Patient Demographics > Gender > Male
You are looking at 61 - 70 of 418 items
Search for other papers by Evangelos Karvounis in
Google Scholar
PubMed
Search for other papers by Ioannis Zoupas in
Google Scholar
PubMed
Search for other papers by Dimitra Bantouna in
Google Scholar
PubMed
Center for Diabetes and Endocrine Research, University of Toledo College of Medicine and Life Sciences, Toledo, Ohio, USA
Search for other papers by Rodis D Paparodis in
Google Scholar
PubMed
Search for other papers by Roxani Efthymiadou in
Google Scholar
PubMed
Search for other papers by Christina Ioakimidou in
Google Scholar
PubMed
Search for other papers by Christos Panopoulos in
Google Scholar
PubMed
Summary
Large-cell neuroendocrine carcinoma (LCNEC) is a rare neuroendocrine prostatic malignancy. It usually arises after androgen deprivation therapy (ADT), while de novo cases are even more infrequent, with only six cases described. The patient was a 78-year-old man with no history of ADT who presented with cervical lymphadenopathy. Diagnostic approaches included PET/CT, MRI, CT scans, ultrasonography, biopsies, and cytological and immunohistochemical evaluations. Results showed a poorly differentiated carcinoma in the thyroid gland accompanied by cervical lymph node enlargement. Thyroid surgery revealed LCNEC metastasis to the thyroid gland. Additional metastases were identified in both the adrenal glands. Despite appropriate treatment, the patient died of the disease. De novo LCNEC of the prostate is a rare, highly aggressive tumor with a poor prognosis. It is resistant to most therapeutic agents, has a high metastatic potential, and is usually diagnosed at an advanced stage. Further studies are required to characterize this tumor.
Learning points
-
De novo LCNECs of the prostate gland can metastasize almost anywhere in the body, including the thyroid and adrenal glands.
-
LCNECs of the prostate are usually associated with androgen-depriving therapy, but de novo cases are also notable and should be accounted for.
-
Further studies are required to fully understand and treat LCNECs more effectively.
Search for other papers by Nicole Oosterom in
Google Scholar
PubMed
Faculty of Electrical Engineering, Mathematics and Computer Science, University of Twente, Enschede, the Netherlands
Search for other papers by Niala den Braber in
Google Scholar
PubMed
Faculty of Electrical Engineering, Mathematics and Computer Science, University of Twente, Enschede, the Netherlands
Search for other papers by Gozewijn D Laverman in
Google Scholar
PubMed
Summary
This study compares the effects of metformin, sulfonylurea derivative (SU) and no treatment in HNF4A-MODY on glycemic control. In two patients with HNF4A-MODY, we changed the existing metformin treatment to SU derivative. The effect on the glycemic control was registered with a Freestyle Libre Flash glucose monitoring device. Each treatment period had a duration of 2 consecutive weeks, and in between, an intermediate period without medication. Data from the first 2 days after changing medications were excluded. We calculated time in range (TIR), and differences in the mean glucose level were tested with a one-way ANOVA test. The 24-h average glucose levels were significantly lower with either metformin (7.7 mmol/L; P < 0.001 and 6.3 mmol/L; P < 0.001) or gliclazide (7.6 mmol/L; P < 0.001 and 5.8 mmol/L; P < 0.001) compared to no treatment (9.4 and 8.9 mmol/L). The TIR with metformin or gliclazide was higher than without treatment (patient 1: 87 and 83 vs 61% and patient 2: 83 and 93 vs 67%). Treatment with either metformin or gliclazide effectively decreases blood glucose, rendering both drugs appropriate for treating HNF4A-MODY.
Learning points
-
HNF4A-MODY has a mild phenotype.
-
Blood glucose was responsive to long-term metformin treatment in HNF4A-MODY.
-
Metformin and gliclazide seem appropriate treatments for HNF4A-MODY.
