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Adrenal cortical insufficiency secondary to destruction of the cortex by a metastatic tumor is a rare condition. Addison's disease is usually caused by an autoimmune process or by a tuberculous infection. We report a case of adrenal insufficiency as the first clinical manifestation of a metastatic prostate carcinoma that occurred simultaneously with an active pulmonary infection by M. tuberculosis.
BACKGROUND: The incidence of pancreatic tuberculosis is extremely rare, and it frequently misdiagnosed as pancreatic neoplasms. The nonsurgical diagnosis of this entity continues to be a challenge. CASE PRESENTATION: A 33 year old male with six-month history of intermittent right epigastric vague pain and weight lost had found a solitary pancreatic cystic mass and diagnosed as pancreatic cystadenocarcinoma. The chest X-ray film and physical examination revealed no abnormalities. Abdominal ultrasound (US) examination showed an irregular hypoechoic lesion of 6.6 cm x 4.4 cm in the head of pancreas, and color Doppler flow imaging did not demonstrate blood stream in the mass. The attempts to obtain pathological evidence of the lesion by US-guided percutaneous fine needle aspiration failed, an exploratory laparotomy and incisional biopsy revealed a caseous abscess of the head of pancreas without typical changes of tuberculous granuloma, but acid-fast stain was positive. CONCLUSIONS: Pancreatic tuberculosis should be considered in the differential diagnosis of focal pancreatic lesions, especially for young people in developing countries.
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Tuberculosis affecting the thyroid gland is a rare condition. We present the case of a 30-year-old man with thyroid tuberculosis whose presenting complaints were dyspnoea and hoarseness. There was a cystic mass in the posterosuperior right thyroid lobe extending into the paraglottic space. There was also recurrent laryngeal nerve involvement. We performed surgery and administered post-operative antituberculous treatment.
A 36-year-old female presented with generalized bone pain, muscular weakness and enlarged cervical lymph nodes. The biochemical findings and skeletal survey was suggestive of primary hyperparathyroidism (PHPT). CT of neck and thorax showed enlarged multiple lymph nodes in the cervical and superior mediastinal region. With a diagnosis of PHPT she underwent cervical exploration and excision of enlarged right inferior parathyroid gland along with biopsy of nodes were done. Histopathology revealed the features of right parathyroid adenoma with few foci of epithelioid granuloma and granulomatous lymphadenitis. AFB smear and culture sensitivity was negative. A positive PCR for Mycobacterium tuberculosis of the homogenates of parathyroid tumor confirmed tuberculous inflammation within the parathyroid adenoma. To the best of our knowledge this is the first reported case of parathyroid adenoma associated with tuberculous pathology in a case of PHPT.
The adrenal gland is one of the organs which tuberculosis infects. In most clinical settings bilateral adrenal tuberculosis has been clarified after adrenal insufficiency is overt. On the contrary, active adrenal tuberculosis is rarely detected during the survey of infectious disease. A 68-year-old man was admitted because of intermittent fever. The fever had continued for the last 3 months. The intermittent fever was accompanied with leukocytosis and elevation of C-reactive protein. Serum soluble interleukin-2 receptor was 1920 U/ml, and beta2-microglobulin was 4.0 mg/l. Bacterial cultures of blood, sputa, urine, bone marrow and cerebrospinal fluid did not show any particular bacteria. Mycobacterium tuberculosis was negative in culture of sputa, and there was no tuberculin reaction. Plasma ACTH and serum cortisol were 18.5 pmol/l and 527.0 nmol/l, respectively. Abdominal CT scan showed right adrenal mass with a size of 28 x 20 mm, which was low density and had a well-encapsulated homogenous appearance. After the adrenalectomy, histology verified active adrenal tuberculosis. The intermittent fever disappeared, and white blood cells and C-reactive protein normalized. These findings indicate an atypical, rare case of unilateral, active adrenal tuberculosis closely linked to intermittent fever, and without any other organ involvement.
Cushing's disease is a disorder of hypercortisolism caused by a pituitary micro- or macro-adenoma. Most patients with Cushing's disease have a bilateral adrenal enlargement, which depends on the duration of the disease, as a result of the long standing ACTH stimulation of both adrenal glands. However, in macronodular adrenocortical hyperplasia (MNH) that is caused by Cushing's disease, if the MNH gains autonomy, a bilateral adrenalectomy, as well as the removal of pituitary adenoma, is often essential. We encountered a patient diagnosed with Cushing's disease with bilateral adrenal tuberculosis simulating MNH. She had taken anti-tuberculosis medications one year prior to admission due to spinal tuberculosis. Sellar MRI revealed a pituitary macroadenoma, but adrenal CT showed enlargement in both adrenal glands that appeared to be MNH. A hormonal study and bilateral inferior petrosal sinus sampling revealed Cushing's disease. Therefore, she underwent trans-sphenoidal surgery of the pituitary mass. The pituitary surgery was successful and the serum cortisol returned to normal range. However, the adrenal mass rapidly enlarged after removing the pituitary tumor without showing evidence of a recurrence or adrenal autonomy of hypercortisolism. Accordingly, a laparoscopic left adrenalectomy was performed to examine the nature of the mass. The resected left adrenal gland was pathologically determined to have a lesion of tuberculosis with some part of the intact cortex. So we assumed that the cause of rapid adrenal enlargement might be due to adrenal tuberculosis. In summary, to the best of our knowledge, this is the first case of Cushing's disease coexisting with both adrenal tuberculosis simulating a bilateral MNH.
