Tag: Addison’s disease

Adrenal histoplasmosis: a case series and review of the literature

Abstract:

Adrenal histoplasmosis is an uncommon mycotic disease typically caused by Histoplasma capsulatum. The objective was to determine the clinicopathological findings in adrenal histoplasmosis.

Pathological records were searched from the database at the Department of Pathology, Faculty of Medicine Ramathibodi Hospital, Mahidol University from 1993 to 2008 for cases of adrenal histoplasmosis. The keywords were “histoplasmosis” and “adrenal gland”.

Adrenal histoplasmosis was diagnosed by histopathology and Gomori-Grocott methenamine silver staining. Histoplasma capsulatum was confirmed by tissue culture and/or serology. The authors report seven cases of adrenal histoplasmosis in immunocompetent patients. The mean age at diagnosis was 67 years. All patients presented as chronic fatigue syndrome.

The onset of symptoms ranged from one to three months. Addison’s disease was found in adrenal histoplasmosis in one case (14.3%). The computed tomography revealed adrenal nodules measuring 1.2 to 7.8 cm in diameter.

The histopathology showed granulomatous inflammation with caseous necrosis. Culture of adrenal tissue from two patients revealed Histoplasma capsulatum. Serum Histoplasma antibodies were positive in four cases. A cure was accomplished in 6 out of 7 cases (85.7%). The patients were followed up for 2.5 to 16.5 years.

 

Source: Larbcharoensub N, Boonsakan P, Aroonroch R, Rochanawutanon M, Nitiyanant P, Phongkitkarun S, Poonvutikul S, Watcharananan SP, Ngarmukos C. Adrenal histoplasmosis: a case series and review of the literature. Southeast Asian J Trop Med Public Health. 2011 Jul;42(4):920-5. https://www.ncbi.nlm.nih.gov/pubmed/22299474

 

Chronic fatigue syndrome, exercise, cortisol and lymphadenopathy

Dear Sir,

As in the past [1], the effects of exercise in the treatment of chronic fatigue syndrome (CFS) are conflicting. Indeed, while Powell et al. [2], in 2004, reported that graded exercise was beneficial to CFS patients, Black et al. [3] have lately written that ‘overall mood, muscle pain intensity, and time spent each day with fatigue worsened following increased activity’ [3] in CFS patients, despite the fact that their increase in daily physical activity was rather moderate (28%) [3]. The virtually opposite effects of exercise in different groups of CFS patients [1–3] may reflect their different cortisol levels [1], which, just as occurred some years ago [1], continue to be contradictory. For example, Inder et al. [4], in March 2005, reported that cortisol levels were normal in their patients with CFS, whereas Segal et al. [5], in the same month, reported that their subjects with CFS had hypocortisolism.

Considering that most features of CFS, such as ‘debilitating fatigue, an abrupt onset precipitated by a stressor, feverishness, arthralgias, myalgias, adenopathy, postexertional fatigue, exacerbation of allergic responses, and disturbances in mood and sleep are all characteristic of glucocorticoid insufficiency’ [6], it is not surprising that hypocortisolism has been convincingly shown to be implicated in the pathophysiology of CFS [7]. Therefore, especially the postexertional fatigue caused by glucocorticoid insufficiency [6] strongly suggests that exercise could be of benefit to CFS patients with high [1] or normal cortisol levels [4], whereas it could be harmful to CFS patients with hypocortisolism [1, 5, 6]. Unfortunately, because of the misleading coexistence of quite different diagnostic criteria for CFS [1], it is difficult to predict the patients with CFS who are more likely to have hypocortisolism and which would worsen with exercise. However, it is arguable that the presence or absence of lymphadenopathy [8], which is a sign of hypocortisolism [6, 9] and is one of the 43 clinical features that CFS shares with Addison’s disease [10–12], could reliably discriminate CFS patients who may worsen with exercise from those who may improve with it. Indeed, lymphadenopathy, unlike other symptoms of CFS [11, 12], many of which are non-specific and can also be found in depression and other affective disorders [11, 12], is far from being common in physical diseases and is absent in psychiatric conditions.

