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A Case Study of Tuberculosis - Addison’s Disease And Hypoglycaemia

by Claudia Louch(more info)

listed in infections and inflammation, originally published in issue 209 - October 2013


Case Presentation

Who/When     Milaim: 1 Year ago

Age:    Unknown

What: Disseminated Tuberculosis (TB)

Management& Outcome: Antibiotic Therapy: Cured TB But Milaim never regained strength


Problem 1:     Developed dark skin pigmentation

Problem 2:     Past weeks: Symptoms of Hypoglycaemia - 3 hours after meal

Problem 3:     Hypoglycaemic symptoms disappear > drinking orange juice

Problem 4:     Plasma fatty acid levels not elevated when hypoglycaemic  

What happened to Milaim?

Adrenals and other Infected Organs
Adrenals and other Infected Organs

  • Tuberculosis: Contagious bacterial infection via inhaled droplets  containing Mycobacterium tuberculosis.
  • Disseminated disease develops in infected people whose immune systems do not successfully heal the primary infection.
  • Worldwide TB was most common cause of chronic adrenal insufficiency.
  • TB causes granular tumours which infiltrate adrenal glands,  infect tissue, destroying glands.
  • Loss of adrenal cortical function occurs, termed Primary Adrenal Insufficiency known also as Addison’s Disease.


What is Addison’s Disease

  • Described in 1855 by Dr Addison as primary adrenal insufficiency.
  • Original primary cause was TB: termed Primary Adrenal Insufficiency. Now known as Addison’s Disease or tuberculosis of adrenal glands.
  • USA 75% due to idiopathic atrophy of adrenal cortex probably caused by autoimmune processes termed: Autoimmune adrenalitis. Occurs as isolated condition or Polyglandular Syndrome type 1 or 2.
  • Type 1: Rare autosomal recessive condition (AIRE gene) with female predominance in children and adolescents, causing also hypo(para)thyroidism, candidiasis, diabetes I, ovarian failure, malabsorption, pernicious anaemia, hepatitis, alopecia, vitiligo  common in Finnish population and Iranian Jews.
  • Type 2:  ‘Schmidt syndrome’ more common than type 1. Woman aged 20 – 40yrs familial inheritance. Causes also Hashimotos and Graves disease, diabetes mellitus, ovarian failure are all common.
  • Other causes: Metastatic carcinoma, Amyloidosis, adrenal haemorrhage, sarcoidosis, fungal infections, Tumour, congenital adrenal hypoplasia, familial glucocorticoid deficiency, drugs blocking corticosteroid synthesis, inflammatory necrosis.

The adrenal glands

The Adrenal Glands

  • TB granular infiltrates destroys adrenal glands, resulting in Primary Adrenal Insufficiency / Addison’s Disease.
  • Inner medulla, source of catecholamines adrenaline and noradrenaline. Rich innervation by preganglionic sympathetic fibres and extension of the sympathetic nervous system.
  • Adrenal cortex converts cholesterol into glucocorticoids (cortisol), mineral corticoids (aldosterone), and androgens.
  • Loss of adrenal cortical function causes aldosterone and cortisol deficiency.
  • Lack of aldosterone: excess sodium /water excretion from kidneys whilst retaining potassium (hyperkalaemia). Ultimately hypo-tension.
  • Glucocorticoids regulate body glucose levels.


Adrenal Gland (Dis)Function in this Case

The adrenal glands
Adrenal Gland (Dis)function

Glucocorticoid deficiency & Hypoglycaemia

  • Adrenal cortex failed producing adequate amounts of glucocorticoid cortisol.
  • In muscle, cortisol activates protein breakdown, releasing alanine and glutamine into blood – substrates for gluconeogenesis.
  • Alanine taken up by liver for gluconeogenesis. Glutamine used for fuel by small intestine and gluconeogenic substrate for kidneys.
  • Cortisol deficiency therefore inhibits gluconeogenesis  in liver and Kidney, causing severe insulin sensitivity, hypoglycaemia and diminished liver glycogen results.
  • Cortisol deficiency inhibits lipolysis - transfer of fatty acids from adipose cells to the liver. Glycerol also substrate for gluconeogenesis. Hence  plasma fatty acid levels are not elevated during hypoglycaemia.


Addison’s disease & Hypoglycaemia

  • Cortisol deficiency results also in increased pituitary ACTH production and blood β-lipoprotein.
  • Causes melanocyte-stimulating activity and, together with ACTH produces typically skin/mucous membrane hyperpigmentation seen in primary Addison’s disease only (Milaim’s case).


Diagnostic Tests (Plasma):

↓ Cortisol <5µg/dL 

↑ ACTH >50pg/mL  (negative feedback loss)

↑ Eosinophils  - ↑ Serum K - ↑ Urea - ↑ Hct -          

↓ WBC - ↓ Serum Na  - ↓ Fasting blood glucose (<50mg/dL)  -              ↓ Plasma Bicarbonate

Imaging Tests: Calcification in adrenal areas – Renal TB – Pulmonary TB


Summary & Treatment

  • Patients with adrenal insufficiency (cortisol deficiency) develop hypoglycaemia after fasting (ca. 3hrs > meal) because of decreased gluconeogenesis resulting in diminished liver glycogen.
  • In contrast patients with hypoglycaemia due to over-secretion of insulin can have attacks at any time.
  • Cortisol deficiency causes decreased lipolysis (↓ fatty acids).