To evaluate sonographic imaging of the normal adrenal glands, anterior transverse and longitudinal scans were made on 200 patients who had no evidence of adrenal disease. In 78 additional patients who were suspected of having adrenal masses, anterior and posterior transverse and longitudinal scanning and longitudinal oblique scanning were done. Anterior transverse scanning proved to be the best single method of scanning the adrenal gland and small adrenal masses. The normal adrenal gland which is 3-6 mm thick and adrenal masses as small as 1.3 cm can be delineated. Although the frequency of visualizing normal adrenal glands (78.5% on the right and 44% on the left) with sonography is not as high as with CT, masses are more readily detected than the normal glands. The accuracy for detecting adrenal masses is very high, with a false-negative rate of only 3%. Sonography can be a useful screening test for many patients who are suspected of having adrenal masses. However, for obese patients the image is degraded and a higher false-positive rate (3.5%) is obtained. CT provides better resolution for such patients.
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We describe a case of a 42 year old male who presented with Addison's disease resulting from primary lymphoma of the adrenals. Our case and a review of the literature indicates that this distinct entity has some unique clinical and radiologic features. In this entity, the lymphoma tends to be extranodal and have a poor prognosis. In addition, the computed tomography (CT) images have the unique appearance of enlargement of the adrenal gland with maintenance of the adreniform shape. We suggest that primary adrenal lymphoma is a distinct clinical entity and should be considered in patients with an elevated serum lactate dehydrogenase, characteristic CT findings and Addison's disease.
We report a case of a patient who presented with hemophagocytic syndrome (HPS) and adrenal crisis associated with bilateral adrenal gland tuberculosis, and resulted in a poor outcome. A 50-year-old man was transferred to our hospital from a local clinic due to fever, weight loss, and bilateral adrenal masses. Laboratory findings showed leukopenia, mild anemia, and elevated lactate dehydrogenase. Computed tomography (CT) of the abdomen revealed bilateral adrenal masses and hepatosplenomegaly. CT-guided adrenal gland biopsy showed numerous epithelioid cells and infiltration with caseous necrosis consistent with tuberculosis. Bone marrow aspiration and biopsy showed significant hemophagocytosis without evidence of malignancy, hence HPS associated with bilateral adrenal tuberculosis was diagnosed. During anti-tuberculosis treatment the patient showed recurrent hypoglycemia and hypotension. Rapid ACTH stimulation test revealed adrenal insufficiency, and we added corticosteroid treatment. But pancytopenia, especially thrombocytopenia, persisted and repeated bone marrow aspiration showed continued hemophagocytosis. On treatment day 41 multiple organ failure occurred in the patient during anti-tuberculous treatment and steroid replacement.
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OBJECTIVE: To describe a patient admitted with acute adrenocortical failure and a right adrenal mass without evidence of tuberculosis, who was ultimately diagnosed with isolated adrenal tuberculosis after postoperative histopathologic evaluation. METHODS: A case report is presented, with clinical, laboratory, and imaging findings. We also discuss potential factors that may complicate the diagnosis of tuberculosis. RESULTS: A 61-year-old man was admitted with symptoms and signs of acute adrenal crisis. The patient had an erythrocyte sedimentation rate of 30 mm in 1 hour, a negative tuberculin skin test, a 6-cm right adrenal mass, and left adrenal nodularity in conjunction with normal findings on a computed tomographic scan of the chest. He recovered dramatically after intravenous corticosteroid treatment. Investigation, including acid-fast staining and cultures for tuberculosis of all available specimens, gastroduodenoscopy and rectosigmoidoscopy, intestinal x-ray imaging, and autoantibody studies, did not disclose the diagnosis. Subsequently, bilateral adrenalectomy revealed isolated tuberculosis of the adrenal glands on histopathologic evaluation. Quadruple antituberculous therapy was initiated, and continued follow-up of the patient is scheduled. CONCLUSION: Our case indicates that acute or chronic adrenocortical failure can occur as a result of tuberculosis of the adrenal gland, despite the absence of clinical and laboratory evidence of tuberculosis.
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We present the case of a 38-year-old male patient with tuberculosis of the thyroid; the diagnosis was established on histological examination after surgery.
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