You can read the rest of this comment here: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2005.01526.x/full

 

Source: Baschetti R. Chronic fatigue syndrome, exercise, cortisol and lymphadenopathy. J Intern Med. 2005 Sep;258(3):291-2. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2005.01526.x/full (Full article)

 

Cost-effectiveness of cognitive behaviour therapy for patients with chronic fatigue syndrome

Sir,

In their economic evaluations of treatments for chronic fatigue syndrome (CFS), Severens et al. compared the cost-effectiveness of cognitive behaviour therapy (CBT) with those of other interventions, and found that the percentage of CFS patients who improved with CBT performed for 8 months was 31% vs. 9% and 12% for other treatments. Considering that, in one study, 28% of CFS patients treated with low-dose hydrocortisone over just one month virtually recovered,  Severens et al. also should have compared the cost-effectiveness of CBT with that of low-dose hydrocortisone.

Treatment with low-dose hydrocortisone for CFS, besides being intuitively far less costly than CBT, is also better-founded clinically than any psychological therapy, because hydrocortisone corrects the hypocortisolism that characterizes at least some CFS patients. Given that ‘frank hypocortisolism’, rather surprisingly, was one of the exclusion criteria for enrolment in the trial of Cleare et al., the percentage of CFS patients who can be effectively treated with low-dose hydrocortisone in day-to-day health care is likely to be higher than the 28% found in that trial.

You can read the rest of this comment here: http://qjmed.oxfordjournals.org/content/97/6/378.long

Comment on: Cost-effectiveness of cognitive behaviour therapy for patients with chronic fatigue syndrome. [QJM. 2004]

 

Source: Baschetti R. Cost-effectiveness of cognitive behaviour therapy for patients with chronic fatigue syndrome. QJM. 2004 Jun;97(6):378-9. http://qjmed.oxfordjournals.org/content/97/6/378.long (Full article)

 

Chronic fatigue syndrome: an endocrine disease off limits for endocrinologists?

Abstract:

Endocrinologists were not included in the multidisciplinary working groups that prepared two recent reports on chronic fatigue syndrome, despite its unequalled clinical overlap with Addison’s disease, which is a classic endocrine disorder. The failure to include at least one endocrinologist in those panels may explain why in their extensive reports there is not a single word about the 42 clinical features that chronic fatigue syndrome shares with Addison’s disease, including all the signs and symptoms listed in the case definition of this syndrome.

Comment in: Dr Baschetti rides/writes again. [Eur J Clin Invest. 2004]

 

Source: Baschetti R. Chronic fatigue syndrome: an endocrine disease off limits for endocrinologists? Eur J Clin Invest. 2003 Dec;33(12):1029-31. http://www.ncbi.nlm.nih.gov/pubmed/14636284

 

Assessing chronic fatigue

Comment on: The head-up tilt test with haemodynamic instability score in diagnosing chronic fatigue syndrome. [QJM. 2003]

 

Naschitz et al.1 studied patients with chronic fatigue syndrome (CFS) in comparison with some controls ‘exhibiting shared clinical features with CFS’, namely, patients with non-CFS chronic fatigue, fibromyalgia, generalized anxiety disorder, and neurally mediated syncope. Considering that those controls were included in the study on the basis of the clinical overlap of their disorders with CFS, it is surprising that Naschitz et al. failed to include also patients with Addison’s disease, which resembles CFS far more closely than does any other medical condition.2

You can read the rest of this comment here: http://qjmed.oxfordjournals.org/content/96/6/454.long

 

Source: Baschetti R. Assessing chronic fatigue. QJM. 2003 Jun;96(6):454. http://qjmed.oxfordjournals.org/content/96/6/454.long (Full article)

 

Chronic unexplained fatigue

Comment on: Chronic unexplained fatigue. [Postgrad Med J. 2002]

 

I found the editorial on chronic fatigue syndrome by White both surprising and disappointing, because he used the title “Chronic unexplained fatigue” and the subtitle “A riddle wrapped in a mystery inside an enigma”, but his editorial, by ignoring very important facts about chronic fatigue syndrome, actually perpetuates that riddle, rather than helping to solve it.

