Addison’s disease with primary hypothyroidism in a case of visceral leishmaniasis and HIV coinfection

2021 ◽  
Vol 14 (3) ◽  
pp. e238488
Author(s):  
Monu Rani ◽  
Rakesh Garg ◽  
Venkatesh Darshan Agraharabachalli Nanjunde ◽  
Rajesh Rajput

A 41-year-old man presented with vomiting and loose stools. He had a history of long-term intermittent fever, generalised skin hyperpigmentation, dragging sensation in the left hypochondrium and unintentional weight loss. He was receiving combination antiretroviral therapy since 2010 for HIV infection. He also received antitubercular therapy for tuberculous spondylitis. During the hospital stay, he was found to have postural hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia, pancytopenia, hypothyroidism, hyperglobulinaemia and hypoalbuminaemia with reversal of serum albumin/globulin ratio. The morning plasma cortisol was lower than normal and could not be appropriately stimulated after the Synacthen test. The bone marrow histopathology was suggestive of visceral leishmaniasis. He was diagnosed as a case of visceral leishmaniasis and HIV coinfection with primary adrenal insufficiency (Addison’s disease) and primary hypothyroidism, as a rare and unusual presentation.

2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Anup Bastola ◽  
Mitesh Shrestha ◽  
Bimal Sharma Chalise ◽  
Abhdesh Kumar Mishra ◽  
Lina Devkota

We report the first case of miltefosine rescue treatment carried out for visceral leishmaniasis (VL) relapse patient. Despite undergoing treatment regimens of liposomal amphotericin B (LAMB) 5 mg/kg (standard: 10 mg/kg) daily for 3 days during the first episode followed by LAMB 5 mg/kg stat and paromomycin 15 mg/kg IM for 10 days against the second episode, the patient suffered from a third relapse and was eventually treated with miltefosine 50 mg BID directly observed treatment for 28 days. Prior to treatment, the patient had a history of intermittent fever and vague abdominal pain for one week and epistaxis for 4 days. He had massive splenomegaly, tested positive for the rK39 test, and showed LD bodies in bone marrow aspirate. The patient tested negative for malaria and HIV. Upon treatment completion with miltefosine, the patient had clinically improved and showed no LD bodies in bone marrow.


1987 ◽  
Vol 114 (3) ◽  
pp. 389-395 ◽  
Author(s):  
F. Laczi ◽  
T. Janáky ◽  
T. Iványi ◽  
J. Julesz ◽  
F. A. László

Abstract. The osmoregulation of arginine-8-vasopressin (AVP) was investigated in 14 patients with primary hypothyroidism and in 6 with Addison's disease. Plasma AVP was measured by radioimmunoassay. Patients with primary hypothyroidism were classified into subgroups with elevated (6.81 ± 1.12 pmol/l) or normal (3.92 ± 0.96 pmol/l) basal levels of plasma AVP. Following the infusion of 2.5% saline, a positive correlation was established between plasma AVP and plasma osmolality. A decreased osmotic threshold was found in hypothyroid patients with augmented basal AVP levels (pAVP = 0.37 (pOs-265), r = 0.71, P < 0.01) as compared with that in hypothyroid patients with a normal AVP level (pAVP = 0.42 (pOs-280), r = 0.93, P < 0.001). A relationship was demonstrated between the alteration in the AVP osmoregulation and the severity of the thyroid insufficiency. Patients with Addison's disease exhibited an increased basal level of plasma AVP (9.59 ± 1.25 pmol/l) and a decreased osmotic threshold (pAVP = 0.42 (pOs-261), r = 0.63, P < 0.01) contrasted to that of healthy volunteers (pAVP = 0.41 (pOs-280), r = 0.83, P < 0.001). The osmoregulation disturbance of the AVP secretion may play a major role in the impaired water metabolism in primary hypothyroidism and in Addison's disease.


Author(s):  
H Cooper ◽  
B Bhattacharya ◽  
V Verma ◽  
A J McCulloch ◽  
W S A Smellie ◽  
...  

Addison's disease is a relatively common disorder to endocrinologists, but is rare and potentially fatal when presenting acutely. Treatment now involves replacement of glucocorticoids and mineralocorticoids with synthetic compounds, although historically patients took common salt and plant-based preparations. We describe the case of a 42-year-old woman who self-treated undiagnosed Addison's disease for several years with soy sauce and liquorice sticks. She presented with a four-week history of decreased energy, malaise and postural dizziness. Our patient described an unusual diet of liquorice sticks and soy sauce, consuming around 46 g of salt per week. There was a family history of Type 1 diabetes mellitus. Physical examination was unremarkable, although subsequent investigation confirmed Addison's disease. Liquorice provided glycyrrhizic acid and glycyrrhetinic acid, which act on 11-beta hydroxysteroid dehydrogenase enzymes. In this case, the net effect was potentiation of glucocorticoid action on renal mineralocorticoid receptors in the context of failing adrenocortical steroid production. The case highlights the importance of taking a dietary history to aid diagnosis.


