Diagnosis and Treatment > Medication
You are looking at 1 - 10 of 492 items
Search for other papers by Ahmad Housin in
Google Scholar
PubMed
Search for other papers by Marc P Pusztaszeri in
Google Scholar
PubMed
Search for other papers by Michael Tamilia in
Google Scholar
PubMed
Summary
Fever of unknown origin is a commonly encountered medical problem. Most common causes include infections, malignancy, and connective tissue diseases. Endocrine causes are rare but are well documented. While fever is common in some endocrine disorders, fever of unknown origin as the sole presenting feature is very rare. We describe a case report of a 63-year-old male who presents with fever of unknown origin. Imaging and biopsy results confirmed the diagnosis of subacute thyroiditis. He was started on prednisone with a good response. We conclude that subacute thyroiditis should be considered in the work up of fever of unknown origin even in the absence of classical signs and symptoms.
Learning points:
-
Fever of unknown origin is a rare sole presentation of subacute thyroiditis.
-
The classic signs and symptoms may not be manifest at the time of presentation.
-
Normal thyroid function tests and elevated markers of inflammation often make infections, malignancy and autoinflammatory conditions the prime consideration.
-
Imaging of the thyroid gland may point to a morphologic aberration and prompt a thyroid biopsy.
-
After exclusion of infection, a rapid response to steroids may be both diagnostic and therapeutic.
Search for other papers by Viktoria F Koehler in
Google Scholar
PubMed
Search for other papers by Patrick Keller in
Google Scholar
PubMed
Search for other papers by Elisa Waldmann in
Google Scholar
PubMed
Search for other papers by Nathalie Schwenk in
Google Scholar
PubMed
Search for other papers by Carolin Kitzberger in
Google Scholar
PubMed
Search for other papers by Kathrin A Schmohl in
Google Scholar
PubMed
Search for other papers by Thomas Knösel in
Google Scholar
PubMed
Search for other papers by Christian Georg Stief in
Google Scholar
PubMed
Division of Endocrinology, Diabetes, Metabolism and Nutrition, Mayo Clinic Rochester, Minnesota, USA
Search for other papers by Christine Spitzweg in
Google Scholar
PubMed
Summary
Struma ovarii is a teratoma of the ovaries predominantly composed of thyroid tissue. Hyperthyroidism associated with struma ovarii is rare, occurring in approximately 8% of cases. Due to the rarity of struma ovarii, available data are limited to case reports and small case series.We report on a 61-year-old female patient with known Hashimoto’s thyroiditis on levothyroxine replacement therapy for years with transition to clinical and biochemical hyperthyroidism despite antithyroid medication with carbimazole (10 mg/day), new diagnosis of urothelial carcinoma and an adnexal mass suspicious of ovarian cancer. The patient underwent resection of the adnexal mass and histopathology revealed a mature teratoma predominantly composed of thyroid tissue showing high levels of sodium iodide symporter protein expression. Following struma ovarii resection and disappearance of autonomous production of thyroid hormones, the patient developed hypothyroidism with severely decreased thyroid hormone levels fT4 and fT3 (fT4 0.4 ng/dL, reference interval 0.9–1.7 and fT3 < 1.0 pg/mL, reference interval 2.0–4.4). This has previously been masked by continued thyroid-stimulating hormone suppression due to long-term hyperthyroidism pre-surgery indicating secondary hypothyroidism, in addition to primary hypothyroidism based on the known co-existing chronic lymphocytic thyroiditis of the orthotopic thyroid gland. Levothyroxine administration was started immediately restoring euthyroidism.This case illustrates possible diagnostic pitfalls in a patient with two concurrent causes of abnormal thyroid function.
Learning points:
-
Struma ovarii is an ovarian tumor containing either entirely or predominantly thyroid tissue and accounts for approximately 5% of all ovarian teratomas.
-
In rare cases, both benign and malignant struma ovarii can secrete thyroid hormones, causing clinical and biochemical features of hyperthyroidism.