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Therese Adrian in
Google Scholar
PubMed
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Mads Hornum in
Google Scholar
PubMed
Center for Clinical Metabolic Research, Copenhagen University Hospital – Gentofte Hospital, Hellerup, Denmark
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Science, University of Copenhagen, Copenhagen, Denmark
Copenhagen University Hospital – Steno Diabetes Center Copenhagen, Herlev, Denmark
Search for other papers by Filip Krag Knop in
Google Scholar
PubMed
Gastro Unit, Medical Division, Copenhagen University Hospital – Amager and Hvidovre Hospital, Hvidovre, Denmark
Search for other papers by Lise Lotte Gluud in
Google Scholar
PubMed
Summary
A 72-year-old man with type 2 diabetes volunteered to participate in the control group of a clinical study. The study evaluated non-alcoholic fatty liver disease in patients with kidney disease. The patient was followed at a gastroenterology department due to Crohn’s disease and post-operative bile acid malabsorption. The patient had no symptoms or biochemical findings suggesting liver disease. Surprisingly, a transient elastography (FibroScan®) suggested advanced fibrosis with a median of 16.1 kPa. A liver biopsy showed non-alcoholic steatohepatitis (NASH)-cirrhosis. The diagnosis was only made incidentally and highlights how NASH-cirrhosis may be overlooked due to the lack of symptoms.
Learning points
-
Clinicians treating high-risk populations, including patients with type 2 diabetes and/or components of the metabolic syndrome, should be aware of the frequently occurring co-existence with non-alcoholic fatty liver disease (NAFLD) and especially non-alcoholic steatohepatitis (NASH).
-
Liver enzymes may be in the normal range even in people with steatosis, NASH, or even cirrhosis.
-
The diagnosis of NAFLD should include evaluation of hepatic fibrosis as this is the most important prognostic factor for liver-related complications and mortality.
-
Guidelines about systematic screening for NAFLD in patients with type 2 diabetes are incongruent.
Search for other papers by Katarzyna Guziejko in
Google Scholar
PubMed
Search for other papers by Łukasz Minarowski in
Google Scholar
PubMed
Search for other papers by Agata Piłaszewicz-Puza in
Google Scholar
PubMed
Search for other papers by Anna Szumera-Ciećkiewicz in
Google Scholar
PubMed
Search for other papers by Robert Marek Mróz in
Google Scholar
PubMed
Summary
Sarcoidosis is an inflammatory, multisystem disease with an undetermined etiology. The presence of noncaseating granulomas in involved organs is a characteristic pathomorphological feature. Sarcoidosis, like a chameleon, can mimic different medical conditions. Although the lungs are most commonly involved, extrapulmonary manifestations can influence any system. The clinical course of the disease may differ. Immediate initiation of glucocorticosteroid therapy is important when critical organs are impaired. A case of a patient with sarcoidosis whose first clinical symptoms were related to diabetes insipidus (DI) was presented. The diagnosis of multiple organ sarcoidosis was delayed because of an adequate response to treatment with vasopressin. The multidisciplinary diagnostic approach validated the involvement of the pituitary gland, lungs, lymph nodes, bones, and subcutaneous tissue. The presented case emphasizes the critical importance of the multifaceted differential diagnosis of patients with DI.
Learning points
-
Sarcoidosis usually affects the lung but can also be a multisystemic disease.
-
The assessment of the extension of sarcoidosis remains complex.
-
A multidisciplinary approach must identify all-organ involvement and initiate appropriate sarcoidosis treatment.
-
Diabetes insipidus (DI) can be the first symptom of a systemic granulomatous disorder.
-
In the differential diagnosis of DI, a comprehensive assessment of rare causes of endocrine disorders, including extrapulmonary sarcoidosis, should be considered.
