scholarly journals Suprarenal cortical extract against adrenal insufficiency (Addison's disease)

2021 ◽  
Vol 25 (11) ◽  
pp. 1232-1232
Author(s):  
N. Kramov

Contrary to the generally accepted view that Addison's disease develops as a result of insufficient epinephrine secretion by the adrenal medulla Rogoff and Stewart (A. MA, 1929, 11 / V) see the cause of this disease in the insufficiency of the adrenal cortex. The product interrenalin isolated from this layer, which was used by the authors on dogs with removed adrenal glands and on patients with Addison's disease, gave extremely favorable results. Interrenaline was administered intravenously to dogs, per os in humans. The authors cite 7 case histories where, after the administration of this drug, the symptoms of Addison's disease improved or disappeared: blood pressure increased, bronze color disappeared, gastrointestinal disorders stopped and weakness disappeared, etc.

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A456-A457
Author(s):  
Ethel G Clemente ◽  
Nina Mathew ◽  
Berrin Ergun-Longmire

Abstract Introduction: Majority of children and adolescents diagnosed with Type 1 Diabetes Mellitus (T1D) present with the classic symptoms of polyuria, polydipsia and polyphagia, associated with hyperglycemia. Concurrent conditions at the time of T1D diagnosis may alter its presentation and potentially lead to challenges in diagnosis and management. Clinical Case: We present a 17-year-old male with worsening fatigue and unintentional weight loss for two months, then one week of emesis and abdominal pain. Initial work-up by his primary care provider showed sodium 125 mmol/L (133–145), potassium 5.7 mmol/L (3.5–5.1), HCO3 20 mmol/L (21–31), anion gap 13 mmol/L (9–18), random glucose 141 mg/dL (70–199). Due to hyponatremia and dehydration, he was sent to a local emergency room where he was found to be mildly hypotensive at 87/57 mmHg. He received intravenous fluids for hydration and was sent home. On out-patient follow up, he appeared well despite being hypotensive. His additional labs revealed a random glucose of 330 mg/dl and elevated HbA1C of 8.3% (4.4–5.6). His urine was positive for glucose but negative for ketones. He was admitted for further management of new onset diabetes. On admission, he was well appearing and in no acute distress. Blood pressure was 86/57 mmHg, heart rate was 109 bpm, and other physical exam findings were unremarkable. Although his hyperglycemia improved after initiation of insulin therapy, his electrolyte abnormalities persisted, raising suspicion for adrenal insufficiency. An ACTH stimulation test was performed, with both baseline and 60-minute cortisol levels low at 1 ug/dl and 0.9 ug/dl, respectively, confirming adrenal insufficiency. He responded well to glucocorticoid and mineralocorticoid replacement. His electrolytes and blood pressure normalized. Further testing confirmed elevated levels of Glutamic Acid Decarboxylase antibodies 0.19 nmol/L (less than 0.02), Islet Antigen 2 Antibodies: 3.38 nmol/L (less than 0.02), and 21-Hydroxylase antibodies, consistent with T1D with concomitant Addison’s disease (AD). Conclusion: About 0.5% of patients with T1D have AD, but the diagnosis of T1D typically precedes AD for several years, thus the coexistence of both autoimmune conditions at diagnosis is rare.


2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Ni Wayan Wina Dharmesti ◽  
Made Ratna Saraswati ◽  
Ketut Suastika ◽  
Wira Gotera ◽  
I Made Pande Dwipayana

Primary adrenal insufficiency, also known as Addison’s disease, is a rare but potentially fatal condition resulting from the failure of the adrenal cortex to produce glucocorticoid and/or mineralocorticoid hormones. Unfortunately, the clinical manifestation of primary adrenal insufficiency is not specific and often progresses insidiously, resulting in late diagnosis, or in severe cases, life-threatening circulatory collapse. Adrenal insufficiency should be considered in patients with unexplained vascular collapse. We report the case of a woman who presented to the emergency ward with unexplainable shock that was later diagnosed as adrenal crisis due to Addison’s disease. The presence of hyperpigmentation in patients with rapid progression of adrenal insufficiency suggests the diagnosis of Addison’s disease presenting with adrenal crisis.


2015 ◽  
Vol 55 ◽  
pp. 1-7 ◽  
Author(s):  
Katharina Schultebraucks ◽  
Katja Wingenfeld ◽  
Jana Heimes ◽  
Marcus Quinkler ◽  
Christian Otte

1980 ◽  
Vol 95 (1) ◽  
pp. 71-74 ◽  
Author(s):  
A. Jara-Albarrán ◽  
J. Bayort ◽  
A. Caballero ◽  
R. Eusebio ◽  
P. García-Peris ◽  
...  

Abstract. Somatostatin (250 μg as a bolus iv and 250 μg as a I h infusion) was administered to 6 patients with primary adrenal insufficiency (Addison's disease). The fall in plasma ACTH during the infusion period ranged between 0–30% with a mean reduction of 11.2 ± 11.6%. These findings suggest that with the method employed, somatostatin is not an inhibitor of ACTH secretion in a condition in which glucocorticoids are lacking.


1994 ◽  
Vol 79 (5) ◽  
pp. 1517-1521
Author(s):  
J Furmaniak ◽  
S Kominami ◽  
T Asawa ◽  
N Wedlock ◽  
J Colls ◽  
...  

2006 ◽  
Vol 91 (5) ◽  
pp. 1637-1645 ◽  
Author(s):  
Graziella Coco ◽  
Chiara Dal Pra ◽  
Fabio Presotto ◽  
Maria Paola Albergoni ◽  
Cristina Canova ◽  
...  

Context: Patients with adrenal cortex autoantibodies (ACA) without overt autoimmune Addison’s disease (AAD) are at risk of adrenal failure. Design: To assess the contribution of different clinical, immunological, genetic, and functional factors in the progression to AAD, we followed up 100 ACA-positive and 63 ACA-negative patients without AAD for a maximum of 21 yr (mean 6.0 yr, median 4.8). ACA were measured by immunofluorescence and 21-OH autoantibodies (Abs) by RIA. Adrenal function was assessed by measuring basal levels of cortisol, aldosterone, ACTH, renin activity, and cortisol response to ACTH. The risk of developing AAD was calculated using survival and multivariate analyses. Results: AAD developed in 31 ACA-positive patients and one ACA-negative patient. The cumulative risk of disease in ACA-positive patients was 48.5% [95% confidence interval (CI) 40.8–56.1]. The cumulative risk was higher in children than adults (100 vs. 31.9%; P < 0.0001), males than females (68.6 vs. 42.7%; P = 0.006), patients with subclinical rather than normal adrenal function at entry (87.4 vs. 30.1%; P < 0.0001), patients with hypoparathyroidism and/or candidiasis than patients with other autoimmune or nonautoimmune diseases (100 vs. 29.7%; P < 0.0001), and patients with high rather than low-medium ACA titers (62.8 vs. 41.2%; P = 0.12). The presence of human leukocyte antigen (HLA)-DRB1 did not appear to contribute to the prediction of AAD. Adjusted hazard ratios by Cox model for the development of AAD were 3.37 for males (CI 1.38–8.24), 5.23 for hypoparathyroidism and/or candidiasis (CI 1.53–17.92), 3.33 for high antibody titers (CI 1.43–7.78), and 6.15 for impaired adrenal function at entry (CI 2.79–13.57). Conclusions: These results were used to construct a risk algorithm for estimating the probability of developing AAD from the combination of gender, age, adrenal function, antibody titer, and associated autoimmune disorders at entry. The values of estimated risk could be used to decide appropriate follow-up intervals and future immunointervention strategies.


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