IntroductionTuberculosis is a chronic granulomatous infection caused by Mycobacterium tuberculosis (MTB). It is a common disease in low- and middle-income countries of the world. Tuberculosis (TB) primarily affects the lungs but can also affect other organs (extra-pulmonary) such as the lymph nodes, genitourinary system, bones and joints, gastrointestinal system, central nervous system, and spine.Breast tuberculosis (BTB) was first described by Sir Astley Cooper in 1829 [1, 2]. It’s characterized by granulomatous inflammation of the breast parenchyma, which may present with cutaneous manifestations including skin changes and ulceration. The breast is a rare site of manifestation of extra-pulmonary tuberculosis, especially as a primary manifestation, even in tuberculosis-endemic countries [3-6]. It generally affects women of reproductive age, commonly between 21 and 30 years old [3, 4, 6, 8, 10].The incidence of BTB is estimated to account for 0.1% of breast diseases in developed countries but reaches 3% to 4.5% in endemic countries [3, 6, 7, 9, 10]. The factors thought to be responsible for the higher incidence of the disease in the developing world include HIV/AIDS, an increase in the prevalence of multi-drug-resistant tuberculosis, and the increasing age of lactating women [5, 11].The clinical presentation of BTB is often insidious and non-specific, mimicking the signs of breast carcinoma. It can present as a breast abscess, a unilateral painless mass, or a sinus and it may sometimes mimic breast cancer [10]. Clinically and radiologically, BTB can resemble a pyogenic breast abscess, fibroadenoma, or carcinoma. The most concerning differential diagnosis is carcinoma of the breast because of the inherent consequences of the treatment, including chemotherapy. The role of microbiology tests in the diagnosis of BTB is, therefore, paramount. Histologic confirmation requires demonstration of acid and alcohol fast bacilli (AAFB), GeneXpert, culture, or polymerase chain reaction (PCR) as means of identifying the causative mycobacterial organism.This report illustrates a case of GeneXpert-confirmed BTB encountered in a tertiary hospital in Ethiopia and highlights the salient features that may aid in diagnosis.

A case of double ANCA negative Granulomatosis with polyangitis:

A document by Gashaw Solela . Click on the document to view its contents.