College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia
King Abdullah International Medical Research Center, Jeddah, Saudi Arabia
Department of Medicine, King Abdulaziz Medical City, Ministry of National Guard Health Affairs, Jeddah, Saudi Arabia
Search for other papers by Raad Alwithenani in
Google Scholar
PubMed
Search for other papers by Danielle M Andrade in
Google Scholar
PubMed
Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, Ontario, Canada
Search for other papers by Lingxin Zhang in
Google Scholar
PubMed
Search for other papers by Karen E Gomez-Hernandez in
Google Scholar
PubMed
Summary
Myopathy caused by thyrotoxicosis is not uncommon. Skeletal muscles are commonly involved, but dysphagia is a rare manifestation of thyrotoxicosis. We aim to raise awareness of dysphagia caused by hyperthyroidism and review similar cases in the literature. We present a case of severe dysphagia caused by hyperthyroidism. We also summarize similar case reports in the literature. Our patient is a 77-year-old man who presented with thyrotoxicosis related to Graves’ disease (GD), dysphagia to both liquid and solid food, and weight loss. Further investigations revealed severe esophageal dysphagia and a high risk for aspiration. He required the placement of a G-tube for feeding. After 8 weeks of methimazole treatment, his thyroid function normalized and his dysphagia improved significantly, leading to the removal of the feeding G-tube. We summarize 19 case reports published in the literature of hyperthyroidism leading to dysphagia. Patients with thyrotoxicosis and dysphagia are at higher risk for aspiration pneumonia and thyroid storm. Based on previous case reports, on average, approximately 3 weeks of treatment with anti-thyroidal drugs and beta-blockers is needed before patients can eat normally. We report a case of dysphagia associated with GD, which is rare and needs prompt recognition to restore euthyroid status. Dysphagia generally resolved with normalization of thyroid function.
Learning points
-
Myopathy caused by thyrotoxicosis is not uncommon.
-
Skeletal muscles are commonly involved, but dysphagia is a rare manifestation of thyrotoxicosis.
-
Dysphagia due to hyperthyroidism resolves with normalization of thyroid function.
-
Early recognition of dysphagia related to hyperthyroidism and early initiation of therapy may help reverse the dysphagia and prevent complications.
Search for other papers by Simone Antonini in
Google Scholar
PubMed
Search for other papers by Alessandro Brunetti in
Google Scholar
PubMed
Search for other papers by Benedetta Zampetti in
Google Scholar
PubMed
Search for other papers by Davide Boeris in
Google Scholar
PubMed
Search for other papers by Andrea Saladino in
Google Scholar
PubMed
Search for other papers by Renato Cesare Cozzi in
Google Scholar
PubMed
Summary
Osilodrostat is a novel, orally administered cortisol synthesis inhibitor, approved in 2020 by the European Medicines Agency (EMA) for the treatment of Cushing’s syndrome in adults. A significant amount of the studies currently available in the literature focus on treatment in patients with Cushing’s disease. However, data collected from patients treated with osilodrostat in real-life settings still represents a small entity. For this reason, in this article, we will discuss two real-life cases of patients with Cushing’s disease treated with this drug. The first report is about a 35-year-old woman with an adrenocorticotrophic hormone (ACTH)-secreting adenoma. After non-curative trans-nasal-sphenoidal (TNS) surgery, due to a small remnant of the adenoma, medical therapy with osilodrostat achieved fast and effective biochemical and clinical response. During treatment, progressive increase of ACTH levels and an enlargement of the pituitary remnant were documented, with planned radiosurgical treatment. The second case reports a 32-year-old man diagnosed with Cushing’s disease in 2020, who, after surgery refusal, started osilodrostat at progressively up-titrated doses, according to 24 h urinary free cortisol levels, up to 5 mg twice a day. With osilodrostat, the patient reached biochemical and clinical control of disease until TNS surgery in October 2021, with complete remission. The first post-surgical biochemical assessment was equivocal in spite of a transient clinical hypoadrenalism, reverted after 2 months with the restoration of physiological hypothalamic-pituitary-adrenal axis (HPA) function.
Learning points
-
Osilodrostat is a potent oral drug viable for Cushing’s disease as medical therapy when surgery is not feasible or remission cannot be reached.
