2	0 (78)	0
Increased urea	386 (472)	81.7	11 (67)	16.4
Hyponatraemia	427 (533)	80.1	2 (78)	2.6
Increased creatinine	241 (363)	66.4	4 (18)	22.2
Hyperphosphataemia	273 (468)	58.3	0 (68)	0
Increased ALT	85 (257)	33.1	14 (65)	21.5
Increased AST	83 (260)	31.9	16 (41)	39
Increased ALP	79 (260)	30.4	6 (65)	9.2
Hypercalcaemia	144 (492)	29.3	1 (18)	5.5
Hypoglycaemia	88 (553)	15.9	21 (67)	31.3
Hypocholesterolaemia	42 (322)	13.0	45 (62)	72.5
Hypoalbuminaemia	37 (359)	10.3	49 (66)	74.2
Urinalysis (hypoadrenocorticism only)	Mean	Range	Azotaemia and USG < 1.030	%
Urine specific gravity	1.023	1.004–1.055	112 (193)	58

No. Number; ALT Alanine aminotransferase; ALP Alkaline phosphatase; AST Aspartate aminotransferase; USG Urine specific gravity