Introduction: Infective endocarditis is associated with many complications; these include cardiac, metastatic, neurologic, renal, musculoskeletal, and pulmonary complications. Renal complications of IE include glomerulonephritis, renal infarction or abscess following septic embolization, and drug-induced acute interstitial nephritis.( 1) Acute renal failure, defined as a serum creatinine of ≥2 mg/dL (177 mmol/L), has been described in up to one-third of patients with infective endocarditis. Infective endocarditis can rarely be complicated by RPGN, and this poses diagnostic and therapeutic challenges. There are only a few case reports of infective endocarditis associated with RPGN in the literature. In a study of 595 IE-related RPGN, the prevalence of Infective endocarditis-related RPGN was found to be 3.4%. ( 2). These studies have also found that it was difficult to differentiate these cases from other differentials, like vasculitis. In a retrospective review of 24 cases of infective endocarditis associated with RPGN, all patients presented with fever and multi-system organ involvement. The involved organs include the heart, kidney, lung, skin, joint, spleen, lung, nervous system, and eye. (2) All of these patients presented with rapid deterioration of renal function within 1 week to several months, along with glomerular hematuria and proteinuria. The mean peak serum creatinine was 6.7 mg/dl (range 3.0–16.1 mg/dl). The most commonly involved valves are the aortic and mitral valves. All of these patients were treated with intravenous antibiotics, and some of them required surgical and immune suppressive therapies. Here we present the case of a 34-year-old known CRVHD patient for whom a prosthetic mitral valve replacement was done 14 years ago for severe mitral stenosis. The patient presented with flank pain, a decrease in urine amount, and a raised creatinine of 3 days duration. Initial workup with Tran’s thoracic echocardiography missed valvular vegetation. She was about to be started on immune suppressive therapy until repeat echocardiography revealed a 3cm by 3cm aortic and mitral valve vegetation. She was treated with intravenous antibiotics alone and diuretics, and she didn’t require immune suppressive therapy. She was discharged with improvement, and follow-up trans-thoracic echocardiography revealed resolution of the vegetation.Case presentationA 34-year-old female patient who was on follow-up for chronic rheumatic valvular heart disease, for whom a prosthetic mitral valve replacement was done 13 years ago for severe mitral stenosis, came to our hospital OPD with the complaint of flank pain of three days duration. The pain was dull and aching in type and involved both her flank areas. Associated with this, she also had reddish discoloration of the urine, a decrease in urine volume, and lower extremity swelling of the same duration. On further inquiry, she admitted that she had a low-grade intermittent fever, loss of appetite, and easy fatigability, which started during this illness period. She was taking anticoagulation and antibiotic prophylaxis. Other than the symptoms mentioned above, she had no orthopnea, PND, chest pain, or chronic medical illnesses like HIV, diabetes mellitus, or hypertension. On physical examination, she was afebrile; her blood pressure was systolic 110 mmHg and diastolic 80 mmHg; her pulse rate was 78 beats per minute; and her respiratory rate was 18 breaths per minute. Cardiovascular examination revealed a flat JVP and a Grade IV holosystolic murmur that is best heard at the apex. Further examination of the genito-urinary system showed bilateral flank tenderness, and musco-skeleton examination showed grade II pitting edema involving both extremities. We investigated her with a complete blood count, which showed a WBC of 25,000, a neutrophil percentage of 91%, and hemoglobin and platelet counts that were within normal. She had an elevated acute phase reactant (ESR: 68 mm/hr). Her serum creatinine was 8.5 mg/dl; her baseline serum creatinine was normal 2 weeks prior to our hospital visit. (Diagram 1, trend of serum creatinine). Urine analysis showed proteinuria and many red blood cells, and the 24-hour urine protein determination was 244 mg. Serology tests like ANA, hepatitis B surface antigen, hepatitis C antibody, and HIV tests were all negative. She was further investigated with a chest X-ray, which was normal, and an ECG showed features of atrial fibrillation with a fast ventricular response of 165 beats per minute (Figure 1). With the initial suspicion of Infective endocarditis, we investigated her with a blood culture and echocardiography. Blood culture had no microorganism growth. Initial transthoracic echocardiography was normal. Repeated transthoracic echocardiography revealed 3cm by 3 cm of vegetation on the aortic and prosthetic mitral valves, severe aortic stenosis, moderate aortic regurgitation, moderate mitral stenosis, severe tricuspid regurgitation, and mild pulmonary hypertension. Mild biventricular systolic dysfunction with an ejection fraction of 45% She was admitted to our hospital, and a diagnosis of rapidly progressive glomerulonephritis was made, and we planned to give her methylprednisolone pulse therapy. However, the repeated echocardiography showed vegetation over both the native valve (aortic) and the prosthetic valve (mitral valve), as described above. Later, a diagnosis of native and prosthetic Infective endocarditis complicated by rapidly progressive glomerulonephritis was made, and the plan to give pulse therapy was cancelled. For this diagnosis, we treated our patient with intravenous antibiotics and diuretic therapy. After two weeks of these treatments, flank pain and lower extremity edema subsided. Serum creatinine recovered, and the patient was discharged with improvement. She was seen on follow-up, and she was in good condition. The follow up trans-thoracic echocardiography showed aortic vegetation, which has decreased in size; otherwise, prosthetic mitral valve vegetation was not seen (Figure 2), and the follow-up serum creatinine was normal.Discussion Infective endocarditis is an infection of the endocardial surface of the heart, and it can be an infection of one or more heart valves or of the intra-cardiac devices. It is a rare disease with an estimated yearly incidence of 3–10 cases per 10,000 people (3). The term native valve endocarditis refers to a cardiac infection that involves the leaflets of the valves, the endocardial surface, chordae tendinae, congenital defects, and anastomosis sites. Prosthetic valve endocarditis (PVE) is a microbial infection of parts of a prosthetic valve or reconstructed native heart valve. (4). Patients with infective endocarditis (IE) can develop several forms of kidney disease. These include bacterial infection-related immune complex-mediated glomerulonephritis (GN), renal infarction from septic emboli, and renal cortical necrosis. Rapidly progressive glomerulonephritis (RPGN) is a clinical syndrome manifested by features of glomerular disease in the urinalysis and by progressive loss of kidney function over a comparatively short period of time (days, weeks, or a few months). The treatment we give to patients with Infective endocarditis can also lead to kidney injury. ( 5,6,7) Diagnoses of Infective endocarditis as a cause of RPGN have therapeutic implications. Most patients with RPGN need immune suppressive therapy. However, patients whose RPGN is caused by Infective endocarditis may be successfully treated with antibiotics alone and may not need immune suppressive therapy. Our patient has clinical and laboratory features suggestive of RPGN, and we planned to give immune suppressive therapy. It is not uncommon for trans-thoracic echocardiography to miss valvular vegetation. The initial echocardiography didn’t show valvular vegetation, but the repeated one showed three small-sized aortic and prosthetic mitral valve vegetations. Our patient fulfills diagnostic clinical criteria for both native and prosthetic valve infective endocarditis (8), and a diagnosis of native and prosthetic valve infective endocarditis complicated with RPGN was made. Infective endocarditis involving multiple valves has rarely been described, and there are only a few case reports of simultaneous native and prosthetic valve endocarditis. (9) Multi-valvular and simultaneous native (aortic) and prosthetic (mitral) valve involvement is what makes our patient’s presentation unique. Studies have shown that patients with Infective endocarditis-associated RPGN can be treated with intravenous antibiotics, and some of these patients may need immune suppressive therapy, particularly when kidney function does not improve after antibiotic therapy. (2) We treated our patient with intravenous antibiotics, and she showed clinical improvement, and serum creatinine showed recovery over 2 weeks. Our patient would have been subjected to immune suppressive therapy if the diagnosis of infective endocarditis had been missed.Conclusion Native and prosthetic valves Infective endocarditis may be rarely complicated by rapidly progressive glomerulonephritis. The diagnosis of Infective endocarditis may be missed, especially if the vegetation is small, as observed in our patient. Detection of infective endocarditis as a cause of RPGN may eliminate the need for immune suppressive therapy, as observed in our patient. Our case illustrates that not all RPGN require immunosuppressive therapy. So, it is important to have a high index of suspicion of infective endocarditis as a cause of RPGN in appropriate clinical conditions. Author contribution: Yitagesu Getachew: Conceptualization, Investigation, Validation, Writing – review & editing. Zerubabel Getahun: Investigation Writing – original draft. Getachew Wondafrash: Conceptualization, Supervision Validation, Zemenay Asmare: Formal analysis Writing – original draft. Gashaw Solela: Supervision, Writing – review & editing. Beka Aberra: Supervision Validation. Merga Daba: Writing – original draft ,Writing – review & editing.Data Availability Statement The data that support the findings of this case report are available from the corresponding author upon reasonable request.Ethical ApprovalThe authors’ institution does not require ethical approval for publication of single case report.Consent for PublicationThe patient’s family provided written informed consent for the publication of details including, history, physical findings, laboratory reports, and imaging.FundingNo funding was used in this case report.DisclosureWe authors have no conflict of interest.