-
Osilodrostat proves to be a safe drug and its main adverse effect is hypoadrenalism, due to the adrenolytic action of the compound.
-
Osilodrostat needs a very tailored approach in its clinical use because there is no correlation between the level of hypercortisolism pre-treatment and the dose required to reach disease control.
Search for other papers by David Lin in
Google Scholar
PubMed
Search for other papers by Jai Madhok in
Google Scholar
PubMed
Search for other papers by Jason Bouhenguel in
Google Scholar
PubMed
Search for other papers by Frederick Mihm in
Google Scholar
PubMed
Summary
We describe a case of a 47-year-old patient who presented with severe lactic acidosis, troponinemia, and acute kidney injury after receiving 8 mg of intramuscular dexamethasone for seasonal allergies in the setting of an undiagnosed epinephrine-secreting pheochromocytoma. This case was atypical, however, in that the patient exhibited only mildly elevated noninvasive measured blood pressures. Following a period of alpha-adrenergic blockade, the tumor was resected successfully. Steroid administration can precipitate pheochromocytoma crisis that may present unusually as in our patient with mild hypertension but profound lactic acidosis.
Learning points
-
Steroids administered via any route can precipitate pheochromocytoma crisis, manifested by excessive catecholamine secretion and associated sequelae from vasoconstriction.
-
Lack of moderate/severe hypertension on presentation detracts from consideration of pheochromocytoma as a diagnosis.
-
Lactatemia after steroid administration should prompt work-up for pheochromocytoma, as it can be seen in epinephrine-secreting tumors.
-
Noninvasive blood pressure measurements may be unreliable during pheochromocytoma crisis due to excessive peripheral vasoconstriction.
Search for other papers by Cody Harper in
Google Scholar
PubMed
Search for other papers by James Michael in
Google Scholar
PubMed
Search for other papers by Tarek Rahmeh in
Google Scholar
PubMed
Search for other papers by Vicki Munro in
Google Scholar
PubMed
Summary
The most common sites of distant metastases of papillary thyroid carcinoma (PTC) are lung and bone. Widespread distant metastases of PTC are rare and associated with poor overall prognosis. Metastases to sites such as liver and pancreas are extremely rare, and literature is sparse on overall survival. In this report, we present a 57-year-old man whose initial presentation of PTC was with pancreatic, liver, and lung metastases, and subsequently developed metastases to bone and brain. He underwent a total thyroidectomy, neck dissection, and tracheal resection. Pathology revealed a predominant columnar cell variant PTC with focal areas of tall cell variant, and genomic sequencing showed both PIK3CA and BRAF gene mutations. Radioactive iodine ablation with I-131 did not show any uptake in metastatic sites and he had progression of the metastases within 6 months. Therefore, therapy with lenvatinib was initiated for radioactive iodine refractory disease. Our patient has tolerated the lenvatinib well, and all his sites of metastases decreased in size. His liver and pancreatic lesions took longer to respond but showed response 6 months after initiation of lenvatinib, and he remains on full dose lenvatinib 18 months into treatment.
Learning points
-
Papillary thyroid carcinoma (PTC) usually metastasizes to lung and bone but can rarely occur in many other sites.
-
Patients with distant metastases have significantly worse long-term prognosis.
-
Lenvatinib can be an effective treatment of radioactive iodine refractory PTC with rare sites of distant metastases.
-
Lenvatinib can be an effective treatment of PTC with BRAF V600E and PIK3CA mutation.