-
Biochemical features of patients with struma ovarii and hyperthyroidism are similar to those of patients with primary hyperthyroidism. In such cases, thyroid scintigraphy should reveal low or absent radioiodine uptake in the thyroid gland, but the presence of radioiodine uptake in the pelvis in a whole body radioiodine scintigraphy.
-
We give advice on possible diagnostic pitfalls in a case with two simultaneous causes of abnormal thyroid function due to the co-existence of struma ovarii.
Search for other papers by Shunsuke Shimazaki in
Google Scholar
PubMed
Search for other papers by Itsuro Kazukawa in
Google Scholar
PubMed
Search for other papers by Kyoko Mori in
Google Scholar
PubMed
Search for other papers by Makiko Kihara in
Google Scholar
PubMed
Search for other papers by Masanori Minagawa in
Google Scholar
PubMed
Summary
Ammonium acid urate (AAU) crystals are rare in industrialized countries. Furthermore, the number of children with diabetic ketoacidosis (DKA) who develop severe acute kidney injury (AKI) after hospitalization is small. We encountered two patients with AKI caused by AAU crystals during the recovery phase of DKA upon admission. They were diagnosed with severe DKA and hyperuricemia. Their urine volume decreased and AKI developed several days after hospitalization; however, acidosis improved in both patients. Urine sediment analysis revealed AAU crystals. They were treated with urine alkalization and diuretics. Excretion of ammonia in the urine and urine pH levels increased after treatment of DKA, which resulted in the formation of AAU crystals. In patients with severe DKA, the urine and urine sediment should be carefully examined as AAU can form in the recovery phase of DKA.
Learning points:
-
Ammonium acid urate crystals could be formed in the recovery phase of diabetic ketoacidosis.
-
Diabetic ketoacidosis patients may develop acute kidney injury caused by ammonium acid urate crystals.
-
Urine and urine sediment should be carefully checked in patients with severe DKA who present with hyperuricemia and volume depletion.
School of Medicine, University of Queensland, Queensland, Australia
Search for other papers by Mimi Wong in
Google Scholar
PubMed
College of Dentistry and Medicine, James Cook University, Queensland, Australia
Search for other papers by Usman H Malabu in
Google Scholar
PubMed
Search for other papers by Ipeson Korah in
Google Scholar
PubMed
College of Dentistry and Medicine, James Cook University, Queensland, Australia
Search for other papers by YongMong Tan in
Google Scholar
PubMed
Summary
Whilst literature is expanding on pasireotide use in the management of Cushing’s disease (CD), there is still currently much unknown about long-term and low-dose pasireotide use in CD. We present a 60-year-old female with residual CD after transphenoidal surgery (TSS), being successfully managed with S.C. pasireotide for over 10 years. For 6 years, her S.C. pasireotide was inadvertently administered at 360 µg twice daily (BID), almost half the recommended dose of 600 µg BID. Despite the low-dose, her urinary free cortisol (UFC) normalised within 6 months and Cushingoid features resolved. She remained in biochemical and clinical remission on the same low-dose for 6 years, before a medication audit discovered her mistaken dose and directed her to take 600 µg BID. With the higher dose 600 µg BID for the next 5 years, her glycaemia worsened without any changes in her UFC and residual tumour volume. Our case showed the continuing effectiveness and safety of treatment with S.C. pasireotide for more than 10 years, and that a low-dose regimen may be considered an option for responders by its safety profile.
Learning points:
-
A lower dose of pasireotide may be effective in the initial treatment of CD than the recommended 600 µg BID dosage, though more studies are required to explore this.
-
Low-dose pasireotide use has the benefit of minimising adverse effects.
-
In the long-term, pasireotide has a sustained clinical and biochemical effect and is well tolerated.