Rare Association of Plasmodium Vivax Malaria with Pulmonary Thromboembolism: A Case Report Gashaw Solela1 Merga Daba2 Zerubabel Getahun2 Yared Getachew2 Dejene Girma31Department of Internal Medicine, Yekatit 12 Hospital Medical College, Addis Ababa, Ethiopia2Department of Internal Medicine, College of Health Sciences, Addis Ababa University, Addis Ababa, Ethiopia3Department of Internal Medicine, St. Paul’s Hospital Millennium Medical College, Addis Ababa, Ethiopia

Polyserositis Caused by Tuberculosis in a Young Female Patient with Hypothyroidism: A Diagnostic ChallengeGashaw Solela1 Ferhan Kedir1 Merga Daba21Department of Internal Medicine, Yekatit 12 Hospital Medical College, Addis Ababa, Ethiopia.2Department of Internal Medicine, College of Health Sciences, Addis Ababa University, Addis Ababa, Ethiopia.Correspondence: Gashaw Solela, Department of Internal Medicine, Yekatit 12 Hospital Medical College, [email protected], +251-921562995, ORCiD ID - 0000-0002-2233-9270

IntroductionHereditary hemorrhagic telangiectasia (HHT), also referred to as the Osler-Weber-Rendu syndrome, is a rare autosomal dominant hereditary disease that results in abnormal vasculogenesis in the skin, mucous membranes, and visceral organs such as the liver, lungs, and brain [1]. The prevalence of HHT ranges from one in every 5,000 people to one in every 8,000 people with an estimated 85,000 cases in Europe [2, 3] and the rate of diagnosis is lower in lower socioeconomic groups [4].Four important genes, including ENG (endoglin), ACVRL1 (activin receptor-like kinase 1), SMAD4 (mothers against decapentaplegic homolog 4), and GDF2 (growth differentiation factor 2), have recently been linked to the underlying mechanism of HHT [5]. Arterio-venous malformations (AVMs) are caused by mutations in these genes that interfere with the TGF-β (transforming growth factor)-beta signaling pathways in vascular endothelial cells, which impair cell division [5]. Heterozygous mutations are the common cause of the two primary kinds of HHT. Endoglin (ENG) is mutated in HHT1. Patients, especially women, with this type are more likely to develop pulmonary and cerebral AVMs. Activin A receptor-like type 1 (ACVRL1), commonly referred to as ALK1, is mutated in HHT2. Of the mutations known to cause HHT, ENG makes up around 61% and ACVRL1 makes up about 37% [7, 8].About 90% of those with the condition experience recurrent nosebleeds, which usually begin in childhood. Other symptoms include gastrointestinal bleeding (25–30%), which can cause melena and severe symptomatic microcytic anemia; pulmonary AVMs (50%) that can cause dyspnea, hemoptysis, paradoxical emboli, and cerebral abscesses; cerebral AVMs (10%) that can cause headache, seizures, and focal neurological deficits; and hepatic AVM (40–70%), which are typically asymptomatic but might show signs of high output cardiac failure and hepatic decompensation, ultimately necessitating liver transplantation [9].Clinical diagnosis of HHT is made using the Curacao criteria, which include first-degree family history of HHT, visceral involvement, recurrent spontaneous nosebleeds, and mucocutaneous telangiectasias. If three or more criteria are met, the diagnosis is considered to be conclusive; if only two criteria are met, the diagnosis is considered to be suspected HHT [10] [Table 1]. If less than two criteria are met, the diagnosis is considered to be unlikely HHT.Table 1 Curaçao diagnostic criteria for hereditary hemorrhagic telangiectasias