Increased Infection Risk in Addison's Disease and Congenital Adrenal Hyperplasia.

CONTEXT: Mortality and infection-related hospital admissions are increased in patients with primary adrenal insufficiency (PAI). However, the risk of primary care-managed infections in patients with PAI is unknown. OBJECTIVE: To estimate infection risk in PAI due to Addison's disease (AD) and congenital adrenal hyperplasia (CAH) in a primary care setting. DESIGN: Retrospective cohort study using UK data collected from 1995 to 2018. MAIN OUTCOME MEASURES: Incidence of lower respiratory tract infections (LRTIs), urinary tract infections (UTIs), gastrointestinal infections (GIIs), and prescription counts of antimicrobials in adult PAI patients compared to unexposed controls. RESULTS: A diagnosis of PAI was established in 1580 AD patients (mean age 51.7 years) and 602 CAH patients (mean age 35.4 years). All AD patients and 42% of CAH patients were prescribed glucocorticoids, most frequently hydrocortisone in AD (82%) and prednisolone in CAH (50%). AD and CAH patients exposed to glucocorticoids, but not CAH patients without glucocorticoid treatment, had a significantly increased risk of LRTIs (adjusted incidence rate ratio AD 2.11 [95% confidence interval (CI) 1.64-2.69], CAH 3.23 [95% CI 1.21-8.61]), UTIs (AD 1.51 [95% CI 1.29-1.77], CAH 2.20 [95% CI 1.43-3.34]), and GIIs (AD 3.80 [95% CI 2.99-4.84], CAH 1.93 [95% CI 1.06-3.52]). This was mirrored by increased prescription of antibiotics (AD 1.73 [95% CI 1.69-1.77], CAH 1.77 [95% CI 1.66-1.89]) and antifungals (AD 1.89 [95% CI 1.74-2.05], CAH 1.91 [95% CI 1.50-2.43]). CONCLUSIONS: There is an increased risk of infections and antimicrobial use in PAI in the primary care setting at least partially linked to glucocorticoid treatment. Future studies will need to address whether more physiological glucocorticoid replacement modes could reduce this risk.

Tuberculous Addison's disease with increased hydrocortisone requirements due to administration of rifampicin.

A 58-year-old man was referred to our hospital for darkened skin, general fatigue and weight loss. His adrenocorticotropic hormone and cortisol levels indicated a primary adrenal insufficiency. 18Fluorodeoxyglucose positron emission tomography/CT showed bilateral enlargement of the adrenal glands, with 18fluorodeoxyglucose accumulation. Loop-mediated isothermal amplification assays of bronchoalveolar lavage fluid were positive for Mycobacterium tuberculosis The patient was diagnosed with tuberculous Addison's disease and treated with antituberculosis agents, including rifampicin. The patient's fatigue worsened gradually after initiation of rifampicin, and the dosage of hydrocortisone was increased. Serum cortisol level monitoring at 2 hours after administration of hydrocortisone was shown to be clinically useful for determining the optimal dose, especially with concurrent use of rifampicin.

An unusual case of hyponatraemia.

The differential diagnosis of hyponatraemia is manifold and includes hormonal disorders such as primary adrenal insufficiency or hypothyroidism. The diagnosis of adrenal insufficiency is always suggestive in cases of hypotension associated with hyponatraemia, hyperkalaemia and metabolic acidosis. We herein report a case of severe hyponatraemia in a patient with Addison's disease. The underlying cause was disseminated adrenal tuberculosis without any evidence of other organ involvement. To date, tuberculosis remains a frequent cause of adrenal insufficiency although the pathophysiology of adrenal tropism is poorly understood.

Addison's disease due to adrenal tuberculosis: contrast-enhanced CT features and clinical duration correlation.

PURPOSE: To describe CT morphology of untreated adrenal tuberculosis during the different stages of the natural history of the disease and to evaluate the diagnostic implications of CT features. MATERIALS AND METHODS: We retrospectively evaluated CT features in 42 patients with documented adrenal tuberculosis for the location, size, morphology, and enhancement patterns shown on CT images. The clinical duration were correlated with the CT features. RESULTS: Of the 42 patients with untreated adrenal tuberculosis, bilaterally enlarged adrenal glands were revealed in 38 cases (91%), unilaterally enlarged in 3 cases (7%), and normal size in 1 case (2%). Of the 41 cases (98%) with enlargement, mass-like enlargement was seen in 20 cases (49%) and enlargement with preserved contours in 21 cases (51%). Peripheral rim enhancement presented in 22 cases (52%) on contrast-enhanced CT. Non-enhanced CT scan revealed calcification in 21 cases (50%). As the duration of Addison's disease increased, the presence of calcification and contour preservation increased concomitantly (p<0.001), whereas peripheral rim enhancement and mass-like enlargement decreased concomitantly on CT images (p<0.001). CONCLUSION: CT may be helpful in diagnosing adrenal tuberculosis when clinically suspected, and CT features are correlated to the clinical duration of Addison's disease.

[Adrenal tuberculosis as a cause of primary adrenal insufficiency--case report]. / Gruzlica nadnerczy przyczyna niedoczynnosci kory nadnerczy--opis przypadku.