Search for other papers by Rob Gonsalves in
Google Scholar
PubMed
Search for other papers by Kirk Aleck in
Google Scholar
PubMed
Search for other papers by Dorothee Newbern in
Google Scholar
PubMed
Search for other papers by Gabriel Shaibi in
Google Scholar
PubMed
Search for other papers by Chirag Kapadia in
Google Scholar
PubMed
Search for other papers by Oliver Oatman in
Google Scholar
PubMed
Summary
Single-minded homolog 1 (SIM1) is a transcription factor that plays a role in the development of both the hypothalamus and pituitary. SIM1 gene mutations are known to cause obesity in humans, and chromosomal deletions encompassing SIM1 and other genes necessary for pituitary development can cause a Prader–Willi-like syndrome with obesity and hypopituitarism. There have been no reported cases of hypopituitarism linked to a single SIM1 mutation. A 21-month-old male presented to endocrinology clinic with excessive weight gain and severe obesity. History was also notable for excessive drinking and urination. Endocrine workup revealed central hypothyroidism, partial diabetes insipidus, and central adrenal insufficiency. Genetic evaluation revealed a novel mutation in the SIM1 gene. No other genetic abnormalities to account for his obesity and hypopituitarism were identified. While we cannot definitively state this mutation is pathogenic, it is notable that SIM1 plays a role in the development of all three of the patient’s affected hormone axes. He is now 6 years old and remains on treatment for his pituitary hormone deficiencies and continues to exhibit excessive weight gain despite lifestyle interventions.
Learning points:
-
Mutations in SIM1 are a well-recognized cause of monogenic human obesity, and there have been case reports of Prader–Willi-like syndrome and hypopituitarism in patients with chromosomal deletions that contain the SIM1 gene.
-
SIM1 is expressed during the development of the hypothalamus, specifically in neuroendocrine lineages that give rise to the hormones oxytocin, arginine vasopressin, thyrotropin-releasing hormone, corticotropin-releasing hormone, and somatostatin.
-
Pituitary testing should be considered in patients with severe obesity and a known genetic abnormality affecting the SIM1 gene, particularly in the pediatric population.
Search for other papers by Tomomi Nakao in
Google Scholar
PubMed
Search for other papers by Ken Takeshima in
Google Scholar
PubMed
Search for other papers by Hiroyuki Ariyasu in
Google Scholar
PubMed
Search for other papers by Chiaki Kurimoto in
Google Scholar
PubMed
Search for other papers by Shinsuke Uraki in
Google Scholar
PubMed
Search for other papers by Shuhei Morita in
Google Scholar
PubMed
Search for other papers by Yasushi Furukawa in
Google Scholar
PubMed
Search for other papers by Hiroshi Iwakura in
Google Scholar
PubMed
Search for other papers by Takashi Akamizu in
Google Scholar
PubMed
Summary
Thyroid storm (TS) is a life-threatening condition that may suffer thyrotoxic patients. Therapeutic plasma exchange (TPE) is a rescue approach for TS with acute hepatic failure, but it should be initiated with careful considerations. We present a 55-year-old male patient with untreated Graves’ disease who developed TS. Severe hyperthyroidism and refractory atrial fibrillation with congestive heart failure aggregated to multiple organ failure. The patient was recovered by intensive multimodal therapy, but we had difficulty in introducing TPE treatment considering the risk of exacerbation of congestive heart failure due to plasma volume overload. In addition, serum total bilirubin level was not elevated in the early phase to the level of indication for TPE. The clinical course of this patient instructed delayed elevation of bilirubin until the level of indication for TPE in some patients and also demonstrated the risk of exacerbation of congestive heart failure by TPE.
Learning points:
-
Our patient with thyroid storm could be diagnosed and treated promptly using Japan Thyroid Association guidelines for thyroid storm.
-
Delayed elevation of serum bilirubin levels could make the decision of introducing therapeutic plasma exchange difficult in cases of thyroid storm with acute hepatic failure.
-
The risk of worsening congestive heart failure should be considered carefully when performing therapeutic plasma exchange.