If a puzzling and poorly manageable condition shares more than 40 features, including all of its diagnostic criteria, with a well known and easily treatable disease, this astounding clinical overlap should not be ignored, because reason not only suggests that the mysterious illness may simply be a form of the well known disease, but also hints that it is worthwhile assessing whether the classic therapy for that treatable disease could be effective for the enigmatic condition as well.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1757928/pdf/v078p00763a.pdf

 

Source: Baschetti R. Chronic unexplained fatigue. Postgrad Med J. 2002 Dec;78(926):763; author reply 763. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1757928/pdf/v078p00763a.pdf

 

Self-reported sensitivity to chemical exposures in five clinical populations and healthy controls

Abstract:

Two hundred and twenty-five subjects, including normal volunteers and patients with previously documented seasonal affective disorder (SAD),chronic fatigue syndrome (CFS), Cushing’s syndrome, Addison’s disease and obsessive-compulsive disorder (OCD), completed a self-rated inventory of reported sensitivity to various chemical exposures.

Patients with CFS, Addison’s disease and SAD self-reported more sensitivity to chemical exposures than normal controls. In addition, women reported more sensitivity than men.

This report suggests that chemical sensitivity may be a relevant area to explore in certain medical and psychiatric populations. A possible relationship between reported chemical sensitivity and hypothalamic-pituitary-adrenal (HPA)-axis functioning is discussed.

 

Source: Nawab SS, Miller CS, Dale JK, Greenberg BD, Friedman TC, Chrousos GP, Straus SE, Rosenthal NE. Self-reported sensitivity to chemical exposures in five clinical populations and healthy controls. Psychiatry Res. 2000 Jul 24;95(1):67-74. http://www.ncbi.nlm.nih.gov/pubmed/10904124

 

Chronic fatigue syndrome: a form of Addison’s disease

Dear Sir, Evengård et al.’s article [1] on chronic fatigue syndrome (CFS) is disappointing, because in their review, despite its 15 pages and 165 references, there is not a single word about the staggering similarity between CFS and Addison’s disease. As someone whose CFS symptoms resolved dramatically with an old remedy for Addison’s disease [2], I understandably found that review even more disappointing.

To compensate for Evengård et al.’s failure to mention both the impressive overlap of CFS with Addison’s disease and its clinical implications, I summarize here these issues.

CFS and Addison’s disease share 36 features [3–6]. Three others, however, are to be added. In fact, reduction in adrenal gland size [7], antibodies against the adrenal gland [8] and respiratory muscle dysfunction [9], besides being present in CFS [7–9], have also been found in Addison’s disease [10–12]. In view of the 39 features that CFS shares with Addison’s disease [3–12] (see Table 1), which constitute a similarity between two distinctly named diseases that is probably unequalled in the medical literature, it seems arguable that CFS should practically be viewed as a form of Addison’s disease [13]. One could object that CFS patients, unlike Addisonian subjects, do not display hyperpigmentation or basal hypocortisolaemia. Neither abnormality, however, is a constant presenting feature of Addison’s disease [14].