Adrenal tuberculosis is relatively infrequent cause of primary adrenocortical insufficiency in developed countries. Adrenal involvement is most often the result of hematogenous spread of the pulmonary tuberculosis. Isolated adrenal tuberculosis, especially with enlargement of adrenal glands can cause diagnostic problems and requires differentiation from primary or secondary neoplastic disease. In this paper we present a case of 61-year-old man with several months history of adrenocortical insufficiency without signs of pulmonary tuberculosis. Computed tomography scan revealed asymmetrical mass-like enlargement in adrenal glands. Despite of consecutive investigations, the diagnosis remained uncertain. Because of the possibility of neoplastic process of unknown origin, the patient was qualified for surgical exploration during which both enlarged glands were removed. The diagnosis of tuberculosis was made on microscopic examination.

A blackening lady--case report.

A 40 year old lady presented with the classical clinical features of Addison's disease which on further investigations with an ultrasound abdomen showed a right suprarenal mass. This was subjected to a fine needle aspiration which revealed pus which on culture grew Klebsiella pneumoniae. Patient responded well to steroids and antibiotics. To the best of our knowledge this is the first report of Klebsiella pneumoniae in association with Addison's disease.

[Addison's diseases caused by adrenal tuberculosis--case report]. / Przypadek pierwotnej niewydolnosci kory nadnerczy o etiologii gruzliczej.

A case of adrenal tuberculosis with acute Addison's disease is described. The disease manifested acute as suprarenal crisis. Metastatic and autoimmunological (antisuprarenal antibodies were not found) etiology was excluded. Computed tomography demonstrated calcifications in both, enlarged adrenals. After antituberculosis treatment and corticosteroid therapy we observed significant improvement in our patient's condition.

Histoplasmosis presenting as addisonian crisis in an immunocompetent host.

A 71-year-old man with presumptively treated pulmonary tuberculosis ten years earlier and previous alcoholism presented with adrenal insufficiency. HIV serology was negative. A computerized tomography scan of the abdomen showed enlarged right adrenal. He recovered after emergency treatment with hydrocortisone IV. Right adrenalectomy was performed. Histoplasmosis was diagnosed and the patient was treated with itraconazole, corticosteroid replacement, and discharged with good health.

Addisonian crisis and tuberculous epididymo-orchitis.

OBJECTIVE: To describe a case of acute primary adrenal insufficiency in which tuberculosis was subsequently detected as the etiologic factor when the patient presented with tuberculous epididymo-orchitis. METHODS: A case of acute primary adrenal insufficiency associated with bilaterally enlarged adrenal glands is reported, along with the subsequent finding of a scrotal mass diagnosed as tuberculous epididymo-orchitis. Diagnosis, adrenal function, and results of imaging studies after institution of antituberculous treatment are discussed. RESULTS: A 41-year-old Egyptian man, who had immigrated to the United States 5 years previously, had acute psychosis and addisonian crisis. A substantially increased early morning level of plasma adrenocorticotropic hormone and a low level of serum cortisol confirmed the diagnosis of primary adrenal insufficiency. Both adrenal glands were enlarged but without calcification on computed tomography. A previous bacille Calmette-Guérin vaccination complicated the interpretation of a positive tuberculin skin test result. Both lungs were clear on chest radiography and computed tomography. Seven months later, the patient had a left scrotal mass and underwent radical orchiectomy. Examination of the pathology specimen showed caseous granulomatous inflammation and necrosis, and acid-fast bacilli were identified. Culture was positive for Mycobacterium tuberculosis. CONCLUSION: In a patient from a country where tuberculosis is endemic, tuberculosis should be considered in the differential diagnosis when primary adrenal insufficiency is detected, especially in association with enlarged or calcified adrenal glands. Extra-adrenal tuberculous involvement should be actively sought because it may provide indirect microbiologic or histologic clues. Other than the lungs, special attention should be paid to the genitourinary system.

Isolated Pneumocystis carinii infection of adrenal glands causing Addison's disease in a non-immunocompromised adult.

Pneumocystis carinii is primarily an opportunistic pathogen infecting patients with AIDS and other immunocompromised patients, and ordinarily does not affect immunocompetent persons. We report isolated P. carinii infection of bilateral adrenal glands in a non-immunocompromised adult male, leading to fatal Addisonian crisis. Diagnosis of P. carinii was established on the basis of cytopathology and microbiological tests, using conventional staining techniques and direct immunofluorescence on ultrasound-guided fine needle aspirates and trucut needle biopsy specimen from adrenal glands. P. carinii pneumonia and other fungal infections of the adrenal glands were excluded by appropriate tests. Absence of HIV infection was established by negative ELISA for HIV I and II antibodies and Western blot analysis at the time of presentation and 45 d later. Normal blood total leukocyte and CD4 lymphocyte counts and IgG and IgA levels confirmed the immunocompetent status of the patient. The patient improved with anti-Pneumocystis treatment and corticosteroid replacement, but succumbed to an episode of Addisonian crisis triggered by a diarrheal illness.

A critical examination of adrenal tuberculosis and a 28-year autopsy experience of active tuberculosis.