Addison’s Disease Treatment

  • Oral Hydrocortisone 3 x day (15mg-30mg in total – less at night due to insomnia risk).
  • Oral Fludrocortisone once/day to replace Aldosterone.
  • Treatment delay may be fatal in hypoglycaemic patients!


Hypoglycemia Treatment

  • Diet: Complex CHO & shorten intervals of food intake.
  • Sucrose water - Glucose solution / tablets.
  • Oral dextrose - IV dextrose in severe cases only.
  • Candy other CHO foods
  • Orange or other juice



Conlon JM. Evolution of the insulin molecule. Insights into the structure, activity and phylogenetic relationships. Peptides 2001;22:1183–93.

Cox M, Sterns RH, Singer I. The defense against hyperkalemia – the roles of insulin and aldosterone. New Engl J Med 1978;299:525–32.

Guyton AC, Hall JC. In: Textbook of Medical Physiology, Xth ed. 2000; p. 336–9, [chapter 29].

Irvine WJ, Barnes EW. Adrenocortical insufficiency. Clin Endocrinol Metab 1972; 1: 549–94.

Kong M-F, Jeff coate WJ. Eighty-six cases of Addison’s disease. Clin Endocrinol 1994; 41: 757–61.

Wang W. Regulation of renal potassium transport by dietary potassium intake. Annu Rev Physiol 2004;66:547–69.


  1. Candy B. said..

    Dear Dr. Lousch,
    There is so little information available on how to treat latent tb in patients with Addison's disease and a compromised immune system, as using corticosteroids is out of the question as it causes severe systemic fungal overgrowth with it's immunosuppressive action.
    The two times before I tried steroid treatment I nearly died with so much fungus and bacterial infection in my body becoming overwhelming.
    Can I learn from you, how to go about this? How to treat both diseases naturopathically?
    There are many MANY things I am taking to support myself. I am a 63yo female and unbelievably, have survived all this time in the presence of these two diseases and also with asthma, severe allergies, fibromyalgia/ CFS, many retroviruses, severe systemic fungal overgrowth, hypothyroid, moderately severe scoliosis.
    I think it is a miracle I am still alive; I practice and have learned much in the fields of naturopathic medicine to use it on myself, and have a large team of exceptional integrative/ naturopathic/ M.D. practitioners working to save my life.
    But knowing how to treat latent tb in the presence of Addison's with IgG compromise causing high systemic fungal overgrowth-- there is hardly any information available.
    Can you help me or point me in any direction?
    Thank you very much!

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About Claudia Louch

Claudia Louch BSc Hons MCPP MSc MPharm MNutr PGCert MBasl at the Natural Dermatology Clinic is a Health Scientist with a background in Advanced Dermatology Practice, Pharmacology, Allergology, Clinical Nutrition and Medicinal Plant Science. She specializes in: Skin Disease, Customised Botanical Cosmetics, Skin Cosmeceuticals, Allergies, Clinical Nutrition and Phytomedicine.

As a phytomedical practitioner and pharmacologist Claudia is able to formulate and issue her patients with unique customized plant based medicines for most conditions. Claudia has also her own range of medicinal plant based skin care products, which are completely preservative-free and do not contain chemicals such as paraben, sodium lauryl sulphate or titanium dioxide. Each of her skin care products is customized for her patients after a consultation. Claudia supports a wide range of skin conditions and customises anti-ageing and line prevention cosmeceuticals.

Claudia Louch at the Natural Dermatology Clinic, obtained a BSc Honours degree in Phytomedicine (Plant based Medicine) and is a fully registered member of the College of Practitioners of Phytotherapy. Claudia was offered a studentship/bursary by King's College London at the world renowned Guy's, King's and St Thomas School of Biomedical & Health Sciences, the Department of Pharmacology & Therapeutics, for a Masters Degree in conventional Drug Discovery. During this course she undertook her Masters Project at the Immuno-Pharmacology Department of a major Medicine Research Company in the UK.

Claudia continued her postgraduate research at King's College London at the School of Biomedical & Health Sciences and the Department of Nutrition and Dietetics to study for a second Masters Degree in Human Nutrition. Claudia developed a strong interest in childhood and adult obesity and patients with eating disorders during this time. Claudia continued her professional  development at the University of Leeds whilst completing a course in Clinical Nutrition, approved by the British Dietetic Association. Claudia attended also postgraduate research course at Imperial College London in Gastrointestinal and Allergic Skin Diseases and also attended a postgraduate course in 'Advanced Dermatology Care' at King's College London.

Claudia founded the Natural Dermatology Clinic in 2005 and practises from her own clinic in Harley Street, London. Claudia Louch is a member of the following professional bodies: Nutrition Society UK, College of Practitioners of Phytotherapy, British Association for The Study Of The Liver, Royal Anthropological Institute, Member of the NHS Directory of C&A Practitioners, Recognized PruHealth and Cigna Health Provider. Please contact Claudia via

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