Search for other papers by Jai Madhok in
Google Scholar
PubMed
Search for other papers by Amy Kloosterboer in
Google Scholar
PubMed
Search for other papers by Chitra Venkatasubramanian in
Google Scholar
PubMed
Search for other papers by Frederick G Mihm in
Google Scholar
PubMed
Summary
We report the case of a 76-year-old male with a remote history of papillary thyroid cancer who developed severe paroxysmal headaches in the setting of episodic hypertension. Brain imaging revealed multiple lesions, initially of inconclusive etiology, but suspicious for metastatic foci. A search for the primary malignancy revealed an adrenal tumor, and biochemical testing confirmed the diagnosis of a norepinephrine-secreting pheochromocytoma. Serial imaging demonstrated multiple cerebral infarctions of varying ages, evidence of vessel narrowing and irregularities in the anterior and posterior circulations, and hypoperfusion in watershed areas. An exhaustive work-up for other etiologies of stroke including thromboembolic causes or vasculitis was unremarkable. There was resolution of symptoms, absence of new infarctions, and improvement in vessel caliber after adequate alpha-adrenergic receptor blockade for the management of pheochromocytoma. This clinicoradiologic constellation of findings suggested that the etiology of the multiple infarctions was reversible cerebral vasoconstriction syndrome (RCVS). Pheochromocytoma remains a poorly recognized cause of RCVS. Unexplained multifocal cerebral infarctions in the setting of severe hypertension should prompt the consideration of a vasoactive tumor as the driver of cerebrovascular dysfunction. A missed or delayed diagnosis has the potential for serious neurologic morbidity for an otherwise treatable condition.
Learning points:
-
The constellation of multifocal watershed cerebral infarctions of uncertain etiology in a patient with malignant hypertension should trigger the consideration of undiagnosed catecholamine secreting tumors, such as pheochromocytomas and paragangliomas.
-
Reversible cerebral vasoconstriction syndrome is a serious but reversible cerebrovascular manifestation of pheochromocytomas that may lead to strokes (ischemic and hemorrhagic), seizures, and cerebral edema.
-
Alpha-adrenergic receptor blockade can reverse cerebral vasoconstriction and prevent further cerebral ischemia and infarctions.
-
Early diagnosis of catecholamine secreting tumors has the potential for reducing neurologic morbidity and mortality in patients presenting with cerebrovascular complications.
General Surgery, Mount Druitt Hospital, Mount Druitt, New South Wales, Australia
Search for other papers by Pratima Herle in
Google Scholar
PubMed
Search for other papers by Steven Boyages in
Google Scholar
PubMed
Search for other papers by Rina Hui in
Google Scholar
PubMed
Search for other papers by Najmun Nahar in
Google Scholar
PubMed
Search for other papers by Nicholas K Ngui in
Google Scholar
PubMed
Summary
In most developed countries, breast carcinoma is the most common malignancy in women and while thyroid cancer is less common, its incidence is almost three to five times greater in women than in men. Since 1966, studies have demonstrated an association between thyroid and breast cancer and despite these studies, the mechanism/s by which they are related, remains unclear. We present a case of a 56-year-old lady who initially presented in 2014 with a screen detected left breast carcinoma but was subsequently found to have occult metastatic thyroid cancer to the axilla, diagnosed from a sentinel node biopsy from the primary breast procedure. The patient underwent a left mastectomy, left axillary dissection and total thyroidectomy followed by three courses of radioactive iodine ablation. Despite this, her thyroglobulin level continued to increase, which was secondary to a metastatic thyroid cancer parasternal metastasis. Breast and thyroid cancer presents metachronously or synchronously more often than by chance. With improving mortality in primary cancers, such as breast and differentiated thyroid cancer, it is likely that as clinicians, we will continue to encounter this association in practice.
Learning points:
-
There has been a long-standing observation of an association between breast and thyroid cancer although the exact mechanism of this association remains unclear.
-
Our patient presented with thyroid cancer with an incidental diagnosis from a sentinel node biopsy during her primary breast operation for breast cancer and was also found to have a parasternal distant bony metastasis.
-
Thyroid axillary metastases are generally rare.
-
The interesting nature in which this patient’s metastatic thyroid carcinoma behaved more like a breast carcinoma highlights a correlation between these two cancers.
-
With improving mortality in these primary cancers, clinicians are likely to encounter this association in clinical practice.
-
Systemic therapy for metastatic breast and thyroid cancers differ and therefore a clear diagnosis of metastasis is crucial.