Search for other papers by Nnennaya U Opara in
Google Scholar
PubMed
Summary
Diabetes mellitus type 2 (DM-2) is one of the important causes of low-grade chronic inflammation (meta inflammation) seen in almost all tissues in the body. Other possible mechanisms involved in the development of lower urinary tract symptoms (LUTS) with DM-2 are the hypertonicity of the peripheral sympathetic nerves and hyperinsulinemia effects on the autonomous nervous system activity. These further suggests that abnormalities in glucose homeostasis influence the hyperproliferation of the prostate cells resulting in benign prostatic hyperplasia (BPH). Similarly, hepatic steatosis, a form of non-alcoholic fatty liver disease (NAFLD) prevalence among patients with DM-2, is as high as 75%. NAFLD has no symptoms in most diabetic patients. In this study, we present a case of a 64-year-old Black male who had worsening urinary urgency and hesitancy for 4 months, with increasing abdominal girth. Patient was found to have symptoms, diagnostic studies, and physical exam findings indicative of BPH and fatty liver disease. He was treated with hepato-protective medications, tighter control of his blood glucose levels, and blood pressure meds for 13 months. Upon follow-up, most of his symptoms were resolved. Timeline of BPH resolution and decrease in liver size following treatment suggest that DM-2 has a strong correlation with the development of BPH and fatty liver disease in most patients living with diabetes.
Learning points
-
Men with type 2 diabetes mellitus (DM-2) tend to have significantly lower serum PSA level, lower testosterone levels, and larger prostate volume compared to non-diabetic male patients.
-
Patients with DM-2 have higher prevalence of hepatic steatosis, liver cirrhosis, and end-stage liver failure.
-
The role of metformin in reducing hepatic steatosis as stated by several studies is yet to be validated as our patient has been on metformin for 22 years for the management of DM-2 with fatty liver disease.
Search for other papers by Keerthana Haridas in
Google Scholar
PubMed
Summary
Human T-cell lymphotropic virus-1 (HTLV-1) causes adult T-cell leukemia and lymphoma (ATLL) and is a rare but important cause of hypercalcemia. A 53-year-old male with HTLV-1-associated myelopathy presented with acute on chronic bilateral lower extremity weakness and numbness. Initial blood work revealed hypercalcemia with corrected calcium of 16.2 mg/dL (8.5–11.5) with normal levels of phosphorus and alkaline phosphatase. Workup for hypercalcemia revealed parathyroid hormone (PTH) of 14 pg/mL (10–65), 25 hydroxy vitamin D at 19.6 ng/mL (30–100), 1,25 dihydroxy vitamin D at 6.7 pg/mL (19.9–79.3), thyroid-stimulating hormone of 1.265 μIU/mL (0.5–5), undetectable PTH-related protein (PTHrP) and lactate dehydrogenase of 433 U/L (100–220). The urine calcium creatinine ratio was 0.388. Reverse transcriptase PCR was positive for HTLV-1 and negative for HTLV-2. Peripheral blood flow cytometry and lymph node biopsy confirmed ATLL. He received treatment with fluids, calcitonin and denosumab after which serum calcium levels fell (nadir: 7.7 mg/dL) and then normalized. Humoral hypercalcemia in this setting is mediated by receptor activator of nuclear factor-kappa B ligand (RANKL), PTHrP and other cytokines. PTHrP levels depend on levels of the TAX gene product, cell type and lymphocyte-specific factors. Thus, a low level, like in our patient, does not rule out HTLV-1 infection/ATLL as the cause of hypercalcemia. Hypercalcemia is known to be responsive to monoclonal antibodies against RANKL given the compound’s role in mediating hypercalcemia in these cases.
Learning points
-
Human T-cell lymphotropic virus-1 infection and adult T-cell leukemia and lymphoma are associated with high rates of hypercalcemia and hypercalcemic crises.
-
Hypercalcemia in these cases is mediated by osteoclastic bone resorption carried out by several agents including receptor activator of nuclear factor-kappa B ligand, parathyroid hormone-related protein (PTHrP), macrophage inflammatory protein 1 alpha, interleukins, etc. A normal PTHRrP does not rule out humoral hypercalcemia of malignancy in this setting, as indicated by this case.
-
Hypercalcemia in such settings is highly responsive to monoclonal antibodies against RANKL given the role the ligand plays in resorptive hypercalcemia.