You can read the rest of this comment here: http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.2000.00695.x/full

 

Source: Baschetti R. Chronic fatigue syndrome: a form of Addison’s disease. J Intern Med. 2000 Jun;247(6):737-9. http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.2000.00695.x/full (Full article)

 

Cortisol deficiency may account for elevated apoptotic cell population in patients with chronic fatigue syndrome

Comment in: Single aetiological agent may not be feasible in CFS patients. [J Intern Med. 1999]

Comment on: Elevated apoptotic cell population in patients with chronic fatigue syndrome: the pivotal role of protein kinase RNA. [J Intern Med. 1997]

 

Dear Sir, Vojdani et al. [1] report that patients with chronic fatigue syndrome (CFS) display an increased apoptotic cell population. This abnormality, according to the authors, is due to the activation of protein kinase RNA pathway, which, in turn, ‘could result from disregulated immune system or chronic viral infection’[1].The latter explanation, however, seems unlikely, because no specific virus has been identified in CFS patients, despite extensive research [2]. Special attention, therefore, should mainly be paid to the immune system of CFS patients, because its repeatedly reported abnormalities may help reveal both the aetiology of CFS and an effective treatment against it.

As Vojdani et al. [1] point out, decreased natural killer (NK) cell activity and altered cytokine production characterize CFS patients. These immunological abnormalities, however, may simply reflect the hypocortisolism of CFS patients [3], because a mere lack of steroid restraint on the immune system may well account for its derangement [3]. In fact, since NK cell activity is directly associated with the circadian rhythm of cortisol [4], the decreased NK cell activity observed in CFS patients may simply be due to their cortisol deficiency [3]. The latter, additionally, may also explain why the release of the cytokines interleukin-lβ, interleukin-6, and tumour necrosis factor-α has been found to be increased in peripheral blood mononuclear cell cultures from patients with CFS [5]. All those cytokines, in fact, have been reported to rise during hypocortisolism [6]. This suggests, therefore, that the cortisol deficiency of CFS patients may play a central role in causing both their immunological abnormalities and, presumably, their elevated apoptotic cells.

In view of the role of hypocortisolism in CFS, Vojdani and coworkers might be interested in determining whether the enhanced apoptosis found in their subjects with CFS could be reduced by giving them small daily doses of hydrocortisone and fludrocortisone. The latter, notably, already has been reported to be of great benefit to CFS patients [7]. The rationale for treating CFS patients with the two steroids that are routinely administered to Addisonian patients [8] lies primarily in the fact that no medical condition, except Addison’s disease, shares 20 features with CFS [3]. Five additional symptoms (dizziness upon standing, orthostatic tachycardia, nausea, diarrhoea, and constipation) can be found in both CFS [9] and Addison’s disease [8, 10, 11]. Rather surprisingly, however, despite the staggering similarities between CFS and Addison’s disease, as yet no published attempt has been made to treat CFS patients with both hydrocortisone and fludrocortisone.

You can read the rest of this comment here: http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.1999.00478.x/full

 

Source: Baschetti R. Cortisol deficiency may account for elevated apoptotic cell population in patients with chronic fatigue syndrome. J Intern Med. 1999 Apr;245(4):409-10. http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.1999.00478.x/full

 

Chronic fatigue syndrome

Comment on: Phosphate diabetes in patients with chronic fatigue syndrome. [Postgrad Med J. 1998]

 

Sir, De Lorenzo and colleagues’ report a previously undefined relationship between chronic fatigue syndrome (CFS) and phosphate diabetes. They also report that mean serum phosphate concentration was found to be significantly lower in CFS patients than in control subjects. They explain their findings by the hypothesis that CFS patients have a metabolic defect that is secondary to their chronic underutilisation of skeletal muscle. Another hypothesis can, however, be proposed.

Hypophosphataemia in sepsis has been recently reported to be associated with high levels of tumour necrosis factor-a and interleukin-6.’ However, these inflammatory cytokines are also produced to excess in both CFS patients 3 and hypocortisolaemic subjects.4 De Lorenzo and colleagues’ findings,’ therefore, may simply reflect the hypocortisolism of CFS patients, 5 which is one of the 20 features that CFS shares with Addison’s disease.5

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2431605/pdf/postmedj00143-0063a.pdf

 

Source: Baschetti R. Chronic fatigue syndrome. Postgrad Med J. 1998 Nov;74(877):701. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2431605/ (Full article)