2013 ◽  
Vol 49 (1) ◽  
pp. 54-57 ◽  
Author(s):  
Kathryn M. McGonigle ◽  
John F. Randolph ◽  
Sharon A. Center ◽  
Richard E. Goldstein

A dog with an unexpected presentation of primary hypoadrenocorticism was evaluated for clinical signs and electrolyte abnormalities characteristic of Addison’s disease. Although the initial adrenocorticotropic hormone (ACTH) stimulation test documented serum cortisol concentrations within the reference range, subsequent assessments confirmed hypoaldosteronism. Mineralocorticoid replacement promptly normalized electrolytes and transiently improved clinical illness. Six weeks after initial ACTH stimulation testing, the dog became glucocorticoid deficient. Concurrent primary hypothyroidism was also documented. Hypoaldosteronism preceding hypocortisolemia is a unique presentation of canine Addison’s disease.


1998 ◽  
Vol 44 (6) ◽  
pp. 22-26
Author(s):  
V. V. Fadeev ◽  
I. I. Buziashvili ◽  
I. I. Dedov

A retrospective analysis of case histories of 426 patients with primary chronic adrenal insufficiency (1-AI), followed up at Endocrinology Research Center, Russian Academy of Medical Sciences, and/or Endocrinology Clinic of I. M. Setchenov Moscow Medical Academy in 1954-1977, was carried out in order to assess the etiological and clinical structure of this disease. The idiopathic form of Addison 's disease prevailed over its tuberculous form (70 and 30%), respectively); dynamic assessment of morbidity over the above period showed a progressive predominance of the idiopathic form. 1-AI is more than 2 times more incident in women, and the incidence of the disease in women vs. men is ever growing. There are at least 2.5 times more women than men among patients with idiopathic Addison's disease, while for the tuberculous form the ratio is 1:1. The mean age of 1-AI manifestation is 34.3 ± 0.46 years. The peak of clinical manifestation of idiopathic Addison's disease occurs between 20 and 40 years (at the age of 32.8 years on average), while for the tuberculous form this age is 30-50 years (37.4), which indicates a later manifestation of this form (p < 0.01). In 28%) cases idiopathic Addison's disease coursed in the presence of autoimmune polyglandular syndromes (APS): type 1 in 3%o and type II in 25% cases. Dynamic assessment of the ratio of the incidence of 1-AI alone to that in the presence of APS showed that from the thirties to the fifties, idiopathic Addison's disease was a component of APS in 13 % cases and by the eighties and nineties this values increased to 34%), which permits a conclusion about pathomorphism of 1-AI, consisting in gradual transfer of this disease into APS. Many patients with 1-AI develop concomitant autoimmune diseases; analysis of family history of such patients reveals autoimmune diseases in close relatives in many cases, while the majority of patients with the tuberculous form of Addison 5 disease have a family history of tuberculosis.


2018 ◽  
Vol 56 (6) ◽  
pp. 896-900 ◽  
Author(s):  
Jacopo Manso ◽  
Raffaele Pezzani ◽  
Riccardo Scarpa ◽  
Nicoletta Gallo ◽  
Corrado Betterle

Abstract Autoimmune Addison’s disease (AAD) is the most frequent cause of adrenocortical insufficiency. The natural history of AAD usually comprises five consecutive stages with the first stage characterized by the increase of plasma renin consistent with the impairment of pars glomerulosa, which is usually the first affected layer of the adrenal cortex. We describe a 19-year-old female with Hashimoto’s thyroiditis (HT) who underwent an autoantibody screening due to having the personal and family history of other autoimmune diseases in the absence of relevant clinical manifestations. She was positive for adrenal cortex autoantibodies (ACA) and steroid 21-hydroxylase autoantibodies (21-OH Ab) at high titers. She had increased basal levels of ACTH with normal basal cortisol not responding to ACTH stimulation, reduced levels of dehydroepiandrosterone-sulfate but normal levels of orthostatic renin and aldosterone. This scenario was consistent with a subclinical AAD presenting with first impairments in pars fasciculata and reticularis and conserved pars glomerulosa function. Only subsequently, progressive deficiency in pars glomerulosa function has become evident. Review of the literature showed that there was only one case, reported to date, with a similar atypical natural history of AAD. The strategies for screening for ACA/21-OH Ab in patients with HT are discussed.


