Addison’s disease

Vinothini*

Physician Assistant, General Medicine Department, Kauvery Hospital, Hosur, Tamil Nadu

*Correspondence

Introduction

  • A 40-year-old male patient with complaints of generalized tiredness, fatiguability, weight loss, hyperpigmentation, which affected daily activities and overall health
  • Clinical examination and Laboratory investigations revealed hormonal imbalance and electrolyte disturbances, leading to the final diagnosis
  • This case highlights the importance of early recognition, proper assessment and timely management to prevent complications and improve patient outcomes.

Chief Complaints

The patient presented with the following complaints

  • Paresthesia sensation over the feet for the past 4 months
  • Progressive weakness in both over limbs
  • Weight loss for 2months
  • Hyperpigmentation all over the body
  • Difficulty in walking

Presenting Complaints

The patient was apparently normal before 4 months ago after which they gradually developed decreased appetite

  • Fatiguability
  • Weight loss
  • Dizziness
  • Nausea and vomiting
  • Muscle ache
  • Low blood pressure
  • Salt craving
  • Depression
  • Low blood sugar episodes
  • Constipation

No h/o- fever, URT symptoms

Past medical history: Nil

Past surgical history: Nil

Personal history: Nonsmoker /Nonalcoholic

N/K/C/O: DM/HTN /IHD/ TB /Epilepsy

On Examination

Patient is conscious, oriented, and afebrile

Bp100/60mmhg
Pr120/min
Rr20/min
Temperature98.30
Spo298%on ra
CvsS1s2 (+)
RsB/l ae (+)
P/aSoft ,non tenderness
CnsNFND

Local Examination: Hyperpigmentation noted all over the body

Investigation

InvestigationResult
CBCHB-12.g/dl
CBCTc- 5880/cumm
CBCPlatelet count- 206000/cumm
CRP<5.0mg/dl
Vitamin B12215pg/ml
Vitamin D 125 ,Dihydroxy-17.5 ng /mL
RFTNa-127 /mmoIL
RFTK+ - 7.3/mmolL1 (12/5/26 K+ - 6.2mmoIL; 13/5/26 K+ - 4.3mmoIL)
RFTUrea - 40.6mg/dl
RFTCreatinine -1.1mg/dl
LFTTotal bilirubin -0.7mg /dL
LFTDirect bilirubin -0.3 mg/dL
LFTIndirect bilirubin - 0.4mg/dL
LFTSGOT - 26/UL
LFTSGPT - 24 /UL
LFTALP - 71 /UL
TFTTSH -2.650mlu /l
TFTT3 -10.2 mcg/dl
TFTT4 -1.60ng/dl
Urine routinePus cells - 02 to 04 hpf, ep cells - 02 to 03/hpf

Serum Cortisol Report

ACTH – Adrenocorticotropic Hormone

Case Presentation

  • A 40-year-old male was admitted in the ward above mentioned complaints and underwent relevant clinical and laboratory investigations
  • Based on the clinical findings and investigation results he was diagnosed with Addison’s Disease, which is primarily adrenal insufficiency caused by inadequate production of adrenal hormones
  • After admission strict monitoring of vital signs and intake -output charting was maintained
  • The patient was managed conservatively with appropriate medical treatment. K+ correction was initiated to manage electrolyte imbalance
  • Hormonal replacement therapy was started with Hydrocortisone to replace cortisol deficiency and Fludrocortisone to maintain mineralocorticoid balance
  • Supportive treatment include iv fluids ,anti -emetics ,ulcer productive medications to prevent gastric irritation due to steroid therapy
  • During the hospital stay the patient showed significant symptomatic improvement. His general condition became stable. Vital signs remains normal and symptoms reduced considerably.
  • Since the patient improved clinically, he was discharged with medication advice and follow up OPD basics.

Condition at Discharge

Patient conscious, Oriented, Afebrile

BP110/70mmhg
PR90/min
Temperature98.30F
SpO298%on RA
CVSS1 S2 (+)
R/SB/L AE( +)
P/Asoft, non-tenderness
CNSNFND

Advice on Discharge

MedicationsMorning Afternoon Night Days
Tab.Gabawin 100mg0015days
Tab.Hisone 10mg20mg010mgTo continue
Tab.Fludrocortisone 100mcg100To continue
Tab. Pan D 40mg1005 days (B/F)
K bind sachet 100-
Tab.D Rise 60k---Once a week x8weeks

Patient Education and Dietary Counselling for Addison’s Disease

Patient Education

  • Explained the nature of Addison’s disease as a chronic endocrine disorder caused by insufficient production of adrenal hormones.
  • Emphasized the importance of strict adherence to prescribed corticosteroid replacement therapy.
  • Advised the patient not to discontinue medications abruptly without medical consultation.
  • Educated the patient regarding signs and symptoms of adrenal crisis, including severe weakness, dizziness, nausea, vomiting, abdominal pain, hypotension, and altered consciousness.
  • Instructed the patient to seek immediate medical attention during episodes of severe illness, persistent vomiting, or inability to take oral medications.
  • Advised regular follow-up visits and laboratory monitoring as recommended by the physician.
  • Encouraged the patient to carry a medical identification card or bracelet indicating the diagnosis of Addison’s disease.
  • Discussed the need for dose adjustment during periods of stress, infection, trauma, or surgery as prescribed by the healthcare provider.