OBJECTIVE: Tuberculosis is potentially fatal and adrenal gland involvement is uncommonly reported. The aims of the current study were to define the characteristics of tuberculosis in hospitalized patients and to analyse the features of adrenal tuberculosis. DESIGN: Retrospective analysis of autopsies and adrenalectomies. PATIENTS: 13,762 patients (13492 at autopsies and 270 at adrenalectomy). MEASUREMENTS: The presence of active tuberculosis, the predisposing factors, the pathological features and organs of involvement were examined. RESULTS: Active tuberculosis was present in 871 patients (6.5% of all 13492 autopsies). It was first diagnosed in 70% of these patients during autopsy. Cancers and a history of recent major operations were the 2 main concomitant factors in the patients with tuberculosis. Extra-pulmonary tuberculosis was seen in 261 patients (30%). The five most common extra-pulmonary sites of tuberculosis were the liver, spleen, kidney, bone and adrenal gland. Adrenal tuberculosis was seen in 52 of the 871 patients (6%) with active tuberculosis at autopsy and in 3 patients at adrenalectomy. The adrenal gland was the only organ involved by active tuberculosis in 14 of these 55 patients (25%; 35 men, 20 women). Tuberculosis was evident on macroscopic examination of the adrenal glands in 46% of the patients. On histological examination, caseous necrosis and granulomatous inflammation with Langhan's giant cells were seen in 71% and 40% of patients, respectively. Seven patients presented with signs and symptoms of Addison's disease due to bilateral adrenal involvement. Langhan's giant cells were frequently seen in histological sections and bilateral enlargement of the adrenal glands was often noted. Fine needle aspiration cytology was not useful for diagnosing adrenal tuberculosis. CONCLUSION: Unexpected and extra-pulmonary tuberculosis such as adrenal tuberculosis has been a common problem. A high index of suspicion, correct diagnosis and proper treatment are essential for the management of tuberculosis.

Disseminated tuberculosis causing bilateral adrenal enlargement and Addison's disease.

The clinical features and computed tomography imaging of a patient with acute adrenal failure following disseminated tuberculosis is described.

Female genital coccidioidomycosis (FGC), Addison's disease and sigmoid loop abscess due to Coccidioides immites; case report and review of literature on FGC.

We describe a woman with unusual complications of infection with Coccidioides immitis--infection of the genital tract and adrenal insufficiency. The patient also had intestinal coccidioidomycosis (cocci) in conjunction with presumed pulmonary, and asymptomatic central nervous system cocci. To our knowledge, concurrent FGC, intestinal and adrenal cocci have not been reported previously. A MEDLINE review from 1966-1997 revealed only 1 case of adrenal insufficiency due to cocci. FGC is rare; we identified 12 reported cases since 1929. No combination of investigations or clinical features is sensitive enough to predict FGC. Diagnosis is usually made after microscopy of surgical specimens. FGC presents either as tubo-ovarian disease or endometritis. Treatment generally involves surgical excision and antifungal agents. We hypothesize that an initial trial of antifungals may obviate the need for surgery.

Helicobacter pylori infection is markedly increased in patients with autoimmune atrophic thyroiditis.

Infection by viral or bacterial pathogens has been suspected in playing a role in the development of autoimmune thyroid disease. Because Helicobacter pylori might be involved in the development of nongastrointestinal conditions such as rosacea, ischemic heart disease, and diabetes mellitus, we evaluated the prevalence of H. pylori infection in patients with autoimmune thyroid disease. Fifty-nine patients with autoimmune thyroid disease were included: autoimmune atrophic thyroiditis (n=21), Hashimoto's thyroiditis (n=18), and Graves' disease (n=20). Twenty patients with nontoxic multinodular goiter served as controls for nonautoimmune thyroid disease, and 11 patients with Addison's disease served as controls for nonthyroid endocrine autoimmune disease. The levels of anti-H. pylori immunoglobulin G (IgG) were determined, and a radiolabeled urea breath test were performed. The prevalence of H. pylori infection was markedly increased in the patients with autoimmune atrophic thyroiditis (85.7%), compared with the controls with nontoxic multinodular goiter (40%) and Addison's disease (45.4%). Infection by H. pylori resulted in increased levels of gastrin, pepsinogen I, and pepsinogen II in the H. pylori-positive groups, compared with the H. pylori-negative groups. A positive linear regression was found between the levels of microsomal autoantibodies and those of anti-H. pylori IgG in patients with autoimmune atrophic thyroiditis (n=21; r=0.79; p < 0.01). Finally, and although the overall prevalence of H. pylori infection was not increased, the anti-H. pylori IgG levels and the results from the breath test were higher in the patients with Graves' disease and Hashimoto's thyroiditis patients than in the controls. Clearly, the prevalence of H. pylori infection is increased in autoimmune atrophic thyroiditis and results in abnormalities of gastric secretory function. The strong relation between the levels of anti-H. pylori IgG and the levels of microsomal antibodies suggests that H. pylori antigens might be involved in the development of autoimmune atrophic thyroiditis or that autoimmune function in autoimmune atrophic thyroiditis may increase the likelihood of H. pylori infection.