1995 ◽  
Vol 133 (1) ◽  
pp. 38-47 ◽  
Author(s):  
Secondo Lastoria ◽  
Annamaria Colao ◽  
Emilia Vergara ◽  
Diego Ferone ◽  
Paola Varrella ◽  
...  

Lastoria S, Colao A, Vergara E, Ferone D, Varrella P, Merola B, Lombardi G, Salvatore M. Technetium-99m pentavalent dimercaptosuccinic acid imaging in patients with pituitary adenomas. Eur J Endocrinol 1995;133:38–47. ISSN 0804–4643 We studied the tumor-seeking agent technetium-99m-labeled pentavalent dimercaptosuccinic acid ([99mTc](V)DMSA) to visualize 21 growth hormone (GH)-, nine prolactin (PRL)-, two mixed GH/PRL-, six adrenocorticotropin (ACTH)-secreting and 15 clinically non-functioning pituitary adenomas, three craniopharyngiomas and one dysgerminoma of the sella. All non-adenomas and 31 out of 53 adenomas were studied before treatment: 22 after surgery and/or radiotherapy. Eight cases of acromegaly were studied before and after chronic treatment with octreotide, whereas three cases of acromegaly, one of prolactinoma and two of non-functioning adenoma were imaged before and after adenomectomy. As a control group, 27 patients without any clinical evidence of pituitary adenoma were studied: 10 of them were operated on previously and treated with iodine-131 for metastatic thyroid carcinoma, 10 had brain tumors and the remaining seven patients had functional pituitary hypersecretion (four Klinefelter's syndrome, two primary hypothyroidism and one Addison's disease). The scintigraphy was repeated after testosterone in Klinefelter's syndrome, l-thyroxine in primary hypothyroidism and cortisone administration in Addison's disease. Seventeen GH-secreting (81%), seven PRL-secreting (78%), three ACTH-secreting (50%), 15 non-functioning (100%) and one (50%) mixed adenoma significantly concentrated [99mTc](V)DMSA, showing elevated tumor-to-background (T/B) ratios. The T/B ratios were similar in untreated and surgically treated adenomas (11.2 ± 5.6 vs 11.8 ± 6.2). Radiotherapy significantly lowered the [99mTc](V)DMSA uptake to 5.1 ± 2.8 (p < 0.1 vs untreated patients). Non-adenomatous lesions of the sella turcica did not concentrate [99mTc](V)DMSA in the pituitary as well as brain tumors and 8 out of 10 metastatic thyroid cancers. The treatment with octreotide normalized GH and insulin-like growth factor I levels and reduced [99mTc](V)DMSA from 15.7 ± 4.8 to 13.5 ± 3.9 (p < 0.05). Conversely, adequate substitutive therapy completely inhibited the uptake of the radiotracer in Klinefelter's syndrome, in primary hypothyroidism and in Addison's disease. The [99mTc](V)DMSA scintigraphy showed an overall sensitivity of 81% (43/53) in detecting pituitary adenomas, which was increased to 95% for lesions greater than 10 mm in size. High-quality images with minimal total body radiation were obtained, enabling a good in vivo characterization of viable adenomatous tissue as well as an accurate monitoring of the effects of different therapeutic regimens. Secondo Lastoria, Department of Nuclear Medicine, National Cancer Institute, Fondazione G Pascale, via M Semmola, 80131 Napoli, Italy


2021 ◽  
Author(s):  
Sunao Matsubayashi ◽  
Madoka Tanaka ◽  
Takeshi Hara

Abstract Objective: Widespread attention has been paid to the misdiagnosis of life-threatening Addison's disease as anorexia nervosa. However, there are no reports on the possible comorbidity of Addison's disease and other adrenal insufficiencies with anorexia nervosa.Methods: A case-series presentation of anorexia nervosa concomitant with central adrenal insufficiency.Results: Four anorexia nervosa patients (21-35 years old, all females) complained of severe fatigue during their treatment. After a thorough examination of the hypothalamus-pituitary-adrenal axis using stimulation with a rapid adenocorticotropic hormone test of 250-µg Cortrosyn®, a corticotropin-releasing hormone test, and an insulin tolerance test, central adrenal insufficiency was diagnosed. Two of the four patients had a history of exogenous steroids for their history of comorbidity. One of the residual two patient had Rathke’s cleft cyst. After the initiation of hydrocortisone replacement the patient's fatigue symptoms improved and they were able to return to school and their workplace. In some cases, their weight obsession was reduced after the initiation of hydrocortisone replacement.Conclusion: Anorexia nervosa may be concomitant with central adrenal insufficiency partly in relation to exogenous steroids used for their history of comorbidity, which needs to be kept in mind when treating such patients.Level of EvidenceLevel V, descriptive study.


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