Dietary Advice

  • Advised consumption of a well-balanced diet containing adequate carbohydrates, proteins, fats, vitamins, and minerals.
  • Encouraged adequate fluid intake to maintain hydration.
  • Recommended sufficient dietary sodium intake, particularly during hot weather, excessive sweating, or strenuous physical activity, as advised by the physician.
  • Advised inclusion of protein-rich foods such as pulses, legumes, eggs, milk, fish, and lean meat.
  • Recommended calcium- and vitamin D-rich foods to support bone health.
  • Encouraged daily intake of fresh fruits and vegetables.
  • Advised avoidance of prolonged fasting and skipping meals.
  • Recommended limiting excessive intake of processed foods, sugary beverages, and caffeine.

Counselling Provided

  • Medication adherence counselling.
  • Disease awareness and self-management education.
  • Recognition and prevention of adrenal crisis.
  • Importance of regular follow-up and monitoring.
  • Lifestyle modification and dietary counselling.

Discussion

  • Addison’s disease is a chronic condition in which your adrenal glands don’t produce enough of the hormones cortisol and aldosterone.
  • Your adrenal glands also known as suprarenal glands ,are small triangle -shaped glands that are located on top of each of your two kidneysthey are part of your endocrine system
  • Cortisol is a hormone that helps your body responds to stress , including the stress of illness ,injury or surgery.it also helps maintain your blood pressure ,heart function ,immune system and blood glucose (sugar ) levels. Cortisol is essential for life
  • Aldosterone is a hormone that affects the balance between sodium (salt) and potassium in your blood. This in turn controls the amount of fluid your kidneys remove as urine, which affects blood volume and blood pressure.

These clinical images show the hyperpigmentation seen in our hospital

Addison’s disease is also called primary adrenal insufficiency .a related disorder , secondary adrenal insufficiency , happens when your pituitary glands does not release enough adrenocorticotropic hormone (ACTH) which activates your adrenal glands to produce cortisol .

Symptoms

  • Fatigue
  • Patches of the skin (Hyperpigmentation) especially around scars and skin creases on your gums
  • Abdominal pain
  • Nausea and vomiting
  • Diarrhea
  • Loss of appetite and unintentional weight loss
  • Muscle pain ,muscle spasm, or joint pain
  • Dehydration
  • Low blood pressure
  • Dizziness
  • Depression
  • Hypoglycemia

Pathophysiology

Image Source: Shutterstock

  • This slide explains Adrenal insufficiency, which means the adrenal glands are not producing enough hormones, mainly cortisol and sometimes aldosterone

On the left side we can see the normal hormonal pathway

  • The Hypothalamus in the brain releases CRH, which stimulates the pituitary gland to release ACTH
  • ACTH then stimulates the adrenal glands to produce cortisol and aldosterone these hormones help regulate stress response, blood pressure and electrolyte balance

On the right slide shows three types of adrenal insufficiency

  • Type 1 is primary adrenal insufficiency, also called Addison’s disease. Here the problem is in the adrenal glands themselves, so cortisol and aldosterone levels decreased and ACTH level increase because the pituitary tries to stimulate the damaged adrenal glands.
  • Type II is secondary adrenal insufficiency. In this condition, the pituitary glands fail to produce enough ACTH, so cortisol decreased but Aldosterone usually remains normal.
  • Type III is tertiary adrenal insufficiency here the Hypothalamus does not produce enough CRH, leading to low ACTH and low cortisol levels.
  • Aldosterone is usually normal.
  • In our case the patient has primary adrenal insufficiency where the adrenal glands are unable to produce significant hormones, leading to symptoms like weakness, weight loss, skin Hyperpigmentation and electrolyte imbalance.

Causes

The most common cause of Addison’s disease is an autoimmune response, which occurs when your immune system attacks healthy tissues for an unknown reason. Which Addison’s disease your immune attacks the outer portion of your adrenal glands (The Adrenal Cortex) where they make cortisol and Aldosterone

In the past Tuberculosis was a major cause of Addison’s disease. It remains a prominent case of the condition in developing countries

Other less common causes of Addison’s disease include:

  • Repeat infections , including HIV/ AIDS – related infections and fungal infections
  • Bleeding ( Hemorrhaging )into your adrenal glands

Treatment

  • Hydrocortisone -cortisol replacement
  • Fludrocortisone -Aldosterone replacement
  • Iv fluids
  • Electrolyte correction
  • Supportive care
  • Regular follow up

Conclusion

  • This case highlights the importance of early recognition and timely diagnosis of Addison’s disease, a rare but potentially life-threatening endocrine disorder
  • Through detailed clinical evaluation , laboratory investigations and appropriate management, the patients’ conditions was effectively stabilized
  • Prompt initiation of hormone replacement therapy Plays a crucial role in improving symptoms and prevention complications
  • This case emphasizes the need for careful assessment of nonspecific symptoms such as fatigue, weight loss and hyperpigmentation which can aid early diagnosis and better patient outcomes.

 

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