Search for other papers by Tzy Harn Chua in
Google Scholar
PubMed
Search for other papers by Wann Jia Loh in
Google Scholar
PubMed
Summary
Severe hyponatremia and osmotic demyelination syndrome (ODS) are opposite ends of a spectrum of emergency disorders related to sodium concentrations. Management of severe hyponatremia is challenging because of the difficulty in balancing the risk of overcorrection leading to ODS as well as under-correction causing cerebral oedema, particularly in a patient with chronic hypocortisolism and hypothyroidism. We report a case of a patient with Noonan syndrome and untreated anterior hypopituitarism who presented with symptomatic hyponatremia and developed transient ODS.
Learning points:
-
Patients with severe anterior hypopituitarism with severe hyponatremia are susceptible to the rapid rise of sodium level with a small amount of fluid and hydrocortisone.
-
These patients with chronic anterior hypopituitarism are at high risk of developing ODS and therefore, care should be taken to avoid a rise of more than 4–6 mmol/L per day.
-
Early recognition and rescue desmopressin and i.v. dextrose 5% fluids to reduce serum sodium concentration may be helpful in treating acute ODS.
Search for other papers by Takuya Higashitani in
Google Scholar
PubMed
Search for other papers by Shigehiro Karashima in
Google Scholar
PubMed
Search for other papers by Daisuke Aono in
Google Scholar
PubMed
Department of Internal Medicine, Keiju Medical Center, Nanao, Ishikawa, Japan
Search for other papers by Seigoh Konishi in
Google Scholar
PubMed
Search for other papers by Mitsuhiro Kometani in
Google Scholar
PubMed
Search for other papers by Rie Oka in
Google Scholar
PubMed
Search for other papers by Masashi Demura in
Google Scholar
PubMed
Search for other papers by Kenji Furukawa in
Google Scholar
PubMed
Search for other papers by Yuto Yamazaki in
Google Scholar
PubMed
Search for other papers by Hironobu Sasano in
Google Scholar
PubMed
Department of Health Promotion and Medicine of the Future, Kanazawa University, Kanazawa, Ishikawa, Japan
Search for other papers by Takashi Yoneda in
Google Scholar
PubMed
Search for other papers by Yoshiyu Takeda in
Google Scholar
PubMed
Summary
Renovascular hypertension (RVHT) is an important and potentially treatable form of resistant hypertension. Hypercortisolemia could also cause hypertension and diabetes mellitus. We experienced a case wherein adrenalectomy markedly improved blood pressure and plasma glucose levels in a patient with RVHT and low-level autonomous cortisol secretion. A 62-year-old Japanese man had been treated for hypertension and diabetes mellitus for 10 years. He was hospitalized because of a disturbance in consciousness. His blood pressure (BP) was 236/118 mmHg, pulse rate was 132 beats/min, and plasma glucose level was 712 mg/dL. Abdominal CT scanning revealed the presence of bilateral adrenal masses and left atrophic kidney. Abdominal magnetic resonance angiography demonstrated marked stenosis of the left main renal artery. The patient was subsequently diagnosed with atherosclerotic RVHT with left renal artery stenosis. His left adrenal lobular mass was over 40 mm and it was clinically suspected the potential for cortisol overproduction. Therefore, laparoscopic left nephrectomy and adrenalectomy were simultaneously performed, resulting in improved BP and glucose levels. Pathological studies revealed the presence of multiple cortisol-producing adrenal nodules and aldosterone-producing cell clusters in the adjacent left adrenal cortex. In the present case, the activated renin-angiotensin-aldosterone system and cortisol overproduction resulted in severe hypertension, which was managed with simultaneous unilateral nephrectomy and adrenalectomy.
Learning points:
-
Concomitant activation of the renin-angiotensin-aldosterone system and cortisol overproduction may contribute to the development of severe hypertension and lead to lethal cardiovascular complications.
-
Treatment with simultaneous unilateral nephrectomy and adrenalectomy markedly improves BP and blood glucose levels.
-
CYP11B2 immunohistochemistry staining revealed the existence of aldosterone-producing cell clusters (APCCs) in the adjacent non-nodular adrenal gland, suggesting that APCCs may contribute to aldosterone overproduction in patients with RVHT.
